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ALL YOU NEED TO KNOW ABOUT AKI Sumayyah Imran & Emma McEwen Here’s what we do: ■ Weekly tutorials open to all! 18:00 every Thursday ■ Focussed on core presentations and If you’re new here… teaching diagnostic technique from a clinical perspective ■ Reviewed by doctors to ensure W elcome to accuracy T eaching ■ We’ll keep you updated about our Things! upcoming events via email and groupchats! AKI Causes Sumayyah ImranKidney anatomy: a quick refresher ■ On average 11 x 6 cm in size, 120-150g in weight ■ Receive 20-25% of cardiac output ■ Approximately 1 million nephrons per kidney ■ Left kidney higher than right kidneyKidney function: a quick refresher Three essential functions: ■ Filtration of waste products from blood to form urine ■ Regulation of fluid, acid-base, and electrolyte balance ❏ RAAS system ● Endocrine functions ❏ 1a-hydroxylation of 25-hydroxyvitamin D from liver ❏ EPO productionKidney function: a quick refresherWhat is an acute kidney injury (AKI)? - AKI can be defined as: an acute decline in kidney function leading to a rise in serum creatinine and/or a fall in urine output - Diagnostic criteria for an AKI:Signs + Symptoms - Reduced urine output - Signs related to underlying cause: sepsis, pain - Signs of fluid overload: pulmonary and peripheral oedema - Severe: signs of uraemia e.g. fatigue, nausea, pruritus, pericarditis, encephalopathy - Might be asymptomatic!AKI stagingWhat are the potential causes of an AKI?Categorising the causes of AKISBA A 75-year-old man presents to A&E following a fall in his kitchen. He was found on the floor the morning after he fell. He has a past medical history of left-sided heart failure, and takes bisoprolol, ramipril, spironolactone, and occasional paracetamol for headaches. His blood and urine results are shown below: Serum sodium: 137 mmol/L Serum potassium: 4 mmol/L Serum creatinine: 160 umol/L Serum urea: 30 mmol/L Urine sodium: 10 mmol/L Urine osmolality: 600mOsm/kg What is the single most likely cause of his presentation? 1. Acute heart failure 2. Acute tubular necrosis 3. Renal tubular acidosis 4. Dehydration 5. RhabdomyolysisPre-renal AKIPre-renal AKI: causes ● Renal vasoconstriction: ❏ ACEis and ARBs ● Renal artery stenosis ● Dehydration/poor oral intake/diarrhoea and vomiting ● Impairment of systemic circulation: ❏ Haemorrhage ❏ Septic shock ❏ Heart failureIntra-renal AKIIntra-renal AKI: causes ■ Glomerular diseases (see later): ■ Interstitial diseases: ❏ Conditions causing nephritic ❏ Acute interstitial nephritis (AIN) syndrome (glomerulonephritides) ❏ Conditions causing nephrotic ● Systemic diseases affecting the syndrome kidney: ❏ Sarcoidosis ■ Tubular diseases: ❏ Amyloidosis ❏ Acute tubular necrosis (ATN) ❏ Haemolytic uraemic syndrome ❏ Drug reaction ❏ Thrombotic thrombocytopenic ❏ Rhabdomyolysis (causes ATN) purpuraPost-renal AKIPost-renal AKI: causesSummarising intrinsic renal pathology…Glomerular diseasesNephrotic vs nephritic syndrome Nephrotic syndrome Nephritic syndrome All 3 of: May include: ● Proteinuria >3g/day ● Hypertension ● Hypoalbuminaemia (<30g/L) ● AKI ● Oedema ● Acute urinary sediment made up red cells and/or red cell castsNephritic vs nephrotic syndrome Nephrotic syndrome Nephritic syndrome Focal segmental glomerulosclerosis (FSGS) Anti-GBM disease = Goodpasture’s syndrome Membranous nephropathy Membranoproliferative glomerulonephritis Minimal change disease Post-streptococcal glomerulonephritis Diabetic nephropathy IgA nephropathy (similar to Amyloidosis post-streptococcal glomerulonephritis) Alport’s syndrome “If it ends in “itis” it causes nephritis (nephritic syndrome)” + The eponymous conditions are also nephritic!Minimal change disease Signs and symptoms Pathology features Prognosis/complications ● Normotension ● “Minimal change” on light ● Rule of thirds: ● Nephrotic syndrome: microscopy ● ⅓: One episode ❏ Periorbital oedema ● Podocyte fusion and foot ● ⅓: Infrequent relapses ❏ Swollen legs process effacement on ● ⅓: Frequent relapses electron microscopy stopping before adulthood Causes ● Mostly idiopathic ● Hodgkin’s lymphoma Treatment ● EBV infection 1) Oral corticosteroids ● NSAIDs, rifampicin 2) Cyclophosphamide for steroid resistance Pathophysiology The child ● T cells and cytokines with damage GBM, causing polyanion loss and nephrotic increasing permeability to syndrome albuminSBA A 45-year-old woman presents to her GP with a 1-week history of puffy eyes and swollen legs. Her urine dip results are shown below: Protein +++ Glucose - Ketones - Blood + Leucocytes - Nitrites - What is the single most likely cause of her presentation? 1. Goodpasture's syndrome 2. Focal segmental glomerulosclerosis 4. Membranous nephropathyglomerulonephritis 5. Post-streptococcal glomerulonephritisSBA A 45-year-old woman presents to her GP with a 1-week history of puffy eyes and swollen legs. Her urine dip results are shown below: Protein +++ Glucose - Ketones - Blood + Leucocytes - Nitrites - What is the single most likely cause of his presentation? 1. Goodpasture's syndrome 2. Focal segmental glomerulosclerosis 4. Membranous nephropathyglomerulonephritis 5. Post-streptococcal glomerulonephritisFSGS Pathology features Signs and symptoms ● Focal and segmental Prognosis/complications ● Nephrotic syndrome sclerosis and hyalinosis on ● Higher rates of ● Nonspecific proteinuria light microscopy development of chronic ● Haematuria ● Foot process effacement renal failure on electron microscopy Treatment ● Steroids ● Other Causes immunosuppressants ● Idiopathic ● Secondary to other renal pathology ● Sickle cell The young ● HIV adult with nephrotic syndrome Membranous nephropathy Pathology features Signs and symptoms ● Subepithelial deposits ● Nephrotic syndrome thickening basement ● Proteinuria membrane on electron microscopy ● “Spike and dome” Causes appearance on electron ● Malignancy microscopy and light ● Idiopathic microscopy with PAS stain ● Infection due to deposits ● Drugs, e.g. gold, NSAIDs, and Prognosis/complications penicillamine ● Rule of thirds: ● SLE, thyroiditis, RA ● ⅓: Spontaneous remission ● ⅓: Continued proteinuria Treatment ● ⅓: Frequent relapses stopping before adulthood ● ACEI/ARB ● Immunosuppression ● Anticoagulation The older adult with nephrotic syndrome and a history of malignancyMembranoproliferative glomerulonephritis Prognosis/ Signs and symptoms Pathology features complications ● Haematuria (nephritic syndrome) ● Primary: “Tram-track” appearance ● Variable ● Mild to nephrotic-range on electron microscopy (and light proteinuria (nephrotic syndrome) microscopy below) ● Some patients ● Hypertension ❏ Subendothelial and/or subepithelial develop ESRF ● AKI immune complexes Treatment ● Corticosteroids Causes with or without ● Primary (immune additional immunosuppressi complex-mediated) on ● Secondary (systemic diseases) ● C3 glomerulopathy ● Eculizumab (C5 (complement-mediated) inhibitor) for C3 glomerulopathy ● Underlying disease treatment Pathophysiology ● Supportive care ● Mesangial cell proliferation ● GBM thickening Immune-mediated ● Immune complex and/or glomerulonephritis with complement deposition “tram-track” appearance and other characteristic histology Goodpasture’s syndrome Signs and symptoms ● Rapidly progressive glomerulonephritis causing proteinuriathology features and haematuria ● Linear IgG deposits along ● Pulmonary haemorrhage (respiratory basement membrane on risk factors and male sex increase immunofluorescence (right) risk) Causes Treatment ● Anti-GBM antibodies to type IV ● Plasma exchange collagen, causing small-vessel ● Steroids vascultitis ● Cyclophosphamide Young man coughing up blood with acute renal impairment Alport’s syndrome Features Pathology features ● Microscopic haematuria ● “Basket weave” ● Bilateral sensorineural appearance on deafness electron microscopy l a ● Lenticonus ❏ Lamina densa o ● Retinitis pigmentosa splitting N Cause Prognosis/ ● X-linked dominant complications inheritance of gene defect ● Renal transplant in type IV collagen, leading may fail due to to abnormal GBM and other presence of t manifestations anti-GBM antibodies o l ● 10-15% autosomal → Goodpasture’s A recessive inheritance syndrome The failing renal transplant Rule of pairs: The due to anti-GBM antibodies. kidneys, eyes, and ears come in pairs and are all Patient has ocular and ENT affected manifestationsSBA A 35-year-old man presents to his GP with blood in his urine. He has had a cough and flu-like symptoms since yesterday. His urine dip results are shown below: Protein - Glucose - Ketones - Blood +++ Leucocytes - Nitrites - What is the single most likely cause of his presentation? 1. Rapidly progressive glomerulonephritis 2. Focal segmental glomerulosclerosis 3. Membranoproliferative glomerulonephritis 4. IgA nephropathy 5. Post-streptococcal glomerulonephritisSBA A 35-year-old man presents to his GP with blood in his urine. He has had a cough and flu-like symptoms since yesterday. His urine dip results are shown below: Protein - Glucose - Ketones - Blood +++ Leucocytes - Nitrites - What is the single most likely cause of his presentation? 1. Rapidly progressive glomerulonephritis 2. Focal segmental glomerulosclerosis 3. Membranoproliferative glomerulonephritis 4. IgA nephropathy 5. Post-streptococcal glomerulonephritisPost-streptococcal glomerulonephritis and IgA nephropathy Post-streptococcal glomerulonephritis IgA nephropathy ■ Mesangial deposition of IgA immune ■ Immune complexes made up of IgM, IgG complexes and C3 deposited in glomeruli → low ■ Recent respiratory tract infection (past 1-2 complement levels days) → visible haematuria ■ Following group A B-haemolytic Streptococcus infection (7-14 days ago) ■ Often young males ■ Renal failure rare ■ Systemic symptoms, haematuria, proteinuria, hypertension, oliguria ■ persistent proteinuria, andnuria, ACEi if ■ Subepithelial deposits on electron immunosuppression if active renal microscopy. “Starry sky” appearance on involvement or failure of ACEi response immunofluorescence (staining for C3) ■ Mesangial hypercellularity on light microscopy. IgA and C3 on immunofluorescence. IgA nephropathy develops more acutely following infection!Tubular disease Acute tubular necrosis Damage to Pathology features tubules, often Signs and symptoms ● Tubular epithelial necrosis and following “long shedding of dead cells into lumens ● AKI ● Tubular dilatation lie” or ● Muddy brown urinary administration casts of other nephrotoxic Dead epithelial cells drug Dilated tubules Causes ● Ischaemic ❏ Shock Treatment ❏ Sepsis ● Nephrotoxins Diffusely Supportive care epithelium ❏ Aminoglycosides ❏ Lead ❏ Radiocontrast ❏ Myoglobin due to rhabdomyolysisInterstitial disease Acute interstitial nephritis Signs and symptoms ● Fever Pathology features ● Rash ● Interstitial oedema and “Asthma of the ● Arthralgia interstitial infiltrate kidneys”, often ● Eosinophilia following ● Hypertension ● Renal impairment medication administration Treatment Causes ● Drugs, including: Stop causative medication ❏ Penicillin ❏ Rifampicin ❏ Allopurinol ❏ NSAIDs ❏ Furosemide ● SLE ● Sarcoidosis ● Sjogren’s syndrome ● Staphylococcus infection AKI Management Emma McEwenInvestigations: Urine Collection What urine output is considered to be AKI for a 70kg adult? A: <56ml/hour for >6 hours B: <56ml/hour for >8 hours C: <35ml/hour for >4 hours D: <35ml/hour for >6 hours E: <21ml/hour for >4 hoursInvestigations: Urine Collection What urine output is considered to be AKI for a 70kg adult? A: <56ml/hour for >6 hours B: <56ml/hour for >8 hours C: <35ml/hour for >4 hours D: <35ml/hour for >6 hours E: <21ml/hour for >4 hours Explanation: <0.5ml/kg/hour for >6 hours suggests AKI 0.5ml/kg x 70kg = 35ml Not diagnostic: must take in whole clinical pictureInvestigations: Urine Collection ■ Urine output: <0.5ml/kg/hour >6 hours ■ Urine dipstick: supports diagnosis of underlying cause – Protein: glomerular pathology – Blood: glomerular pathology / urological problems – Protein + blood: rapidly progressive glomerular disease – Nitrites: UTI – Leukocytes: UTI / glomerulonephritis / acute interstitial nephritis – Glucose: diabetes ■ MC&S only if symptomatic / evidence of UTI on dipstick ■ Protein:creatinine ratio if glomerulonephritis is suspectedInvestigations: Bloods Which of the following is NOT used to investigate AKI? A: Serum creatinine B: FBC C: eGFR D: CRP E: Bone profileInvestigations: Bloods Which of the following is NOT used to investigate AKI? A: Serum creatinine B: FBC C: eGFR D: CRP E: Bone profile Explanation: eGFR is very unreliable in investigating AKI, as it represents a gradual change in serum creatinine. All other investigations can be used to monitor and/or assess for underlying causes.Investigations: Bloods ■ U&Es – Sodium – Potassium: hyperkalaemia may require urgent treatment – Urea – Creatinine ■ FBC ■ CRP ■ Bone profile ■ Unknown cause: – Creatinine kinase – ANA – ANCA – Anti-GBM – Complement levels – Antistreptolysin O titre – HIV – Hepatitis B/CInvestigations: Renal USS & Biopsy What imaging is most appropriate in assessing AKI? A: Abdominal X-ray B: Micturating cystourethrogram C: CT contrast D: MRI E: USS KUBInvestigations: Renal USS & Biopsy What imaging is most appropriate in assessing AKI? A: Abdominal X-ray B: Micturating cystourethrogram C: CT contrast D: MRI E: USS KUB Explanation: AXR does not show kidneys, MCUG assesses urine flow, CT contrast contains nephrotoxic contrast, MRIInvestigations: Renal USS & Biopsy ■ USS KUB – Indications: ■ New case of AKI ■ No identifiable cause: should always have renal USS ■ Suspected post-renal cause: within 24h – Possible findings: ■ Small size: more likely to be long-standing CKD ■ Corticomedullary differentiation (kidney architecture) ■ Pre-renal AKI: renal blood flow (doppler) ■ Post-renal AKI: hydronephrosis ■ Biopsy only if it will change management: risk of thrombosis / bleedingDiagnostic Criteria of AKI (NICE) ■ Rise of serum creatinine >26 micromol/L within 48h ■ >50% rise in serum creatinine within 7 days ■ Urine output <0.5ml/kg/hour for >6 hours – Useful in pre-renal AKI – ESRF: may not have low urine outputKDIGO Classification of AKI Stage Serum Creatinine Urine Output 1.5-1.9x baseline creatinine or <0.5ml/kg/hour for 6-12 hours 1 >26 micromol/L <24h 2 2.0-2.9x baseline creatinine <0.5ml/kg/hour for >12 hours 3 >3.0x baseline creatinine or <0.3ml/kg/hour for 24 hours or Decrease of eGFR to <35ml/min or Anuria for 12 hours Initiation of RRT ■ Gives indication of prognosis: – Stage 3: 30% mortalityPreventing AKI ■ Identifying at-risk patients: monitoring! ■ Consider IV fluids for investigations requiring contrast ■ Avoiding nephrotoxic medications Consider Stopping Should Be Stopped Metformin NSAIDs Lithium ACE inhibitors & ARBs Digoxin Diuretics AminoglycosidesPreventing AKI ■ Identifying at-risk patients: monitoring! ■ Consider IV fluids for investigations requiring contrast ■ Avoiding nephrotoxic medications Consider Stopping Should Be Stopped Metformin NSAIDs Lithium ACE inhibitors & ARBs Digoxin Diuretics AminoglycosidesManagement of AKI ■ Largely supportive: – Careful fluid balance: avoid hypoperfusion & fluid overload – Stopping nephrotoxic drugs – Treat underlying cause ■ Pre-renal: correct volume depletion / circulatory support ■ Renal: biopsy + specialist management of intrinsic renal disease ■ Post-renal: catheter / urological intervention ■ Renal Replacement Therapy (RRT) – Indications: ■ Not responsive to treatment ■ Risk of complicationsComplications of AKI ■ CKD: bidirectional relationship ■ Fluid overload – Heart failure / pulmonary oedema ■ Metabolic acidosis ■ Uraemia → encephalopathy & pericarditis ■ Hyperkalaemia – Management: ■ Stabilisation of cardiac membrane – IV calcium gluconate ■ Short-term shift of K+ to intracellular compartment – Combined insulin/dextrose infusion – Nebulised salbutamol ■ Removal of K+ from body – Calcium resonium – Loop diuretics – DialysisRecovery from AKI ■ Renal function improves graduallyover 1-3 weeks ■ GFR recovers faster than tubular reabsorptive capacity – Leads to large volume diuresis for few days ■ Warrants careful fluid balance monitoringTHANKS FOR WA TCHING! Tutor 1: Sumayyah Imran Tutor 2: Emma McEwen Please fill out the feedback form on Medall and see you next week!