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Summary

This on-demand teaching session led by Fadi Al-Shoaibi and Soma Lengyel dives deep into the topic of flank pain, with a specific concentration on the anatomy and pathophysiology of the kidneys. Highlights include detailed descriptions of the kidneys' internal and gross anatomy, their neurovascular supply, the hallmarks of pyelonephritis, and differences compared to LUTI. The course equips medical professionals to understand renal calculi's signs, aetiology, and management, as well as recognise clinical signs of renal cell carcinoma. The session also explores congenital abnormalities of the kidney and their surgical significance. Ideal for medical professionals, this course not only expands their theoretical knowledge but also their practical skills.

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Learning objectives

• Identify and explain different causes of flank pain, especially focusing on renal and urological etiology • Differentiate between the presentations of pyelonephritis and other lower urinary tract infections and grasp the significance of flank pain in the diagnosis of these conditions • Have a thorough comprehension of the renal and ureter anatomy and its neurovascular supply, and comprehend its clinical implications • Develop an understanding of conditions such as renal calculi and renal cell carcinoma; being able to describe their aetiology, clinical presentation, management options and potential complications • Understand and explain the congenital abnormalities affecting kidneys and ureters, and recognize their surgical implications.

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Flank pain Fadi Al-Shoaibi and Soma LengyelLearning Objectives • Describe the internal and gross anatomy of the kidneys including their neurovascular supply • Understand the clinical features of pyelonephritis, and the differences compared to LUTI, as well as the investigations and basic medical management • Understand the anatomy and neurovascular supply of the ureters • Describe the signs and aetiology of renal calculi, with the medical and surgical management, as well as complications including Infection and hydronephrosis. • Recall congenital abnormalities of the kidney and their surgical significance • Describe the mechanism of renal cell carcinoma, and be able to recognise clinical signs of thisObjectiveExternal kidney anatomy •Retroperitoneal •Level of kidney: T12 and L3 •Left kidney: protected by rib 11 and 12 •Right kidney: protected by rib 12 •Left kidney Hilum: L1 •Right kidney hilum: L1/L2 VAP Anterior to posterior: •Vein (from the IVC) •Artery (from descending aorta) •- Superior mesenteric: L1 - Celiac trunk: T12 - Superior suprarenal artery: above Celiac Vascular supply • Renal arteries make posterior and anterior branch. • Posterior branch: supply posterior kidney. • Anterior branch: makes 5 segmental arteries (supplying each renal segment) • Segmental arteries make arcuate arteries that make interlobular arteries. • Interlobular arteries make the afferent arterioles.Gonadal veins • vein.gonadal vein drains into left renal • Right gonadal vein drains into the IVC. • Renal cancer can present with left sided varicocele (enlarged vein in scrotum). • Other causes of left sided varicocele is increased hydrostatic pressure in renal vein.Nutcracker phenomenon • Enlargment of superior mesenteric artery can compress the left renal vein. • Affects the left gonadal vein. • Obstructs the drainage. • Leads to decreased arterial blood inflow. • Leads to Flank pain. • Can lead to testicular infarction and lower quadrant pain in females.Innervation of the kidney •Sympathetic input: Throacolumbar splanchnic and celiac ganglia. the renal •Parasympathetic input: via the vagus nerve. •Sensory nerves from spinal cord T10-T11 (Flank pain suggestive of kidney problem). Renal Fascia •renal fascia (Gerota’s fascia) – anterior, posterior and lateral to kidney. •Fascia enclosed kidney and adrenals with perinephric fat. •Separates compartment from paranephric fat (posterior kidney). •Kidney is not covered inferiorly.clinical significance of the fascia •Fascia acts as a natural barrier. 1. Prevents further spread of infection. 2. Allows for a self-contained hematoma in the perinephric space to create a tamponade. •Features can be lost in unascended or ectopic pelvic kidneys. •Non-contained fluids can leak into the inferiorly into the pelvis yet not medially (kidney rupture).Kidney Relations Left Kidney: •“Pancreas tickles the spleen” •Inferior medial is peritoneum of jejunum. Right Kidney: •Hepatorenal pouch of Morison (pouch usually empty of fluid). •Inferior pole is in contact with peritoneum of jejunum.Posterior surface of the kidney •1 artery: subcostal artery (from thoracic aorta - level of T12). •3 nerves: subcostal, iliohypogastric and ilioinguinal. •4 muscles: diaphragm, Psoas major, quadratus lumborum and transvMnemonic: “1-2-3-4 All Boys Need Muscle”. Nerves are considered when doing a nephrectomy.Internal anatomy of the kidneyNephronAnatomy of ureters • begin at the kidneys' ureteropelvic junction (UPJ). • pass anterior to the psoas muscle. • enter the bony pelvis at the iliac bifurcation • follow the posterolateral pelvic wall. • and enter the bladder posterolaterally via the trigone. • ureterovesical junction (UVJ) – has anti-reflux mechanisms.Renal calculi •Commonly get entrapped at: 1. Pelvi-ureteric junction (PUJ). 2. Crossing the iliac vessel. The ureters then enter to pelvic brim, entering at an acute angle as ureter plunges posteriorly in pelvis. 3. Vesicoureteric junction (VUJ).Vesicoureteral reflux •Congenital anomaly at the Vescico-Ureteral Junction (VUJ) level. Primary vesico-ureteral reflux: •child born with defective VUJ. •Normally, ureter has a 2 cm intramural segement. •As the bladder fills it stretches and closes the junction (passive anti-reflux mechanism). •If junction is abnormal, this mechanism fails. Secondary vesico-ureteral reflux: •obstruction in the tract causing a backflow into the ureters and kidney •Due to bladder obstruction with urinary retention.Wall of the ureter 1. Mucosa (innermost layer) = Transitional epithelium 2. muscularis (middle layer) = of 2 longitudinal muscle circular muscle layer. The circular layer is peristaltic and disappears in the distal ureter segments. 3. Adventitia (outer layer).Blood supply of ureter - vesical and uterine arteries, which are internal iliac artery branches. - arteries course along the ureter, creating an anastomotic plexus. This arterial network allows for the safe mobilization of the ureter during surgeryInnervation of ureter •Motor impulses for ureteral peristalsis: intrinsic smooth muscular pacemaker sites in the minor renal calyces. •Preganglionic sympathetic stimulation comes from The T12 to L2 roots create a ureteric plexus and innervate the ureters. •S2 to S4 sacral pelvic splanchnic nerves provide ureteral parasympathetic innervation.Pyelonephritis •bacterial infection causing inflammation of the kidneys. •A complication of ascending urinary tract infection. •Spreads from bladder to kidney. •Chronic pyelonephritis: recurrent renal infections induce inflammation and scaring. (associated with vesicoureteral reflux and renal calculi etc)Aetiology of pyelonephritis •Spread can be via hematogenous spread (less common) or ascending infection (most common). •Contamination of periurethral area from the rectum. •More common in females (proximity and shorter urethra). •associated with bacterial infection, vesicoureteral reflux, renal calculi and kidney transplant patients etc Urinary outflow obstruction can lead to urinary stasis allowing bacteria multiplication without being flushed out.Microbiology of pyelonephritis •Escherichia coli (most common). •Inflammatory response = scarring (connective tissue) of parenchyma. •All organisms: Most are Gram negative. •Escherichia coli (60-80% of uncomplicated infections). •Klebsiella species (10%). •Proteus mirablis (5%). •Pseudomonas species. •Enterobacter species.Symptoms (pyelonephritis vs LUTI) •Reminder: pyelonephritis is a complication of Lower UTI (LUTI). •LUTI symptoms: - Frequency of urinating - Urgency •Pyelonephritis symptoms: - Dysuria - Frequency of urinating - Urgency - Fever - Nausea - Vomiting - Flank pain (typically unilateral)Tests and diagnosis •Mid stream-urine sample / catheter specimen of urine to identify organism. •Dipstick urine test (nitrites and leukocytes). •A definitive diagnosis of pyelonephritis is made in people with flank pain/fever and a UTI is confirmed in culturing of urine sample. Management of pyelonephritis •Antibiotics (treat infection). •Analgesics (treat pain). •NSAIDS (reduce fever and pain). •Start antibiotic treatment once sample for culture has been obtained. •Culture review: adjust treatment. improving = narrow-spectrum antibiotics.Management of LUTI 1. mid stream urine sample. 2. antibiotics (considering the local antimicrobial resistance data). 3.Review the choice of antibiotic: adjust treatment. If we detect bacterial resistance and the symptoms are not improving, we can give narrow-spectrum antibiotics. -Patients with indwelling catheter: 1. (tachycardia and hypotension).ittion if severely unwell 2. removing/changing.eded: check catheter efficacy/considerRenal Calculi •Renal calculi: kidney stones are hard deposits made of minerals and salts inside the kidney and may travel down the tract. Aetiology •Intrinsic factors: genetical predisposition, ethnicity and gender (3:1 ratio of men to women). •Extrinsic factors: water intake, lifestyle and climate. - Meta-analysis: 21% increase in risk of stones per 5 units increase in body mass index (BMI) (Aune et al (2018)). - were much higher in obese subjects (Poore et al (2020))., oxalate, and urate levelsPathophysiology •Increased urinary supersaturation (urine solvent contains more solutes than it can hold in solution). •There are several types of stone, grouped according to their biochemical composition: - Calcium-based stones (60-80%)= calcium oxalate and calcium phosphate stones, usually a mixture of both (hypercalciuria). - magnesium and ammonium phosphate (infection leading to ammonia production – Proteus,ium, Klebsiella, staphylococcus). - Uric acid stones (10%): via increased uric acid production (protein catabolism and metabolic disorders (Gout, type 2 diabetes and obesity)).Symptoms •“Loin to Groin” pain. •Renal colic pain is caused by increased peristalsis contractions (steady pain followed by waves of severe pain). •Haematuria . •Pyuria due to increased irritation by the stone or infection due to the blockage.Investigation •Urine dipstick (Haematuria/ Pyuria) •Blood test: Full blood count (FBC), C-reactive protein (CRP), serum creatinine and electrolytes and calcium. •CT to adults with suspected renal colic. If a woman is pregnant, offer ultrasound instead of CT . •Ultrasound is first-line imaging for children and young people.Management •NSAIDs. •Intravenous paracetamol for adults, children and young people if NSAIDs are contraindicated or are not giving sufficient pain relief. •Opioids for adults, children and young people if both NSAIDs and intravenous paracetamol fail). •Alpha blockers (muscle relaxant). •Stenting (prevents blockage) – can be done by surgically (via the urethra) or radiologically (via skin using nephrolithotomy tube). •Surgical intervention.Surgical interventions • Shockwave lithotripsy (SWL): minimally invasive procedure to fragment small kidney stones. • Ureteroscopy: guidewire inserted past the stone and up the kidney. An instrument is passed along the wire, and stone is broken with laser fibre/ultrasound probe (fragments are extracted with baskets).Surgical intervention – percutaneous nephrolithotomy • “keyhole” approach to kidney an incision. • ultrasound or X-ray guidance) and make a “track” for the telescope. • lithoclast (small pneumatic drill) or an ultrasonic suction probe. Reserved fcomplex kidney anatomy. patients withComplications of renal calculi •Infection - Urinary outflow obstruction can lead to urinary stasis allowing bacteria adherence and multiplication without being flushed out. - Inability to filter metabolic waste (retention of nitrogenous wastes) makes a reservoir for bacteria. - Can lead to sepsis. •Hydronephrosis - Dilation of the kidney due to obstruction of outflow in the tract. - Severe hydronephrosis can lead acute kidney injury.Congenital Abnormalities of the Kidneys •Horseshoe Kidney •Polycystic Kidney DiseaseCongenital Abnormalities of the Kidneys •Horseshoe Kidney Most people are asymptomatic Due to the abnormal anatomy of the kidney, there's an increased risk of: • Kidney stones • Hydronephrosis • Infection • Carcinoid tumours and Wilms tumours infoKID - https://infokid.org.uk/conditions/horseshoe-kidney/ Congenital Abnormalities of the Kidneys •Polycystic Kidney Disease Autosomal dominant (ADPKD) - Most common inherited renal disease - Third most common cause of end stage kidney disease - Caused by a mutation in the polycystin gene (a tumour suppressor gene) which is necessary for the inhibition of cell proliferation. Water moves into the proliferating cells causing the cysts. Autosomal recessive Presents in infancy and may present with oligohydramnios due to renal failure before birth. Congenital Abnormalities of the Kidneys Polycystic Kidney Disease Presentation • Haematuria • Loin pain Investigations • Hypertension • Renal US – first line • Recurrent UTI • MRI – More sensitive for smaller cysts and can be good O/E for seeing cysts elsewhere • Palpable abdominal mass • Hepatomegaly due to hepatic cysts Congenital Abnormalities of the Kidneys Management: Symptomatic Renal transplant – generally offered based on patients but GFR below 20% Complications • Hepatic cysts • Increased risk of CVD • Intracranial aneurysms • Increased incidence of gestational hypertension and preeclampsia https://radiopaedia.org/articles/autosomal-dominant-polycystic-ki dney-disease-1 Renal Cancer -Renal cell carcinoma - Presentation • Originates from the epithelial tissue in the PCT • Haematuria • Microscopically they appear clear due to the • Loin pain dissolution of the fat and glycogen • Flank mass • Hence the most common type is called clear cell • Uncommon: can present with a left sided carcinoma (75%-85%) of renal cell carcinomas varicocele if the tumour is big enough Renal Cancer Risk factors - Paraneoplastic syndromes - Non-Modifiable Can part of the presentation in 10-40% of patients • North American and European heritage • Polycythaemia – Ruddy Complexion due to • PTHrP secretion – leading to hypercalcaemia - Modifiable leading to fatigue, weakness and • Obesity • Diet low in vitamins and minerals • Hypertension Renal Cancer Investigations 2 week wait criteria • Haematuria (visible and unexplained) either without urinary tract infection or that persists or recurs after successful treatment of urinary tract infection, age 45 years and over Complications - Metastasis Imaging - IVC invasion - Anaemia • US KUB first line imaging - Polycythaemia • Contrast CT for dx and staging - Varicocele Biopsy not commonly done for RCC due to low chance of a benign RCCRenal Cancer Management RCC is resistant to chemo and radiotherapy, so surgery is often the only option Two main options – 1 – partial nephrectomy 2 – radical nephrectomy Partial offered if a tumour is t1 or below OR If the other kidney cannot support the body by itself Renal Cancer Transitional cell carcinomas Presentation • 5-10% of all renal cancer (majority of bladder • Painless intermittent haematuria cancer) • Pain – suprapubic if there's local invasion • Most common form of LUT cancer • Dysuria • Stems from the transitional cells (urothelium) • Increased frequency • Urothelium runs all the way up the renal pelvis • NocturiaRenal Cancer Risk Factors P-SAC Investigation and Management P – phenacetin – common analgesic back in the day though now banned Pretty much the same as RCC S – smoking – BIGGEST risk factor A – aniline – rubber and dye manufacturing More likely to offer segmental resection of the C – cyclophosphamide – cytotoxic ureter and the renal pelvis in smaller tumours as Other: male, HPV, not voiding bladder for well as laser treatment long time Wilms Tumour One of the most common childhood malignancies typically presenting before the age of 5 Clinical Features Abdominal mass that does NOT cross the midline Painless haematuria Flank pain NICE CKS referral criteria •“Consider very urgent referral (for an appointment within 48 hours) for specialist assessment for Wilms' tumour in children with any of the following: • A palpable abdominal mass. • An unexplained enlarged abdominal organ. • Unexplained visible haematuria.” Image references: • Kidney - Location, Function, Anatomy, Diagram and FAQs • Renal Arteries and Veins Visualization - SONOSIF - by SIFSOF, California • Kidneys: Anatomy, function and internal structure | Kenhub • Testículos: Anatomía | Concise Medical Knowledge • [PDF] Hemodynamic and Radiological Classification of Ovarian Veins System Insufficiency | Semantic Scholar • Renal Nutcracker Syndrome Pathophysiology Nutcracker ... | GrepMed • The renal and abdominal sympathetic nervous system. (Picture courtesy... | Download Scientific Diagram • Renal Fascia: Anatomy and Function | Learn from doctor • Kidneys – Earth's Lab • Ureter – Anatomy QA • Ureter Anatomy & Function - Ectopic Ureter, Ureter Pain & Ureter Cancer • Pyelonephritis - acute | Health topics A to Z | CKS | NICE • Unenhanced CT in the evaluation of renal/ureteric colic • Ureteroscopy for kidney stones. Laser lithotripsy - KidneyStoners.org • PCNL.pdf • https://radiopaedia.org/articles/autosomal-dominant-polycystic-kidney-disease-1 • https://infokid.org.uk/conditions/horseshoe-kidney/