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So we'll be live in a second. Mhm. Hi, everyone. Welcome back. Uh, we're just going to be resuming the next session of the day, which is renal session in a minute or so. So we'll just give everyone else a chance to come back for any breaks and, and we'll hand over, um, go if you introduce. Yeah. Hello. Hi. So we have uh, Doctor S Shema here. He's a renal registrar. Uh, and I'm here. So we'll get all your questions answered for renal session today. Uh So doctor Ss over to you. Thank you and thank you everyone. Thank you, Gareth. So, um, I'm, I'm one of the renal registrar. I just finished my I MT three Renal in General hospital. So, um, have been working in renal medicine for the last six months. So I'm covering as much as I can about renal medicine in around two hours and some electrolyte disturbances. So I'm gonna just go through topic by topic and not gonna go through too much on physiology, but just to, um, give her a little bit of whistle stop to her. So I'll be talking about uh physiology, the nephrotic and nephritic syndromes all the nephritis, renal vein, throm renal vein and renal artery and problems. Polycystic kidney disease, pyonephritis, A KD, then going on to dialysis and then some of the rarer conditions such as HH US and HSP uh rhabdomyolysis very commonly seen in the hospital and just a little bit about electrolyte disturbances. Um as that's also very important for hospital medicine and comes up in exams as well. So just to have a quick recap of um renal physiology here, just on the slide. So, looking at the right, you've got your afferent arterial um glomerular capillaries which go into Bowman's capsule and then your urinary duct and everything and then your efferent arterial and the peritubular capillaries go around the, the proximal conjugated tubule, distal conjugated tubule. And this is all you have your various areas of where things are. So, um Bowman's Bowman's capsule is your glomerular filtrate area. Then you've got your um PCT. So where all the multiple different transporters are? I won't go into detail on each, each one. But um you've got your N ACL transporter, your potassium is transported, then you go into your loop of, you're descending them and you're sending them. So on each side, you've got your filtration of water and filtration of various ions as um as you'll know from physiology and then you've got your distal convul tubule. Now, the key thing of the key thing about all of this is just knowing where various things act So, for example, on your PCT, you've got actions of diuretics in your um in your DCT, you've got thiazides acting here and the distal part of your D CT is where osmotic and potassium sparing diuretics act. And then in the collecting tubules, you've got the osmotic effect of ADH. But again, that's just very, just very, very briefly one slide. So now starting with um some of them, um some of the topics that you'd want to know about. So, nephrotic and nephrotic syndrome. So I've just stolen this diagram from on online. So firstly, um there's a lot of distinctions in the clinical presentation and there's a lot of distinctions and the ex exact definitions. So starting with nephrotic syndrome, nephrotic syndrome is defined when you have a low serum albumin, high amount of protein in the urine. So above 3.5 g in 24 hours, um A clinical syndrome of edema um dyslipidemia because of um dysregulation and lipids and lipid metabolism, hypercoagulability and reduced immunity. Your hypercoagulability is due to loss of antithrombin three in the kidneys. Now, the clinical syndrome is considered, let's say a a middle aged person presenting with peripheral edema, facial edema, frothy urine recurrent infections. Um in nephrotic syndrome, as I mentioned, there's a high amount of protein leak. So your protein of above 3.5 g a day will give you a very, very high amount of proteinuria. So if you did a urine dipstick, the protein would be plus plus plus and that's what gives you the frothy urine. Now, um in terms of red cells being in your being in your urine, they are generally not present present in your urine, but sometimes they may be present as well. Now, the causes of nephrotic syndrome, which will go into a bit more detail are minimal change, disease, membranous, nephropathy, and focal segmental glome glomerulosclerosis. Now, all of these conditions are part of multiple other conditions which can cause nephrotic syndrome as well. But I'll just be going into details about a few of them. Um The a whole two hour talk could be on nephrotic syndrome. Now, looking at nephrotic syndrome, it's slightly different. So you generally get hematuria, patients generally present quite, quite high hypertensive. So with um with quite high blood pressures, um the proteinuria is found but the proteinuria is a little bit more milder. So you might get a slightly lower amount of protein in the urine there. Um You also sometimes present if the patients present with very very severe Nephritic syndrome, you can get oligouria and uremia. So you can get symptoms of uremia such as uremic pericarditis, uremic encephalopathy, the uremic itch, nausea, vomiting. Now, looking at the key symptoms, you've got the hematuria, as I mentioned, the edema and the signs of uremia. Again, they will have protein in their urine but less protein. The key thing here is hematuria, hematuria is always present and red blood cell casts in the urine if you were there to send them off for further analysis, always present. Now, some of the causes of these um of uh Nephritic syndrome are iga nephropathy, which I'll go on to talk about post streptococcal glomerulonephritis, rapidly progressing glomerular nephritis such as anti GBM and anca vasculitis. Now, all of these conditions are generally less common than the conditions. So, nephrotic syndrome is generally slightly more common than nephrotic syndrome. Now, just a quick, I'm looking at the, looking at the causes again, another slide from online. So you sometimes get overlap between the two conditions. So looking at the nephrotic syndrome, we talked about post streptococcal, the rapidly progressing ones iga nephropathy, which is also known as Buerger's Disease Alport syndrome, which is one of the congenital ones. Now, there are some conditions which can give you an overlap of both such as diffuse proliferative goal, nephritis and membranal proliferative glomerulonephritis. Now, looking at nephrotic syndrome itself, I talked about these being quite important causes. The other one which is actually the most common cause of nephrotic syndrome right at the bottom is diabetic. So, diabetic um diabetic nephropathy presents as a nephrotic syndrome and looking at slightly rarer causes amyloidosis as well. So, again, in medicine, as I'm sure you've um known for ages common is common. So looking at this whole slide, you may not see any of these conditions, but you will see diabetic nephropathy and diabetic nephropathy is something you'll encounter almost every day in patients in hospital. And in general practice. Now, looking at, looking at a little bit of about each one and a little bit of detail. So minimal change nephropathy, the most common cause of nephrotic syndrome in Children presentation typically occurs with facial swelling around the age of two. And now that's um and it's, it's diagnosed based on the urine sample. Um, Children often it's a very difficult decision about doing a renal biopsy or not doing a renal biopsy. Again, taking by a pediatric nephrologist, the treatment is usually with steroids, so, steroids and if not responsive to steroids, you give immunosuppression treatment. So if your asked, an exam is the most common cause of um nephrotic syndrome in Children, minimal change. Now, the next one is membranous glomerulonephropathy. That's the most common cause of nephrotic syndrome in adults, apart from diabetic nephropathy. Now, approximately 80% of cases are primary and 70% of these primary cases are associated with anti pla two antibodies. So let's say you get somebody presenting with nephrotic syndrome. As an adult, you will do, you will do blood tests, just look at the kidney function, you'll do the urine sample, you'll also send off antibodies for anti pla two antibodies. And if these anti pla two antibodies are positive, you will, you will make a diagnosis of membranous glom nephropathy and that's the most associated antibody with that. Now, FSG S. So focal segmental occurs when scar tissue forms across the glomeruli. So this damages the filtration barrier. Now, this can be idiopathic or this can be secondary. Now, the key secondary causes are medications. So, and drugs. So, heroin bisphosphonates such as alendronic acid, risedronic acid or chronic steroid use, sickle cell disease can also cause this. Um you've got HIV infection where um HIV viral load is not controlled or just things aren't controlled. Therefore, you're, you're causing scarring on the kidneys from the HIV uh or reflux nephropathy. So, reflux nephropathy is when you have a chronic reflux of urine back into the kidney and this causes scarring over time. Now, when possible this diagnosis because it's scarring and often permanent damage, it should be confirmed by a renal biopsy with immunostaining and electron microscopy. Now, managing FSGS is often just managing the course. So you stop the, um, you stop the drug that's causing the problem. You control the sickle cell disease, you control the HIV, you control the reflux nephropathy. Um There are more and more treatments you can give steroids and you can give immunosuppression. But again, it's something that's taken by a nephrologist. That decision. That wouldn't be something taken by people who are F one F twos or trainees as such, even even renal registrars wouldn't be taking that decision. It would be discussed with a consultant. Now, the next one diabetic nephropathy. So this is known as diabetic kidney disease. It's a complication of both type one and type two diabetes, high blood glucose levels, damage the renal blood vessels over time. This um damages the glomerulus. So causes nephrotic syndrome. Protein leaks, approximately 30 or 40% of diabetic patients will go on to develop this. Now, think about the number of diabetic patients you see on a day to day basis as doctors almost it's very, very prevalent. So anyone with diabetes and edema bilaterally on the legs could have diabetic nephropathy. Now, the management of nephrotic syndrome depends on the cause. So, treatment can be divided supportive immunosuppression and renal transplant. So supportive measures, for example, dietary. So low sodium diet reduces peripheral edema, reduces swelling, reduces fluid retention diuretics. So, diuretics can be given to manage the um to manage the fluid overload. Um ace inhibitors and SGL T two inhibitors have been shown to reduce protein leaks. So, in the ace inhibitors Ramipril. So, in um in patients with diabetes and hypertension with a protein leak, ramipril is always recommended SGL T two inhibitors. So, um DPO Glyzin has been licensed now with nephrotic um syndrome. You get a leak of anti throm thrombin three which can cause clotting. So, VT prophylaxis is very important in patients with ang clotting, regular vaccinations due to the um um immunoglobulin losses and due to just you have a relative immunocompromised state statin therapy. So, giving, giving um um patients atorvastatin simvastatin or a statin for those with um deranged lipids and diabetic control. Now, with the SGL T two inhibitors, you get dual. So you get the diabetic control and you get the protein leak. Now, immunosuppression depends on the course. So the first two minimal change in membranous can be steroids, riTUXimab and further treatments. Now where uh where um nephrotic syndrome progresses rapidly or progresses to the point where you've got endstage renal failure, which we'll go on to talk about, you can be considered for a renal transplant or dialysis. So, again, those decisions are made by nephrologists and those are very specialist decisions. But any of these four conditions and all the other causes of nephrotic syndrome can lead you to having a renal transplant or can lead you to having dialysis as well. Now looking at Nephritic syndrome, so, IGA nephropathy. So, um as I think you'll remember during medical school, so this is when you get deposition of iga immune complexes in the kidneys, most common form of glomeris. So, the Nephritic syndrome worldwide, so you normally get hematuria one or two days after a upper respiratory tract or sinus infection. So it's it's rapid onset. So um it's similar to the second condition, but we'll talk about that treatment is usually supportive. So you treat the underlying infection, you can give ace inhibitors and SGL T two inhibitors to prevent, to um prevent further protein leak steroids can be given for progressive dis progressive disease. Most of these uh most of the IGA nephropathy resolves over some time. Now again, like with every condition, you can have the severe ovarian. So where you have advanced disease and iga nephropathies and responding to the conventional methods methods, you may need transplant. You may need renal replacement therapy, which is or you may need immunosuppression. Now, looking next at post streptococcal glomerulonephritis. So this is caused most commonly by group A beta hemolytic streptococci. So type 12 which causes pharyngitis and type 49 which causes impetigo. Now, this is presenting with hematuria or asymptomatic hematuria uh just about a week after the initial infection. So, IGA nephropathy is 1 to 2 days. So up to two, well, 2 to 4 days, I'd say maximum and post streptococcal is more than seven days after. Now, symptoms and signs of this can vary quite a lot. So sometimes you can get asymptomatic hematuria, sometimes you'll get symptomatic hematuria and sometimes you can get a full bone nephritis. So this can be quite a serious condition as well. So where you get a full bone nephritis, you may require admission to hospital and you may require further further investigations. Now, the key investigation here is a blood test for anti streptolysin O level. Now, this is to see whether you've responded to a streptococcal infection, usually finding titra of above 200 can be diagnostic of this condition. Um You'll also do complement three levels and ch 50 levels which can fall during active disease. Now, treatment of this condition is usually supportive. Again. So, restriction of protein, sodium fluid and in some severe cases, you will treat the edema and hypertension because as you, as um previously said, nephritic syndrome presents with quite severe hypertension. Now, in this condition, dialysis can be necessary but it doesn't normally lead to long term dialysis. It can just be in the short term where you've treated the initial full blown nephritis, the kidneys have recovered and you wean them off dialysis. Now treating the infective course or treating the group a strep and can cause remission. So where that's treated very, very quickly, some studies have shown treating it within the 1st 24 hours induces a remission of nearly 100% in some patients. Now looking at the other cause it's a rapidly progressive glomerulonephritis. This is another acute nephritic syndrome and that is uh associated with anti GBM antibodies. So, um anti glomerular basement membrane antibodies and it's an autoimmune glomerular nephritis and that's around 10% of cases. Now, the next slide, we'll talk about that in a bit more detail. But treatment for that is usually with steroids with or without cyclophosphamide or riTUXimab and sometimes plasma exchange to get rid of the antibodies. Now looking at um one second. Yep, looking at them, looking at these conditions in a bit more detail. Everyone will remember your ankar vasculitis as well. So looking at um looking at ankar vasculitis, you've got your pr three anca and you've got your MPR Anchor. So PMC and P ANCA. So looking at granulomatosis with polyangiitis, which was previously known as Wagner's granulomatosis. You get renal failure, epistaxis, hemoptysis and C ANCA positive. I'm looking at your Shag Strauss syndrome which is adult onset asthma, um eosinophilia and um sinusitis, shortness of breath. That's P ANCA positive. Now, looking just to remember your Anca cian is anti pr three Bianca's anti mpo. Now, these, these um these are generally positive in these conditions. Now, looking at another type of nephritis. So this is interstitial interstitial nephritis. So this is when inflammatory cells infiltrate the interstit of the kidneys. So looking at this diagram again, I've stolen from another website. So this can often be caused by allergic reactions. So you can get allergy reactions to various drugs. So, nsaids, beta lactam antibiotics, diuretics, PPI S anticancer drugs reaction to various types of infections or legionella, some cytomegalovirus streptococcus sarcoidosis or sl e. So, autoimmune conditions can cause it. Now, generally with this, you get what we call a rash, fever and eosinophilia. So that's the triad. Now, the key difference here is your in your urine, you'll get sterile pyura and you'll get eosinophil uria. So where you send your urine off a sampling to the lab, you're gonna ask for an eosinophil eosinophils in the urine to see whether there is eosinophils and often you'll find eosinophils in the urine. Now, in this condition, biopsies are often done as well. So you've got, um you've got um histopathology. We'll look at the biopsy slide and we'll tell you that there is deposition of eosinophils on the kidney. Now, the treatment is to often remove the drug or just treat the infection. So this is the best way to do that. Now, looking at, looking at the histopathology again, so you'll get interstitial edema with white cell infiltration and granulomatosis granuloma. Sorry. Now, this can become chronic with fibrosis, scarring and atrophy of the kidneys as well. But again, the key thing here where you get this condition, you get eosinophiluria, you get um it's caused by, caused by various drugs and the the key thing is to remove the drug and treat the infection. Now, looking at uh looking at a question for you guys. So I just, I've got a couple of MC QS in this talk. So a 45 year old type one diabetic arrives at the GP for his annual diabetic review, which of the following should be performed in this patient to assess if he has any signs of diabetic nephropathy. So, a 24 hour urinary protein B, serum, urine electrolytes, C renal ultrasound D urine acr in an early morning specimen or e urine acr in a late night specimen. What are your thoughts here? So, yeah, so the an the correct answer for this would be D as all of as all of you, as all of you had said So now all of these conditions will be, all of these, um, investigations will be very useful. Um, 24 hour urinary protein will give you a total amount of protein, serum, urine electrolytes. You, um, you al um, you already know that, um, you can already test that. You're assuming the patient has diabetic nephropathy at this point. So, there is a nephropathy renal ultrasound. Always important to e exclude obstructive uropathy. A urine acr Yes. In an early morning Specimen will tell you if this patient has diabetic nephropathy, cos it's specific to the albumin leak and it's always taken in an early morning Specimen, not a late night specimen. Now, the next next question I've got for you is a 72 year old man presents to his O PD nephrology appointment after a referral by his GP for low G fr and leg swelling. He's recently suffered from an L RTI and UTI both requiring antibiotic treatment. He has a history of sickle cell disease and polymyalgia, rheumatica. He is currently on alendronic acid, 70 mg once a week and prednisoLONE 10 mg once a day weaning go on examination. He has a bilateral leg swelling. What is the most appropriate uh next most appropriate investigation? So I know that somebody has um voted for O option D that. So again, in this, in this, in this, um in this question, all of the investigations are very relevant. So firstly, we need to look at what we're dealing with here. So you've got a 72 year old man. He's got a low G fr he's got leg swelling, so he's got a clinical diagnosis. His clinical diagnosis is nephrotic syndrome. If um if that makes sense to all of you, now, he's got a history of sickle cell disease can cause nephrotic syndrome. PMR not known for causing nephrotic syndrome but he's on steroids for that. He's also got um he's also had a recent L RTI and recent uti. So again, he's getting recurrent infections. So this is nephrotic syndrome. Now, which of these investigations for a fact will tell you he's got nephrotic syndrome. H BSS level will tell you the degree of sickle cell disease. Urine PCR will tell you the protein in the urine. Urine. ACR will tell you diabetic nephropathy, but he's not diabetic renal ultrasound will tell you that there's no hydronephrosis. There's nothing that, but again, there's nothing to really suggest that here. Uh all apart from the uti lipid profile will tell you he's got high cholesterol, but again, that can be a very variety of conditions. So the answer here is B urine PCR. So you want to do your urine protein to creatinine ratio. So you want to know whether the only thing way to actually diagnose he's got nephrotic syndrome here is to look at the amount of protein in the urine. Now, going back to this slide here just here. So, yeah, nephrotic syndrome, 3.5 g a day of protein leak. So you want to know your urine protein leak. And if it's above 3.5 g, you can confirm that this is nephrotic syndrome. So in, in terms of the reason for putting that question in, there was just to say that this is the most appropriate investigation to conclude that a patient definitely has nephrotic syndrome. Because if your urine PCR there's no protein leak, you'll have to think about other causes for this. Now, one more question. So a 33 year old female presents to the ambulatory unit after being referred by her GP for high BP on arrival, she has observations taken showing a high BP, um a slightly high temperature. Otherwise normal observations, blood tests reveal a creatinine of 195 with a slightly impaired um renal function there. We don't know if it's an A, we don't know if it's C KD at this point. And a normal full blood count, urine dip shows protein and blood on further enquiry. She suffered from a sore throat two weeks prior to this episode. What is the like most likely diagnosis here? So again, we're focusing on what's the most likely diagnosis here. So this one as we've gone, um as we've gone through, it is most likely to be post streptococcal glomerular nephritis. So just to just to recap iga nephropathy is 1 to 2 days after a febrile infection. Post streptococcal is more than seven days after um interstitial nephritis is to do with your eosinophils. Eosin eosinophilic granulomatosis with polyangiitis. This has to do with your um this is to do with your asthma in later onset in adults. And anti GBM vasculitis is to do with your antiglomerular basement membrane disease. So yeah, the answer is post streptococcal glomerular nephritis. Now moving on to the next topic. So, moving on to renal vein thrombosis. Now, renal vein thrombosis is where you get a blood clot in the renal vein can occur unilaterally can occur bilaterally. Now, this commonly occurs in nephrotic syndrome due to your loss of antithrombin. Three. Now loss of loss of antithrombin three leads to um hypercoagulability. So, in these hyper hypercoagulability states, you can get renal vein thrombosis. So as you can see in the diagram here, clear renal vein thrombosis. There other causes can include renal cell carcinoma. So tumor thrombus, other hypercoagulable states. So, acute hypercoagulable states. So such as pregnancy, um such as suffering from a malignancy such as suffering from conditions which can cause clots. Essentially. Now, symptoms of a renal vein thrombosis are acute renal vein, thrombosis, R VT, acute flank pain, nausea, vomiting fever and a rapid decline in G fr. Now, I am I appreciate that this can mimic uh other conditions as well. Now, your diagnosis is um made by imaging. So generally done an MRI scan or a CT scan of the kidney. So they generally present having a differential diagnosis here. So you um a patient presenting with something like that can be pyonephritis can be a renal stone, can be a renal vein, thrombosis can be an infarcted kidney can be multiple things. So often you just have to pick um the most appropriate scan, which would be a non contrast CT K UB. And then moving forward, you will do the more detailed scan depending on what you find. Now, treatment depends on the symptoms and severity. So in hospital patients are often given an IV unfractionated heparin infusion. Now, this is purely because unfractionated heparin is less um damaging to the kidneys, outpatients, um Warfarin or no A. So you can titrate the dosage to renal functions. So you've got various no a there, Apixaban riv and doxy. Now, in severe cases where you've got um where you've got a very clear thrombus that's acute or can be removed, you can do mechanical thrombectomy. Now, there are very few centers around the UK which do this. This is an IR procedure in patients who've got, let's say an acutely infarcted kidney who are very unwell. You may consider thrombolysis again, very rare. And the other thing is where you've got where you've got a renal vein, thrombosis causing capsular rupture of the kidney. You may need to do an urgent nephrectomy. So again, the key thing is these patients need to be anticoagulated and in serious you have severe cases depending on what the imaging finds. Contrast imaging to be done, depending on what you see, you may need to consider surgical options. Now, the next one is renal artery stenosis. So this is typically due to vascular disease or due to fibromuscular dysplasia. Now, in patients where this is um important is often you get patients presenting with difficult to control or accelerated hypertension. Um These patients are often given ace inhibitors, very commonly used for treating hypertension such as ramipril. Now, when you uh initiate ramipril, you may get an acute drop in your renal function or you may get recurrent flash, pulmonary edema. So looking at, looking at these two diagrams you've got on the bottom one, you've got a normal renal artery on the right and you've got a stenos renal artery on the left. This is again contrast imaging. Now, the diagnosis of renal artery stenosis is made on an Mr renal angiogram. Now, above 30% stenosis has been defined as having a stenosis renal artery. Now, the treatment of this, because surgical options can be quite invasive, depends on the degree of stenosis and the symptomology. So you can just treat this supportively with treating the hypertension and monitoring it. But percutaneous renal and artery angioplasty is recommended for stenosis above 80%. So, depending on your, depending on your symptoms, depending on how bad your symptoms are it. Um That that's the treatment. Now, sometimes you can just give supportive medications for your hypertension ace inhibitors can often be the treatment. But again, with renal artery stenosis, it's quite um quite difficult to manage. And often in patients who the way the stenosis is getting worse and worse and worse, you may need to really do this renal artery angioplasty. Again, very difficult to very limited centers around the UK do this because it's vascular vascular would be performing this or IR now, one of the most common things, um renal registrars get bleeped about so acute kidney injury. Now, this is a very, very big topic. So um just going through um things in very, very varying degrees. So AK is defined as a rapid drop in kidney function diagnosed by measuring serum creatinine. So looking at the top right, you've got AK one AKI two AK three, everybody would have seen these on blood tests. So AK I one is defined as a serum increase of creatinine of more than 26 within 48 hours or a 1.5 to 2 fold increase from baseline. You've also got a urine output criteria. So less than naught 0.5 mils of urine per, per kilo per hour for six consecutive hours is also the urine output definition of AKI one. Now going to AK two. So creatinine increase of 2 to 3 fold from baseline or um reduced urine output for 12 hours. And now AKI three serum creatinine will increase of a three fold increase of 354 or let's say a patient, let's say a patient comes in without any baseline blood tests and you need to start renal replacement therapy. This is an AKI three by definition. Um You've also got your urine output criteria. So, oligo urea for 24 hours or an urea for 12 hours. Now, the important thing to note is AKI is a reflection of another underlying cause AK I is not a diagnosis. So it's AKI secondary to something else. So as we looked at, we looked under the nice guidelines there. So AKI, I can be defined as prerenal, renal and postrenal. So your prerenal causes are most common. So looking at things like hypovolemia, hypo perfusion. So let's say somebody's come in with dehydration. So nausea and vomiting, gastroenteritis, sepsis, um just not eating and drinking, advanced dementia, um acute blood loss. So for example, somebody who's bled quite a lot post surgery as well. So patients, let's say um a young female has had ac section and has bled quite a lot can cause prerenal AKI. Other ones are heart failures. So, heart failure, when you have fluid overload, this fluid overload often causes hypoperfusion of the kidneys which can cause a prerenal AKI. So the treatment of a prerenal AKI due to heart failure is actually to give diuretics and to to remove the, to um remove the fluid and to get the renal, the kidneys perfusing better. Again. Now, your renal causes are due to intrinsic disease atn um acute tubular necrosis. I'll go on to talk about that glomer, nephritis, acute interstitial nephritis, which we spoke about H US, which I'll talk about rhabdomyolysis and um other conditions as well. Now, looking at, looking at your um this diagram at the bottom. So your AK I will AKI I is an acute condition. So all the definitions are within 24 to 48 hours. So that's acute. When it goes on to be more than three months, you've got deterioration in your kidney function, which then becomes irreversible AKI and then you go into D. So in AK you get adaptive repair and recovery of the kidneys and that would be an acute kidney disease. So AKI secondary to sepsis which has recovered. So you'll often see patient and clinicians saying AKI secondary to sepsis resolving. But when you get to DC KD is generally not reversible. So they will be around the same degree of KD, but you can get progression of KD or you can get AK I on C KD as well. Now, looking at your renal causes of AKI and your post renal causes. So atn so acute tubular necrosis refers to damage and death necrosis of the epithelial cells of the renal tubules. Now, this can occur due to ischemia. So, due to hypoperfusion or nephrotoxin. So as you all know, covered weight throughout medical school, gentamicin is nephrotoxic radio contrast agents. So such as iodine dye CISplatin. So these things can cause what you call an ATN. Now, the path of pneumonic um diag to diagnose ATN is muddy brown cost and urine analysis to confirm the necrosis. So if you do a urine sample, send it to the lab muddy brown cost ATM the epithelial um cells can normally regenerate. This is normally supportive treatment. So at ATN is usually reversible. So where you've got ischemia due to hypoperfusion, you um treat the hypoperfusion, give fluids, give ido give whatever's required with nephrotoxin gentamicin. So, gentamicin, you remove the insulting agent, you give loads of fluids, you check your gentamicin levels, regularly radiocontrast agents. Now, most hospitals have a protocol about um giving contrast with CT scans because there have been increases in ATS related to contrast in the UK, although a very small population CISplatin. So, CISplatin is a platinum based chemotherapy and this causes at and now, in that case, often it might be irreversible, but generally, you will just monitor the renal function over a number of months and often these patients may not need further treatments. Now, acute interstitial nephritis is the second one. So this involves acute inflammation of the interstitium. So the space between the tubules and the vessels, this can be caused by a immune mediated reaction. So, associated with some drugs, infections and autoimmune conditions. So, um it can be associated with nsaids, certain antibiotics, infections such as E coli or HIV can cause this or autoimmune conditions. So, sarcoidosis and Aleve now management again includes um includes treating the underlying course. So getting rid of nsaids, getting rid of the offending antibiotics, getting rid of the E Coli treating the HIV, treating the sarcoid or treating the SL E. Now because this is a inflammation rather than an ischemia, often steroids are given for this condition. So, steroids can reduce inflammation and improve recovery in a a in. So where you've got a in secondary to certain, it's quite common where you get it that there are um in the management of cancer. There are various new immunotherapies wherever you see such as pembrolizumab, um anything where you see Liz. So these are immunotherapies for cancer treatment. They cause an A in and they get, they cause um pembrolizumab induced kidney failure which is due to an A in steroids will be the mode of treatment. So where you have a in where other specialties are coming in, you will have an MDT approach with those specialties and steroids may be may be indicated. Now, post renal causes so involve obstruction to the outflow of the urine away from the kidney, causing back pressure into the kidney. So that's obstructive uropathy. So that can be renal stones can be, tumors can be B ph can be a bladder cancer can be constipation as well. Severe constipation can cause urinary retention again, very, very commonly seen in the elderly. In fact, when I was on call on Friday, I had five renal referrals. Three of those I requested to see TK UB and the answer was obstructive uropathy. So was not a renal renal input wasn't needed. So, and all of those patients were above the age of 65 and male. So, treating an AK I rim involves reversing the underlying cause and supportive management. Um, dialysis may be required in severe cases whether there is complications such as fluid overload, hyperkalemia, acidosis, symptomatic uremia. Now in ATN and A in where you've got very, very severe ATN or severe A in where you've got these criteria for dialysis, it may be required. So for example, I have seen patients with CISplatin induced at three which have required dialysis. I have seen patients, I have seen patients where I'm taking two doses of naproxen causing an A I and requiring dialysis. So again, the degree the clinical degree of these conditions can be very, very, very varied. So, but often the kidneys can recover with good treatment. Now, just looking at just looking at this diagram. So again, looking at your prerenal, intrarenal and P renal. So, prerenal, we mentioned hypovolemia, hypotension, decreased circulation, heart failure. Again, liver failure, I forgot to mention. So where you get liver failure, you can also get fluid overload and which causes decreased effect of circulation. So again, the treatment would be diuretics and getting treating the underlying cause of the liver failure, hemorrhage. So again, ace inhibitor or um angiotensin receptor blocker use can cause a prerenal ache. So, again, treat the cause intrarenal. So we spoke about, we spoke about the glomerular nephritis conditions, vasculitis, TTP and H US which I'll go on to talk about. These are all causes of intrarenal acho. And then we spoke about ATN and A in again, intrarenal causes. Now these again a very big bracket but often not the most commonly seen and finally, post renal causes. So looking at renal stones, bph malignancy and that's just the bladder out, there's various causes there. And again, these often go down into the urology side of things rather than the nephrology side of things unless the kidneys are damaged enough with these conditions to require dialysis or require specific treatments. Now, just another quick M CQ for you guys. So a 23 year old female presents to a with difficulty breathing and a two week history of generally feeling unwell, which started off with a sore throat. She reports a productive cough. Um her medications, her medications are history is significant for nsaids and uh for menorrhagia, chest X ray shows right sided consolidation. She's got a high temperature, high respiratory rate, um low oxygen sats, high heart rate, low BP and low urine output, high white cell count, high urea creatinine, sorry American units is around is around 300 there. So she's got a low G fr now this one again, very easy questions. So the most likely diagnosis here would be a pre renal AKI due to hypovolemia and sepsis. So again, the evidence here, high temperature, low oxygen sats tachycardia. Again, all hypovolemia and sepsis. Now, this could be post streptococcal glomeru because you had two week history. But again, you don't have enough evidence to suggest that iga nephropathy isn't this clinical syndrome? You don't have the urine, um you don't have the urine sample post renal AKI due to renal stones. She is um again, no symptoms there, prerenal AKI due to NSAID use. So the only cause here, she, she may, it may be that NSAID S are contributing to this AKI I but that's not the most likely diagnosis. So, again, on the balance of what's most likely it's a prerenal AKI due to hypovolemia and sepsis. Now, moving on to another very important topic in um renal medicines for chronic kidney disease. It's like we spoke about in AK. It's acute CKD is a chronic reduction in kidney function over three months. Now, d often starts as a asymptomatic syp um syndrome, an asymptomatic disease and as um renal function worsens, symptoms may become worse, symptoms may develop. Now, if you remember from renal physiology, the EGFR is based on somebody's creatinine age and gender. It estimates the glomerular filtration rate. So the rate fluid is filtered from the blood into bowman's capsule. Now, normal, normal kidney function is above 90 above 90. So above 90%. So there are various factors which can cause a decline in um renal function and can cause CKD and can cause this diagnosis. So, diabetic diabe diabetes, diabetic nephropathy, hypertension medications, glomerular nephritis, polycystic kidney disease. We'll go on to talk about some of these more. Now, a diagnosis of CKD is made when there are consistent results over three months. So, uh, here where you've got EGFR of above 90 normal and an EGFR of between 6089 with less than 3 mg per millim of protein. There is no CK D unless there is markers of kidney damage. Now, looking at the rest of your, looking at the rest of this chart to C KD. So you've got your definition by G Fr. So you've got CK D3 3 BC KD four KD five, which is end stage renal failure. And you also define the new definition of KD as per the K IGO guidelines. And the UK Kidney Association includes albumin creatinine ratio categories. So where you've got, let's say A G Fr of 30 on this line and you've got an albumin leak of 3 to 30 that's CK DG three BA two and where you've got, let's say A G fr of less than 15 with a really high albumin creatinine ratio. It's AK DG five A three which is endstage renal failure. Now, see, looking at this chart again, I won't go through each, each one but with, with the increasing albumin leak and with the decreasing G fr, your risk for dialysis goes up or your risk for needing what we call renal replacement therapy. So, renal replacement therapy, either hemodialysis peritoneal dialysis or a transplant. Now, looking at C KD again, we um we need to look at what's important for um people doing their exams and people in terms of um um primary and secondary care. So it recommends referral to a renal specialist when the G fr is less than 30 and a urine acr of more than 70 accelerated progression, five year risk of requiring dialysis over 5%. So, again, there are equations to do that and uncontrolled hypertension with more than four drugs used. Now, often a big degree of renal referrals. I see in my hospital are way before this is there. So a lot of this can be managed in the outpatient setting. KD. Very rarely unless it's severe progression of KD, which will, will bring you into hospital. Dialysis is usually started outpatient. So you have your fistula formed, you have your line put in usually outpatient. Now, treatment involves treating the underlying cause. So, diabetic and hypertension control. Again, we talk about diabetic nephropathy, hypertensive nephropathy, avoiding further nephrotoxic causes and nephrotoxic drugs. Now and treating the underlying cause. So, glomerulonephritis. So, treating that. So, treating all of these um shark straus Weers, treating your rapidly progressing diseases, treating your IG a, treating your post streptococcal because these can all be chronic in nature and cause KD and the damage can eventually become rever irreversible. Now, like we spoke about um medications and treatments. So things to slow disease progression. So in diabetic patients and hypertensive patients, ace inhibitors and angiotensin two receptor blockers are recommended and SGL T two inhibitors and are recommended. So these are often these have a good in and out effect on all conditions. So for example, ace inhibitors are good for diabetes. Ace inhibitors are good for hypertension. Ace inhibitors are good for heart failure, dapagliflozin, your SGLT two inhibitor is good for your kidneys. Protein leak is good for your diabetes and good for heart failure as well and also acts as a mild diuretic because the way it works is flushing out glucose into your urine and causing causing diuresis. So often, um these medications have been have been put there to slow disease progression. Now, management in advanced C KD, you get various complications. So where, where on this chart, you go into a G fr of 30 or below where you come into the referring to nephrologist category. So um where you get the severe reduction in kidney failure. So, in all of these criteria here, so patients often have a metabolic acidosis. So that can be managed with oral oral sodium bicarbonate, um iron and epo for anemia. So, in CKD patients, it's important to check their transferring saturations regularly. If your transferrin saturation is less than 20% you'll have an iron infusion. If it's above 20% you can start epo and you just titrate the dose of epo. Now, as you'll remember, Vitamin D metabolism occurs the last stages in the kidneys. So, Vitamin D alfacalcidol can be given. Now, a low phosphate and low potassium diet is recommended as CKD patients are, are um are um um are quite commonly seen with high phosphates and high potassiums. Hyperkalemia is a complication and sometimes you can get phosphate binders such as calcium acetate. Now where you've got end stage renal failure. So, looking here at your GFR of less than 15 and or you've got any of these criteria there. The renal specialist will begin talking about end stage renal failure and talking about renal replacement. So you often move from your general nephrology clinic to advanced kidney care clinic. So these patients begin to be counseled about dialysis and what they'd want and the various options for dialysis. Now your symptoms of CKD and end stage renal failure. So these symptoms often are when the KD is rapidly progressing or it's a lot worse. So you get fatigue pallor due to the anemia, foamy urine because your protein leak goes up. You can get nausea and vomiting, loss of loss of appetite, pruritus. So your uremic itch, these patients often present with edema and fluid overload, severe hypertension, peripheral neuropathy. So, looking at, looking at all of these, looking at all or at all of these conditions and looking at all of these um these um uh signs and symptoms, yeah, shortness of breath due to fluid overload, you can get a chronic cough, um gi symptoms. So where your C KD is caused by advanced diabetes, you can, you can get gastroparesis of the gut. So, gastroparesis can cause nausea, vomiting, constipation, and again, all of these symptoms are very nonspecific, but generally CD can have a lot of symptoms when it's progressing quite a bit. And often you look at the blood test. So certain things can differentiate between an AK and CKD. So where you have, for example, a metabolic acidosis or you have chronically high phosphate or you have an anemia or you have, you have high calcium or low calcium, you might be able to say this is a CKD rather than an AK. But again, all of these signs and symptoms and it's all clinical context. So now looking at dialysis and end stage renal failure. So going on to where, where you've got um need, need further treatment. So now dialysis is split up into acute dialysis and end stage renal failure causing chronic dialysis or long term dialysis. So, in hospital, your indications for acute dialysis, very important, no resistant acidosis. So, a metabolic acidosis not responding to treating the underlying cause, not responding to bicarbonate, not responding to conventional measures, treatment resistant hyperkalemia. So where you've given multiple rounds of hyperkalaemia treatment and the treatment, patients not responding now, certain drugs can cause um renal failure. So it can cause your ATN or A I which becomes irreversible. And that may present with the requirement with an at three for an acute dialysis. So it might be, let's say an ATM an ATM secondary to gentamicin or an A in secondary to nsaids. So let's say somebody's taking a ibuprofen and naproxen overdose presented with at three. So you'll say um an AK three causing A I secondary to NSAID use requiring acute dialysis, um severe fluid overload. So, where fluid overload is not responsive to diuretics is not respond to, is not responsive to things like CPAP. So sometimes patients with florid heart failure may require dialysis acutely as well. Often a forgotten indication for dialysis. But fluid overload is one of those indications. Um And the other one is it. So we spoke about the uremic nausea, vomiting, urine, uremic encephalopathy, uremic encephalitis, uremic pericarditis. These are all indications. Now, end stage renal failure is the main indication for long term dialysis. Now, your long term dialysis options are hemodialysis or peritoneal dialysis. And your acute dialysis option is hemodialysis or peritoneal dialysis. Again, these are all done on a renal ward. Now, these are various. Um these are divided into patient preference and patient preference and various things. So HD is when you're connected to a hemodialysis machine. We'll talk about that in the next slide. Um your blood is cleaned and um put against the membrane, which toxins come out and then your filtered blood has returned back to your kidneys, sorry, back to your body peritoneal dialysis. You put in a diacylate into your um peritoneal cavity. The filtering occurs again across your peritoneal membrane and all of this is filtered out and then your waste fluid comes out into a waste bag at the bottom there. So patients have various preferences. So HD requires three sessions, four hours a week in general. And PD requires three sessions overnight in a week or sometimes can be every day as well. So firstly, looking at hemodialysis, so you've got your line from artery to the operator, it goes through a pump and it's pump, um, it's um pushed through your tubing on your selectively permeable membrane with your dialyzing solution, your blood with waste products and your waste products pass through the membrane and you get your filtration and your osmotic effect. So your potassium comes out, your excess urea comes out. All of these can, all of this comes out and goes into the waste and your, your, your filtered blood is returned back to through a vein into your body. Now, the most common way this is done is through an A V fistula. Again, a v fistulas ones that are put in by vascular teams take six weeks to work. So like I said, blood is taken out of the body passed through the dialysis machine, pumped back into the body the blood passes are going across a semipermeable membrane, solutes, filter out across the membrane into a fluid called the diacylate the concentration gradients between the blood and the diacylate fluid cause water and solutes to diffuse out and across the membrane. So you can control this. So often dialysis patients during their sessions will have fluid taken off. So you can control the amount of fluid removed through the dialyzing solution and through the machine settings, anticoagulation is sometimes necessary to prevent blood clotting into the machine. And during the process, uh hemodialysis requires good access. So good access can either be done through a tunnel cuff catheter. So like a permacath or through a dialysis line or an A V fistula. So, um again, this is bent on patient and nephrologist. Um preference. Next type is peritoneal dialysis. So PD dialysis uses the peritoneal membrane, like I mentioned to filter the blood, a special solution in your diacylate block is inserted through a tech off catheter which goes into the abdomen. Um your fluid goes in, it's filtered across the peritoneal membrane. So your, your blood is effectively um your blood is cleaned and the solutes and soluble things come in and out. You have a drainage bag where your waste products, drainage from the peritoneal space and this is peritoneal dialysis. The plastic tube is inserted into the peritoneal cavity, as I mentioned. So, continuous ambulatory peritoneal dialysis. This is where dialysis solution is always in the peritoneal cavity. So you can do two hours, four hours depending on your nephrologists recommendations. And automated dialysis is another alternative. So this is where you are sleeping, you connect yourself up to the machine and the dialys laid bags and it just happens 8 to 10 hours overnight. So again, this is patient preference and preference dependence. So some patients prefer PD because it can be done at home. Um A recent interesting thing I found is that PD is one of the can actually be done in war zone. So for example, if somebody presents with has acute renal failure in a war zone, you put in a tube, connect the dili bag, remove the waste very quick and quick and easy to do in a war zone. So it's the, it's the preferential um dialysis in a war zone or a conflict zone. Now, this one has a few more complications. So you can get bacterial peritonitis. So again, and these um infections can be quite serious. Now, eventually, over time, your peritoneal membrane may become less permeable and you might get thickening and scarring. So PD may become less effective. Um Now again, ultrafiltration failure. So in the solution, you have sugars and dextrose. So the dextrose may be absorbed by your body and making ultrafiltration less effective. Now, because of dextrose in high sugar environment causing the infection and the high sugar, you may get weight gain. Now, sometimes some of these patients with PD tubes, they have psychological implications. So you always have a tube in your abdomen. You sometimes appear to be bloated overnight. You um it just uh reduces your quality of life in a different way that hemodialysis does. So, um again, with the advances in renal replacement therapy, you've got various different options and moving on to the last option, which is renal transplant. Now, now this again is a very um very um the ne the la the one of the last resort measures and the transplant waiting list in the UK is above, is currently above 1.5 years. So it's very difficult to get a transplant unless you have a relative wishing to donate to you. Now, your kidney is usually transplanted into your um um iliac fossa region. So either left or right side here. Um Now this one usually adds about 10 years to life compared to dialysis and significantly improves quality of life. And you can have up to three kidney transplants in your lifetime. So some people will have multiple kidney transplants and due to rejection due to failure of one failure of another. So patients and donor kidneys are matched using the HLA A antigen. So HLA A ab and C on chromosome six, you may not always have a perfect match, but you have to go with what you've got. So your in the operation, your native kidneys are not removed um unless it's kidney failure due to certain chronic conditions which you have to remove the kidneys where you may become septic, like chronic, chronic um reflux nephropathy such as pyelonephritis chronic, where you've got renal malignancies and stuff like that causing you to need renal transplant. Now, the kidney is inserted into one of the li fossas and its anastomose with the pelvic vessels, usually the external iliac and the ureter is connected with the bladder. After the transplant, the kidney will function immediately. So, function stat. Now, basiliximab is a monoclonal anti antibody targeting interleukin two receptors on T cells. Two doses are given after the surgery to prevent acute rejection. Now, all renal transplant patients require lifelong immunosuppression. So this is a this is another very important thing. So patients often started on triple therapy in initially after their transplants or tacrolimus, bloo and steroid or tacrolimus, cycloSPORINE and steroid or tacrolimus, uh azaTHIOprine and steroid. Now, um some signs and things you may see on a kidney transplant patient is you may see previous tunneled line scars. You may see the renal transplant scar, you may see PD scars, you may see an existing fistula, you may see a palpable implanted kidney. So for those in um in this talk who are wanting to actually potentially go into medicine, these are very common things in the M RCP exams. Now, where renal transplant patients come in with um with um things into hospital, their immunosuppression always needs review. Now, never hold a patient's immunosuppression without discussion with a nephrologist. So where patients are septic, where patients are anything, the only medication that would be appropriately to hold if somebody's already on another immunosuppressant would be mycolate. But again, this should always be discussed with the renal team on call or a senior medic and where patients are septic, where patients are very unwell hypotensive, you may consider doubling their steroid dose doses or giving IV hydrocortisone. No complications due to kidney transplants can involve rejection. So, hyperacute acute or chronic rejection. This is managed by the nephrology team. So um it can be messing with your immunosuppression treatment can be removing the kidney can be can be transplanting other kidney electrolyte imbalances. So, tacrolimus can cause hypomagnesemia can cause hyponatremia. So, managing the tacrolimus levels, managing the drugs, managing the new kidney working. Now, patients with uh one second patients with renal transplants because they're immunosuppressed, they're also um able to have quite commonly atypical infections. So where you get a renal transplant patient presenting with pneumonia or other things, this may often be atypical. So for example, last week, I had a patient, 40 something year old patient who had had a renal transplant 20 years ago. So it cannot 10 years plus your life had been on chronic steroids presented with uh flu like illness, shortness of breath and exertion and a dry cough on his um chest X ray. There was bilateral pneumonia. So I requested an immediate ct scan of the chest showing ground glass changes bilaterally and of quite severe nature. So we investigated for CMV pneumonitis and we investigated for Pneumocystis, gerovit pneumonia. So, his P JP came back positive and was started on co trimoxazole and was moved to the renal ward. So again, so in a normal patient without a renal transplant that that may have been something else. So COVID pneumonitis or a simple pneumonia, but in this case, it was AP JP or PCP pneumonia. So it's always important where you have patients with chronic immunosuppression to consider atypical things and atypical infections. Now, looking at this, um looking at this question. So um another M CQ. So a 58 year old man with a history of CKD presents to a with a complaining of increasing fatigue, nausea and vomiting. Over two weeks on examination, he appears pale and unwell. He reports no urine output for 24 hours. He denies any fevers or recent infections. Blood tests are performed. So, sodium normal, mildly hyperkalemic, high urea creatinine 900 g fr eight. So he is in um chronic renal failure. We don't know if this is an acute deterioration, but he appears to be fluidic. So, what is your most important next step in management for this patient? What are your thoughts here? So are your thoughts intravenous fluids, intravenous frusemide, referral for dialysis insulin dextrose, starting um starting ace inhibitors, arbs or intravenous antibiotics. So, there appears to be a mix between options, options B and C here. So in this patient, so in a patient with complete anuria. So firstly, let me tell you the answer. So the answer is C. So in this patient, all of these options would be reasonable. Options. Apart from option E now looking at what you've got here, so you've got a patient with D, he's coming in with what looks like progression of his D and he's acutely uremic, he's appears unwell. His potassium is safe. Now, in this case, giving a, if he was dehydrated, giving fluids would be appropriate, but he's got no urine output. So giving him fluids will just make him fluid overloaded, intravenous frusemide. So if this gentleman was oligo UIC, um so he still had some urine output. It would be appropriate to give fursemide. So you can try and see. But again, we don't know here is he fluid overloaded? Is he, is he um saturating low? Is he respiratory distress? Nothing to some, some suggest that c referral for hemodialysis. So yes. So this is a man with an already got a diagnosis of D no urine output for 24 hours, nausea, vomiting, fatigue, G fr of eight creatinine of 900 safe potassium. Give him dialysis. He can be transferred across the ward to a renal ward and start dialysis or in an intensive care setting. Start CVVH. Now, intravenous insulin and glucose. So this would treat hyperkalemia. His potassium level is just below the treatment mark. This is not to say that the blood test you may have done, he may now be hyperkalemic. So that wouldn't be wrong. But the most important next step is hemodialysis. Starting ace inhibitors are angiotensin receptor blockers. No role here, intravenous antibiotics. Now, if you had evidence where he's septic, where his temperature is high, hypotensive tachycardic antibiotics, you've got the golden hour of sepsis. So you could do the antibiotics a very quick measure and then refer for dialysis. But the main thing here is, this patient has got indications for acute dialysis. Now, moving on to your slightly more rarer conditions and slightly more interesting ones, I think. So, polycystic kidney disease. So this is a genetic condition in which healthy kidney tissue is replaced with cysts. It's um autosomal dominant and the genes affected are PKD one and PKD two. So chromosome 16 or chromosome four. So these conditions can often cause a lot of extrarenal manifestations. So you can get cerebral aneurysms, hepatic splenic pancreatic or prosthetic cysts. Uh you can get mitral regurgitation or you can get diverticula in the colon. So your complications can include chronic pain, chronic hypertension, which can be quite difficult to manage hematuria due to cyst rupture, recurrent infections, renal stones, and again, end stage renal failure. So often these patients because the the amount of cysts just goes up, you can get endstage renal failure. Now, ultrasound and genetic testing is used for diagnosis So your ultrasound shows cysts and your P KD one or PK D2 genes shows the genetic disposition, analgesia is given for acute or chronic pain, antibiotics for infection. So, I had one lady patient a few months ago who got kept getting recurrent infected renal cysts. So we had to actually refer her for bilateral nephrectomy for recurrent renal uh P um polycystic kidney cyst infection. And then she had to be started on dialysis and that had to be timed. So, drainage of symptomatic cysts can be performed by aspiration or surgery and dialysis or renal transplant for end stage renal failure. Now again, this um um on a on um where you um on examination for these patients, you can often have palpable kidneys. So, yeah, like I said, supportive measures, analgesia antibiotics and eventually around the age of 50 these patients may need dialysis or renal transplant. But again, before you give the dialysis or renal transplant, you need to make sure the polycystic kidney is ok, not prone to re recurrent infections or these kind of things. Now, pyonephritis, I thought I'd include a quick slide on this. So again, um this is generally a more urological or just general medical condition. So, inflammation of the parenchyma of the kidneys from a bacterial infection, um vesicoureteric reflux. So, bacterial colonization in your bladder vesicoureteric reflex and then causing uh Perris can be quite a severe infection, your child of symptoms of fever, lowering or back pain, nausea or vomiting again, can mimic renal stones, can mimic polycystic kidney disease, can mimic many things. Now, imaging is often done to exclude other pathologies like I mentioned kidney stones or abscesses. Um This can be an ultrasound or CT scan. It can sometimes mimic acute renal vein thrombosis as well. So you need to know these referral to a hospital if there are signs of sepsis on first line antibiotics are Keflex called amoxiclav trime. The key thing to remember in these patients is for a conventional uti 3 to 5 days of antibiotics for pyonephritis, 7 to 10 days because they are more serious infections. So always discharge patients or give patients a prolonged course of antibiotics. And because this is a very high risk condition of sepsis as well. So yeah, just a very quick slide there. Now looking at hemolytic uremic syndrome. So, i it's characterized by low red blood cells, acute kidney injury and low platelets. So this is most commonly occurs after an infective diarrhea. So, e coli 0157, everybody should know this in their head. Hemolytic uremic syndrome. Most common cause E coli 015787 only cause early symptoms are a bloody diarrhea, vomiting and fever. A few days later, you might get bruising low red blood cells and kidney failure diagnosis is made by blood tests showing renal failure, stool sample, showing your causative organism and a urine sample again, which can show hematuria. Often these patients require hospital admission. Al almost certainly supportive management with fluids, managing their hypertension, managing anemia, managing low platelets or blood transfusions, platelet transfusions. And often this can go into a full blown um renal failure. So severe AKI three, but most patients will fully recover from this. So looking again, e coli um 0157. So you can in this condition, you can get some confusion, bruising abdominal pain, pallor and hypertension, renal failure. The other thing is so treat, um you can often treat the E coli with the antibiotics as well. If clinically indicated, treat the fluids and these patients normally recover. So that's a little bit about H US now HSP So this is ox nine purpura again, forgive my pronunciation there. So it's an IG a vasculitis which is presents with a palpable purer rash, affecting the lower limbs and buttocks. Most commonly in Children occurs due to IG A deposits. So you can get ig a Neri uh nephritis, your abdominal pain, purer rash and joint pain. So it's iga depositions and complements C three deposits in the kidneys and blood vessels. This causes a type three hypersensitivity reaction. So your triad of these um of this is purpura arthritis and abdominal pain. Those are your, your triad. This is not IJ nephropathy. This is IJ nephritis. So it can cause affect the kidneys in 50% of patients causing your iga nephritis or uh HS kidney can lead to microscopic or microscopic hematuria or and proteinuria. So there is a criteria which is done by multiple, multiple um forums. So the most common criteria. So the one that we use now is palpable purpura, not particular and at least one of abdominal pain, arthritis, arthralgia, iga deposits on histology, biopsy protein or hematuria. Now, management of this condition is often supportive. So with simple analgesia hydration and just things normally, things normally reverse the use of steroids is debatable. They may shorten the duration of the illness, but they don't really um affect long term outcomes. Most patients recover in 4 to 6 weeks. So now because this is a iga vasculitis, you may get recurrence of the disease within six months and a very small proportion of patients will go on to develop end stage renal failure. So, again, just to recap iga nephritis, abdominal pain, purpuric rash, that's palpable again. So you can see that's 100% criteria, joint pain iga deposits causing inflammation. And this is an example of one of the purpura other. So that's a bit about HSP. Now, looking at rhabdo rhabdomyolysis. So again, very commonly seen in the hospital. So condition where the skeletal muscle breaks down, rapidly causing myoglobin release into the bloodstream, which can cause the kidney damage and myoglobinuria. So this is caused by excessive muscle damage. So in in hospital, often patients with the fall in long life, crush injuries, strenuous exercise. I've actually had a friend who had a very, very long gym workout after years and years having strenuous exercise or having muscle pain, having dark urine actually had rhabdomyolysis. So it can happen in all, in all age groups. Uh often electrical injuries can cause it. Um you've got drugs. So cocaine statins, colchicine and other toxins can cause it. So again, most commonly fall with long line in an elderly patient, but not to forget all of these kind of um other other factors. Now, your signs and symptoms, like I said, muscle pain, muscle weakness, confusion, dark urine. Now your diagnosis is made with an elevated level. So, creatinine kinase level in the blood stream and an AKI. So this patient um will present with uh AKI I secondary to rhabdomyolysis requiring treatment. Now, complications, as I mentioned can be AKI high potassium, low calcium and can lead to D IC. So disseminated intravascular coagulation. Now, treatment of this condition is fluid resuscitation, removing the course. So making sure the patients, let's say you've got compartment syndrome or a cross injury, treating that removing this um insulting agent, uh hydrating them, mobilizing them. So yeah, fluids and removing the course, like I've mentioned in most conditions in the kidney. Now, this condition can often lead to the need for acute dialysis in my six months. So far, I've seen three patients with rhabdomyolysis who we've transferred for acute dialysis because levels remain high. No response in the treatment. No improving AK So again, they're meeting that criteria for acute dialysis. So they've got a treatment resistant to acidosis hyperkalemia, often sometimes can give you fluid overload and um you've got uremia. So again, you've got that confusion weakness again, presenting with uremia there. So yeah, torn muscle, um myoglobin enters bloodstream damages is your kidneys. This is an example of the dark urine. You'll get some myoglobinuria. Again, this is pathognomonic of the conditions. All patients with renal failure should be catheterized if you see this kind of urine and that's the history concerns. Are there for Abdo? Now, looking at, looking at this um next case here. So a 36 year old man presents to the emergency department with bruising all over his body and fatigue. He reports dial illness a few days prior to this but completely resolved. He has no past medical history. Blood tests revealed the following. So sodium is normal potassium, highly, high urea raised. He's 36. So his renal function there is quite severely impaired for his age. He's got a low hb um small, normal white cell count and low platelet count. What is the most appropriate next step in management here? So, looking at this, looking at this, you've got a, you've got a number of number of options here. So what's your feeling here? And again, I'll go through, I'll go through the rationale with the answer as well. Yep. So the, so the answer. So the answer here is this is clearly hus. Now, in this patient, you you have the option here. So I would, I would say the most appropriate step here is renal biopsy. So in this patient, you've got a couple of things. So he's clearly had this dire illness presented with HS. Now, you've got blood tests which are abnormal but not abnormal to the point of specific treatments needed. So, intravenous antibiotics would be appropriate but the illness is completely resolved. So again, neither here nor there red cell transfusion. His HB is only 85. There's no indications there for transfusion referral for hemodialysis. His G fr is only 38 creatinine 350. He's not got any signs of sclero uremia. Apart from fatigue referral for renal biopsies, here you have a golden opportunity in which to get the diagnosis. So you can, although we'll probably know that doing a stool sample would be useful, doing blood cultures, doing all of that can find E coli 157. But in this case, referral for renal biopsy would be the most appropriate next step platelet transfusion. If his platelet count was below 20 he was acutely bleeding, then yes. So yeah, it's about picking the single best most option answer there. Now, looking, looking at your next one. So a 78 year old lady presented to the emergency department after being found by her carer on the floor at 6 a.m. this morning, she was last seen at 9 p.m. the previous day, she has a past medical history of hypertension, left side hydronephrosis type two diabetes and a previous CVA uh blood test. Again, renal failure. Is there. What's the most appropriate next investigation here? What are your feelings? So again, firstly, what do you feel the diagnosis could be here? And what tests do you want to do? So, yeah. So the answer here is rhabdomyolysis. Now looking at the most appropriate answer, yes, it's a so serum level. So all of these options can be considered. So serum level and an AK I will give you the diagnosis of rhabdo renal biopsy. I don't think it's indicated here. Again, technically, all renal disease, the only way to tell is a biopsy. But nope renal ultrasound again, wouldn't be wrong. But because she does have left sided hydronephrosis in the past, she does have abnormal blood tests. So you probably would want to do a routine renal ultrasound as well, but not the most appropriate urine dipstick. So again, you'll probably find protein, you'll find a bit of protein, you'll find a bit of blood, you'll find myoglobin if you did a test. But again, that would not give you the diagnosis, avena's broadcast. So looking at, looking for an acidosis is important, but again, she's at the level where her G fr is 17 where you've got severe or we don't know the degree of this A VBG would also be appropriate. But here to get the diagnosis, it's a serum CK level. So that's all good. Now, the next part of the talk is just looking at your electrolyte abnormalities. So, um uh they asked me to cover a little bit about hypokalemia, hyperkalemia and going on to them electrolyte disturbances. So, so firstly, beginning with hypokalemia. So I've used a lot of my trust guidelines here and just combined things there. So low serum potassium can cause muscle weakness, paralysis, cardiac arrhythmia, susceptible and in susceptible patients, especially with a hepatic encephalopathy, it also um potentiate the effects of cardiac um effects of digoxin. So, digoxin is contraindicated in hypokalemia and drugs up long qt interval. So looking at this chart here. So depending on your serum potassium level, the uh the lower your potassium level, the more the symptoms. So mild 3 to 3.5 usually no symptoms. Sometimes arrhythmias in patients with ischemic heart disease or post cardiac surgery moderate. So you get your weakness, constipation arrhythmia. So often you might get a patient with severe constipation with a pseudo obstruction and your surgeons have magically found low potassium. So this will come on the medical people because constipation due to low potassium. So there can often be a debate there, severe uh hyperkalemia. So you can get muscle weakness, necrosis and arrhythmias and again, paralysis. So, low potassium is commonly secondary due to increased losses. So, vomiting, diarrhea, thiazide loop diuretic steroids. It can also be due to alkalosis. So loss of hydrogen through the persisting, persistent vomiting, low magnesium. So, low magnesium, again, we were never taught this during medical school but low magnesium, magnesium is required for potassium absorption. So, hypomagnesemia can cause hypokalemia, beta blockers, xanthine drugs like colchicine insulin. So again, insulin is the treatment for hyperkalemia, but insulin can cause a relative hypokalemia. So yeah, all of these cause potassium to enter the cells. Now, looking at your management of hypokalemia, again, this differs by your potassium level. Um in um severe hypokalemia, you may require intravenous and monitoring as well. So looking at mild hypokalemia, number one, so be between three and 3.5 oral replacement. So, OK, I'm sure all of you here working in hospital medicine have prescribed s at one point um IV replacement where patients are able to take things orally and that's often 20 to 40 millimoles and 1 L over eight hours. Now, you have to monitor your potassium levels three times a week and, and the maximum infusion rate of potassium is 20 millimoles an hour through a central vein and 10 millimoles an hour through a peripheral vein. Now, where you have moderate hypokalemia, again, orals and OK, can be given but IV replacement is often um recommended. Now where you've got severe hypokalaemia. So less than 2.5 or anything with arrhythmias or anything with symptomatic or where they can't take 40 millimoles over six hours is given and this can require ecg monitoring and require cardiac monitoring. So in these patients and with severe hypokalemia. So going on here. So less than two with uh arrhythmias, you may transfer them to acc kind of setting or a HD kind of setting and they often require repeat infusions of them of intravenous potassium chloride and a little bit more investigations into the course. So controlling the vomiting, controlling the diarrhea, stopping these diuretics, stopping these thiazides um and often just making sure your magnesium levels are ok. Now, hyperkalemia, again, I'm sure all of you at some point have seen hyperkalemia in your um in your um medical career so far. So attempts should be made to lower the potassium of a patient's potassium is above six. Now, symptoms again, are a um are very uh very, so cardiac arrhythmias and very severe hyperkalemia, asystole muscle weakness or paralysis. I was actually looking for AE CG of a patient with VF that I recent I was going to put in a clinical case with a VF secondary to hyperkalaemia, but I couldn't find the E CG. Um So early symptoms can be heart, um irregular heartbeat, skin sensations, numbness, tingling, muscle weakness, muscle, paralysis, and other symptoms. Again, cardiac arrest and your sudden collapse. So again, all of these things can occur, constipation, cramping, weak pulse. But again, as you all know your A LS algorithm and your four Hs and your four Ts. So one of the four HS is hyperkalemia. So, yeah, very important. So causes of increased potassium concentrations. Again, like this is a talk on renal failure. So, r kidney issues, renal failure, potassium sparing diuretics, ace inhibitors, nsaids, Addison's disease. It will give you the hyperkalemia, hyponatremia metabolic um condition potassium leaving cells. So, relative acidosis and it can cause that to your transporters of cells release potassium from your cells, diabetic hyperglycemia again, cell damage. So, rhabdo burns hemolysis trauma. So um we often see patients were referred to as a renal team with diabetic feet. So with diabetic feet causing gangrene. Now, that's a state of necrosis, that necrosis causes potassium release. So unless you get rid of that and debride that you may have recurrent hyperkalemia and often these patients have multimodal things causing the hyperkalemia. So for example, recently in a patient, I saw a patient with hyperkalemia secondary to a new diagnosis of af so um if I, if I hyperkalaemia, sorry, where I, where I see. So they were newly started on um they were newly started on diuretics, they were newly started on bisoprolol which can cause it. They were newly started on Rivaroxaban. So all of these factors are important to consider and often require specialist input. Now, hyperkalemia management, this is the kidney association guidelines. Now I won't go through all of it, but mild hyperkalemia can consider the cause and weight. So, like in the question we discussed earlier, but the general approach is protect the heart shift the potassium into cells, remove potassium from the body monitor and prevent. So if the E CG is abnormal and the patient's potassium is 6.46 to 6.4 or above 6.5. Consider calcium gluconate or calcium chloride. IV. Recent guidelines have suggested repeat doses of up to 30 mils in total. So keep repeating doses until the ECG is normal. Now, after that, you shift your potassium into the cells. So your actrapid and dextrose infusion is very important and considering giving um salbutamol nebs. Now, salbutamol neb should never be given as a monotherapy. This has no response in 40% of patients. And again, it's given in caution with patients with tachycardia or ischemic heart disease as salbutamol can cause tachycardia and can cause um this relative high lactate state. So going onto this diagram, insulin glucose, reduce the risk, um salbutamol and then your next part of the guidelines which used to be calcium resonium is now sodium zirconium cylate. So this is Lama. So 10 g T DS for up to 72 hours. So this is a potassium binder which binds potassium from the gut and releases it in the stools. Now again, where you have hyperkalemia, persisting treatment resistant hyperkalemia, call the renal team or call ICU. There's very clear guidelines here. So consider dialysis. So this chart or every trust or every hospital will have a vague um vague um reflection of this chart. There's also a chart for hyperkalemia management in the community, which is similar but focuses more on speaking when to refer to hospitals. So I won't go too much into that because it's a lot more, it's a lot more detailed. Now E CG changes with potassium. So again, just, just to recap again from life in the fast lane, hypokalemia, T wave inversion, ST depression and a prominent new wave hyperkalemia. So you get these tall 10 T waves, flattening of the P wave, uh pr prolongation and wide widened QR S complex. So let's see, you see a patient coming into your A&E department or you see a patient and GP where you've done an E CG, any of these features in GP, obviously referred to the hospital in, in, in the hospital setting in A&E, let's say you've seen a patient in renal failure and you've done an E CG and that's the only investigation you have and you've got peak T waves on any of these signs. You can give actrapid dextros and you can sorry, calcium gluconate and extra dextrose. There is no relative harm from these measures and the other, the relative harm going into hypokalemia can be controlled. But your key thing here is where you've got E CG changes. You may have go into imminent cardiac arrest. So always treat and again, it's clinical decision, call your senior treat. Now, moving on from potassium to calcium. So, hypocalcemia again um can have this, this is often more symptomatic. So this is where your uh your low plasma concentrations of calcium. So, increased neuromuscular activity. So you get paresthesia, muscle cramps, spasms, stridor and convulsions. So you just to remember chop sticks and tr signs. So where you tap the facial nerve causing facial twitching and also a sign where you uh do put somebody in a BP cuff for 3 to 5 minutes and you get the, you get the carpal pedal spasms. So attempts should be made to um raise a patient's calcium where it's below 1.8 or univocal signs of hypocalcemia with low calcium such as tetany coughs or a seizure. Now where alkalosis suggests in um is increa where, where you've got an alkalosis, you've increased the likelihood of symptoms and signs and occasionally hyperventilation can be the sole cause for the clinical picture. Now, often things to consider our primary hyperparathyroidism. Again, this is not an endocrine talk, but that can be a cause of renal failure where you get um lack of Vitamin D absorption, lack of Vitamin D deficiency. So that may require alfacalcidol to replace the Vitamin D rather than replacing the calcium and malabsorption. And a low plasma magnesium can also cause hypocalcemia without any change in total body calcium. So, in these cases, treat the hypomagnesemia before you treat the hypocalcemia and you can repeat the calcium levels. So again, the symptoms just to revise numbness around the mouth, painful muscle cramps, paresthesia laryngo, spasm, vomiting, seizures and decreased cardiac function. Again, hypocalcemia can cause E CG changes. I'll talk about it on one of the slides later. Now here, hypo, so like I said, hypomagnesaemia related hypocalcemia should be treated with the magnesium alone and then you repeat the calcium levels. You can see unless there are E CG changes indicating both. Now, supplements can be given orally or can be given IV. So oral is your Adal D3 or sandocal. Oh Calci, you now intravenous infusions, you can give 10 mils of calcium gluconate or calcium chloride like you've given in hyperkalemia treatment. Again, that's for acute, the effect is short lasting and should always be followed by calcium gluconate infusion. So you've got 40 mils of calcium gluconate and 500 mils of dextros saline over 24 hours. And often the very interesting thing about this condition is the symptoms often resolve through the infusion. So you can see that the chopsticks and chine disappears. It's quite an interesting clinical phenomenon. Now, hypercalcemia. So, hypercalcemia is a lot more common than hypocalcemia and can be asymptomatic or can be fully symptomatic. So your symptoms are your stones, bone grows and psychiatric overtones. So you can get bone fracture risk, kidney stones, you've got your abdominal cramping, nausea, constipation, ileus, again, hypercalcemia causing bowel obstruction, pseudo obstruction. Again, we'll come on the medicine, psychiatric overtones. So you can get depression, psychosis, cognitive dysfunction. Now, again, as a attempts to lower the serum calcium with any one of serum calcium above three should be made unless the patient is stable and the patient is completely asymptomatic. But generally, many physicians will become uncomfortable if a patient's calcium is above three. Now again, going into the causes. Now again, this is not an endocrine talk, but malignant disease. So can occur without bone mets. So you've got your uh lung cancer where you get P th related peptide secretion. So, hyperparathyroidism related thiazide diuretics, Vitamin D intoxication. So I had a young lady a few months ago. Um she presented with um just fatigue and her calcium levels were 3.5. So we did every test under the sun to look for it. And then in our team, we were like, ok, let's do a Vitamin D level. She reported not taking any supplements, but her Vitamin D level was 300 plus. So we asked her to bring in everything she takes and she was on this herbal medication which contained a lot of Vitamin D So as soon as that was stopped, that was all resolved and other less common causes can be sarcoidosis. So during um during your serum ace levels, tuberculosis causing granulomas, thyrotoxicosis, cortisol deficiency, pheochromocytomas, VIP oas immobilization, post renal transplant, lithium, and Vitamin A. So in that lady, we actually did all these tests. So we did a test for sarcoid TB thyrotoxic. We did all of this. But again, it was just a Vitamin D intoxication. So again, be very careful with Vitamin D intoxication and it's often an under recognized cause of hypercalcemia. Now, to treat it, the key thing is to give Saline. So in the 1st 24 hours, you may require 4 L3 to 4 L. Um and aiming to increase urine volume output. Uh cautious rehydration in patients with risks of CCF in patients with hypercalcemia known to malignant disease. You can give IV Zoledronic acid or IV PMID donate and you can recheck the calcium level 3 to 5 days after treatment. IV zole or IV pidolate does not work immediately. So some physicians and some consultants will have you recheck calcium levels. Tomorrow may need to repeat it. No, you don't need to repeat it, check it after 3 to 5 days. These patients often have asymptomatic and it's definitely due to malignancy, you can discharge them, bring them back to a medical ec or ambulate your care setting if there's persistent hypercalcemia, seek specialist advice. So, endocrine or renal advice. So like I've said treatments of your hypercalcemia. Again, this is the acute setting, but where you've got acute settings of saline bisphosphonates, steroids can be given for chronic granulomatosis disease. So again, with the TB calcitonin parathyroidectomy for primary hyperparathyroidism, dialysis, now, where you've got severe hypercalcemia KD and patients already with severe hyper calcium and during the second secondary to their C KD, their dialysis will often control their calcium levels. Now if you see a dialysis patient come into your department with high calcium, do not give them fluids, do not do all of this. You will cause them more harm than good, contact their renal team and get them on the machine. They will be put onto a low potas, sorry, low calcium diacylate and the calcium will come out avoid thiazides and bisphosphonates. Um So where thiazides can increase calcium reabsorption and cause symptoms and bisphosphonates just to be aware, are associated with jaw necrosis. So, always look at those effects. So again, so yeah, there you are. So that's hypercalcemia. Now, your uh E CG changes with hypo and hypercalcemia, your most important thing with hypocalcemia is QT prolongation. So where you've got your QT prolongation, again, you can do an E CG to monitor and E CG cardiac monitoring is often required for the uh calcium gluconate infusion and hypercalcemia shortening of the ST segment. Now, the last few things, so we'll talk about sodium and we'll talk about magnesium. So hopefully not too long left. So, hyponatremia. So this is one of a query that often comes to renal medicine often comes to endocrine. So now it normally resolves from a lot of lot of issues. So looking into it. So the diagnosis is confirmed by a sodium level of below 100 and 35 you have to measure your urinary sodium concentration to know if they're passing concentrated urine or dilute urine, measure your plasma osmolality and assess volume status. Now, these patients can either be hypervolemic, euvolemic or hypovolemic. So if your osmolality is greater than 275 assume the problem is hyperglycemia or renal failure, entry to such as per guidelines where you've got a low plasma osmolality, then the treatment will determine on, based on what the issue is. See if they're hypovolemic, say if your patient is dry, dehydrated and all of these things has clear losses. So causes can be diuretics, vomiting, diarrhea, or cortisol deficiency, always check a morning cortisol level. It's part of the guidelines before initiating any treatment. So, not before initiating but in the pathway of treatment you volemic. So this can be caused by diuretics, hypothyroidism. Si A DH Polydipsia irrigation with glycine orbitol during turp um and drugs such as ecstasy chloropropamide exercise. Again, looking at your euvolemic states. The most common is si A DH seen in the hospital or subclinical hypothyroidism and like diuretics being newly started such as fursemide or your thiazides. Your hypervolemic is congestive cardiac failure, renal failure. So, in congestive cardiac failure, you'll get fluid overload in renal failure, you'll get fluid overload conditions associated with hypo albuminemia. So, liver failure or poor nutrition, you'll get fluid overload. So these are all your fluid overload ones. So low osmosity, fluid overload, hypervolemic hyponatremia. Now, just to have a quick look at your, look at your um your um your hyponatremia work up just so you know So check your serum osmolality, normal serum osmolality, isotonic. So, hyperproteinemia. So just check your albumin levels, hyperlip tri hyper lipidemia. So this is sometimes seen in patients with where you get a pancreatitis secondary to high lipids. Again, very, very rare where you get high triglyceride levels, low serum osmolality volume state is very important. So if your urinary sodium is less than 10, you've got extra renal salt loss. So, dehydration, diarrhea, vomiting, what I mean, extra renal salt loss. So you, you're vomiting it out, you're diarrhea it out, you're vomit, your diarrhea or your vomiting. So your sodium is coming out from, not from your kidneys. Now, when your urinary sodium is normal and you're hypovolemic and you've got a low osmolality. This is a renal salt loss. So high urinary sodium means your s your kidneys are pushing salt out. So, diuretics, ace inhibitors, nephropathies, mineralocorticoid deficiency and cerebral sodium salt wasting syndrome. Again, I won't go into each one, but that's the pathway and you treat as such. So, stop the offending agent, treat the nephropathy, treating the mineral corticoid deficiency or look into the cerebral sodium salt wasting syndrome, euvolemia. So, si DH so that requires fluid restriction, postoperative hyponatremia. Again, due to a volume shift, hypothyroidism, psychogenic polydipsia. So, where patients are drinking, drinking a lot. Um and all the other ones. So your drug, your drug, um your drug reactions to thiazide diuretics, ace inhibitors, endurance exercise, ACTH deficiency. Now again the key thing here is your volume status. If they're hypovolemic, it's very different to you volemic and the causes are as such. So, patients often require assessment by a specialist although they shouldn't for their fluid status. And now hypervolemia where you've got a low serum osmolality is heart failure, liver failure and nephrotic syndrome around advanced kidney disease. So, these patients require diuretics. Now again, treatment of hyponatremia, hypovolemic saline fluid, stop the causing oh sorry, spelling it, uh stick there, stop the causing agents. Antiemetic supportive measures. Euvolemic fluid restrict, treat the cause hypervolemic restrict sodium intake. IV fursemide don't be afraid to give high high doses of IV flusemide in these patients but always speak to a specialist. Now, hypertonic saline should be reserved to patients with severe hyper hyponatremia and patients with seizures or neurological complications. So, these patients often require ICU care or endocrine input. So where you've got your, where you've got things not responsive to treatment. Again, this is something I won't go into too much detail on, but you just need to know hypo hyponatremia with seizure hypertonic saline. So 1.8% or 3% saline. Again, that will be determined by an endocrinologist, a renal physician or ICU. Now, so I'm now moving on to the opposite side. So hypernatremia. So this is a sodium of above 145 usually only clinically significant when it's above 155 or where there's been a rapid increase of above 2024 hours can be associated with confusion and coma. So these patients are often they have a high hyperosmolar coma, that's diabetic state. So it can be associated with subarachnoid or intracerebral hemorrhage. Now causes include so H2O loss without adequate H two in intake. So there you are dehydration. So, dehydration related hyponatremia fluids, done, they'll be out of hospital diuretic or laxative abuse the way you see patients abusing laxatives or diuretics. So this is often seen in patients with eating disorders, seen in patients trying to lose weight or seeing in patients with that mental health problems, osmotic diuresis or hyperglycemia, be aware of the pseudo hypernatremia here. And also um that's the other thing you need to be aware of. Here is your hyperosmolar hyperosmolar state and diabetes hyponatremia. So that will require very, very, very fluid resuscitation and controlling the sugar state. Now, sodium gains seawater infusion of last volumes of bicarb, sodium bicarb. So high volumes of sodium bicarbonate IV. So 8.4% can cause a relative hypernatremia. Now again, this is not an endocrine drug, but your central and nephrogenic diabetes, insipidus are other causes. So your patients post brain surgery, patients with brain injuries, nephrogenic. So inherited or acquired with certain drugs, I won't go into the treatment there. Like for example, novastan tolvaptan is used to treat severe hyponatremia and or due to si A DH but can then cause hyponatremia. Now, the key thing is stop the um volume loss depending on the cause may involve giving antiemetics, stopping diuretics or treating diarrhea, calculate the water deficit. So there's a water deficit out um equation that's on MD CALC. Use that to see how many liters deplete they are. And if hypernatremia is due to central or nephrogenic diabetes inhibitors or this is suspected, contact the endocrine specialist or contact the renal physician depending on who what the issue is mainly endocrine. Now, the last part of my talk is very quickly looking at hypomagnesemia. So, um um I added this in because it's related to all other electrolytes and quite common in the hospital as well. And we're not often not taught about it. So, symptoms of low magnesium typically occur when magnesium levels are less than naught 0.5 and include nausea, vomiting, weakness, lethargy, tremor, twitching. So similar to your signs of hypocalcemia can lead to arrhythmias and seizures. So, as I mentioned, symptomatic hypomagnesaemia is often um associated with hypocalcemia. Magnesium is required for PT eight secretion and hypokalemia, magnesium is required for normal functioning of the N AK transmembrane there at TP in the kidneys. So, in the, in the, in the um the tubules. So yeah, if that's not functioning, you'll get a relative hypokalemia or hypocalcemia that causes of low magnesium, diarrhea, malabsorption, PPI s laxative. So often newly started on omeprazole or lansoprazole, you can get a related hypomagnesemia or a hypomagnesia as well. Gastrointestinal fistula postintestinal resection, short bowel syndrome, malnutrition, renal losis. So again, your diuretics amphotericin which is an antifungal aminoglycoside antibiotics, immunosuppressants. So, like I mentioned tacrolimus CISplatin. So, CISplatin being your platinum chemotherapy which also causes atn can also cause hypomagnesemia cycloSPORINE. So, one of your immunosuppressants are in, again, tacrolimus, like I mentioned diabetes. So with glycosuria, you can get osmotic diuresis of magnesium into your urine alcoholism. So, chronic alcoholism, hypercalcemic states, um hyperaldosteronism, renal tubular disorder, poral tubular acidosis, uh inherited disorders such as Bartter ments. Again, I won't go into those in too much detail. But yes, post renal transplant in the acute phase and in dialysis patients. Now, the other thing is refeeding syndrome. So in patients with um who are not eating and drinking and you start um feeding them, you can get this hypomagnesaemia due to refeeding syndrome. Now, in most patients with hypomagnesemia, the cause will be obvious from the history. The underlying cause should always be treated. So, if you've got diarrhea or vomiting, treat that medications stop that post intestinal resection, speak to your surgeons, medications, optimize that, optimize diabetic control, optimize try and get patients to give up alcohol intake, optimize your post renal transplant medications and all of this will be treatable. Now, your management. So again, you get E CG changes um with um with uh hypomagnesemia. So in those with a severe deficiency, less than naught 0.4 you can get widened QR S prolonged QT or flat T waves treatment. So, if you're not 0.5 to naught 0.7 mild, you only require oral replacements. If symptomatic, you can increase it in your diet. Otherwise moderate deficiency to 0.4 to 0.5 advise oral replacement of um asymptomatic or IV replacement of symptomatic or E CG changes severe deficiencies, less than naught 0.4 usually require admission five E replacement. So often patients for with this one will have um cardiac monitoring on a CCU bed. Now that um effectively concludes my talk just in time there. So, does anyone have any questions? And thank you for letting me speak about a very long topic, sir. Now, thank you so much, Doctor Soma. I think you have got all the nephrology today. And definitely, I think there would be a lot of candidates here who would have peaked interest in nephrology by now. So hopefully some of them will be your colleagues in future. But II think uh we have a few questions in the chat here. Uh One question was uh can you talk about how ace inhibitors cause at? But ace inhibitors can be used to treat CKD. So, so, so ace inhibitors are in C KD first answering your question about how ace inhibitors treat CKD. So, ace inhibitors cause cause reduced protein leak. So where you get to reduce protein leak and the reduced protein leak is there, you're treating the CKD. Now. Um so ace inhibitors causing AKI I will cause high BP. So they will prevent an enzyme. So made from making angiotensin two which narrows blood vessels which then causes hypertension which causes damage to the glomerular glo glomerulus. So yeah, they can cause AK I that way. But again, the ace inhibitors AKI I is often a transient AKI I treat hypomagnesemia. I think that has already been covered. The question was asked before. Yeah, hypomagnesemia just I'll just go back to this slide there. So, yeah, mild, moderate or severe deficiencies. And then uh is there any specific level of calcium when IV fluids needs to be started? So with calcium, so if your calcium level is below 1.8 you'll need IV magnesium, sorry IV calcium. So IV calcium gluconate. If your calcium level is above 1.8 you can have oral supplements. I think we have a lot of great responses here. People saying fantastic, amazing presentation. No, not boring at all. Amazing session. Very informative. Thank you very much. You are a lot pleased. Uh Thank you so much. You have put so much work. It looks in the slide that you have put so much work into it. Thank you so much for doing this and putting so much work and taking time out. I know Madrid life is busy, so busy. Yeah, that's fine. That's fine. Um It was a effective um just recap for me as well, but thank you very much. Oh Thank you. So much. Does anybody else have any questions? We'll take questions for a few minutes and then I think, uh we'll catch you for the next session. So will you give a minute? Uh If anybody has any questions otherwise, uh we'll take about the stage. Uh So I think there are few candidates who want access to slides. Uh So guys, uh you will receive the recording. All these sessions are getting recorded, uh, as we have mentioned before, after all the sessions are completed, after few editing and stuff, you guys will get the recordings of these sessions. Mhm. What's the next talk then? Yeah, I think uh if nobody else has questions, we'll and next session on interviews and orthopedics will come again. Thank you so much, Doctor Sheer for doing it honestly. No worries. Thank you. Thank you for having me and um yeah, hope that was a good overview for everybody. So I can, I'll stop sharing my screen then. Now that's fine.