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What are the key features of nephrotic syndrome?
Proteinuria >3.5g/day, hypoalbuminemia, hyperlipidemia, edema.
Which histological change is characteristic of minimal change disease?
Normal light microscopy; podocyte foot process effacement on electron microscopy.
What is the most common cause of nephrotic syndrome in adults?
Membranous nephropathy.
What are the key features of nephritic syndrome?
Hematuria with RBC casts, proteinuria (<3.5g/day), hypertension, oliguria, edema.
Which glomerular disease is strongly associated with upper respiratory tract infections?
IgA nephropathy (Berger’s disease).
What is the hallmark histological finding in membranous nephropathy?
Spike and dome appearance on silver stain.
What histological pattern is typical of post-infectious glomerulonephritis?
Diffuse hypercellular glomeruli with subepithelial "hump-like" deposits.
What urinary findings are characteristic of nephritic syndrome?
Dysmorphic RBCs and red cell casts.
What is the primary pathophysiology of diabetic nephropathy?
Hyperglycemia causes glomerular basement membrane thickening, mesangial expansion, and nodular sclerosis.
What are Kimmelstiel-Wilson nodules?
Nodular glomerulosclerosis seen in diabetic nephropathy.
What is the most common cause of AKI in hospitalized patients?
Pre-renal hypoperfusion (e.g., dehydration, sepsis).
What is the typical histological finding in acute tubular necrosis (ATN)?
Tubular epithelial cell necrosis and muddy brown casts.
What is the significance of fractional excretion of sodium (FeNa) >2%?
Suggests intrinsic renal failure, such as ATN.
What are the three phases of AKI?
Initiation, maintenance, and recovery phases.
What is the first-line imaging for urinary tract obstruction in AKI?
Renal ultrasound.
What defines chronic kidney disease (CKD)?
GFR
What are common biochemical findings in CKD?
Elevated creatinine and urea, hyperphosphatemia, hypocalcemia, metabolic acidosis.
What is the typical kidney appearance on ultrasound in CKD?
Small, echogenic, and shrunken kidneys.
What causes anemia in CKD?
Decreased erythropoietin production by the diseased kidneys.
What are the features of CKD-mineral bone disorder (CKD-MBD)?
Secondary hyperparathyroidism, hyperphosphatemia, hypocalcemia, bone pain, and vascular calcification.
What causes secondary hyperparathyroidism in CKD?
Phosphate retention and reduced calcitriol synthesis lead to low calcium and increased PTH.
Which organisms commonly cause UTIs according to the slides?
Escherichia coli, Proteus mirabilis, Klebsiella spp.
What is the most specific urinalysis finding for pyelonephritis?
White cell casts.
What are the risk factors for recurrent UTIs mentioned in the notes?
Female sex, sexual activity, urinary tract anomalies, and catheter use.
What is vesicoureteral reflux and what predisposes to it?
Retrograde flow of urine due to a short or incompetent intramural ureter segment.
How does urine move from kidneys to bladder?
Peristalsis in the ureters.
What mechanism prevents reflux of urine from bladder into ureters?
Oblique insertion of ureters into bladder wall acts as a valve.
What is the nerve responsible for voluntary control of micturition?
Pudendal nerve controls the external urethral sphincter.
What controls bladder contraction during voiding?
Parasympathetic fibers via pelvic splanchnic nerves (S2–S4).
What is the histological hallmark of clear cell renal carcinoma?
Cells with clear cytoplasm and delicate vasculature.
Where does clear cell renal cell carcinoma originate from?
Proximal convoluted tubule.
What is the most common histological type of bladder cancer?
Transitional cell (urothelial) carcinoma.
What is the hallmark histological feature of chronic pyelonephritis?
Thyroidization of tubules with eosinophilic casts.
Which renal tumour is associated with von Hippel-Lindau disease?
Clear cell renal cell carcinoma.
Which urinary stone is associated with urease-producing organisms?
Struvite stones (magnesium ammonium phosphate).
What is the first-line imaging for suspected renal stones?
Non-contrast CT KUB.
What is the typical composition of the most common kidney stone?
Calcium oxalate.
What inherited condition causes hexagonal cystine crystals in urine?
Cystinuria.
What is the most common cause of nephrotic syndrome in children?
Minimal change disease.
What is the key diagnostic feature of minimal change disease on electron microscopy?
Effacement of podocyte foot processes.
What is the most common cause of nephrotic syndrome in adults?
Membranous nephropathy.
What is the hallmark histological finding in membranous nephropathy?
"Spike and dome" appearance on silver stain.
What glomerular disease is associated with obesity and heroin use?
Focal segmental glomerulosclerosis (FSGS).
What histological feature defines FSGS?
Segmental sclerosis of some glomeruli.
Which disease is characterized by Kimmelstiel-Wilson nodules?
Diabetic nephropathy.
What is the earliest change seen in diabetic nephropathy?
Glomerular basement membrane thickening.
What is the hallmark clinical feature of nephrotic syndrome?
Proteinuria >3.5 g/day, hypoalbuminemia, edema.
What disease presents with hematuria, hypertension, and red blood cell casts?
Nephritic syndrome.
What is the most common glomerulonephritis worldwide?
IgA nephropathy.
What histological feature is seen in IgA nephropathy?
Mesangial proliferation with IgA deposits on immunofluorescence.
What is the characteristic feature of post-streptococcal glomerulonephritis?
Subepithelial humps on electron microscopy.
What is the typical trigger for IgA nephropathy?
Mucosal infections, especially upper respiratory tract infections.
What diagnostic test is used to identify glomerular disease subtypes?
Renal biopsy with light microscopy, immunofluorescence, and electron microscopy.
Which glomerular disease is associated with hepatitis B infection?
Membranous nephropathy.
What are the classic features of acute tubular necrosis (ATN)?
Muddy brown granular casts in urine, elevated creatinine, oliguria.
What is the most common cause of AKI in hospital settings?
Pre-renal hypoperfusion (e.g., volume depletion, sepsis).
What lab finding distinguishes intrinsic AKI from pre-renal AKI?
Fractional excretion of sodium (FeNa) >2% in intrinsic AKI.
What is the hallmark of rapidly progressive glomerulonephritis (RPGN)?
Crescent formation in Bowman's space.
What histological feature is diagnostic of amyloidosis in the kidney?
Congo red staining with apple-green birefringence under polarized light.
What is the typical presentation of chronic pyelonephritis?
Recurrent UTIs, renal scarring, and "thyroidization" of tubules.
What is the primary diagnostic imaging for suspected urinary tract calculi?
Non-contrast CT of the kidneys, ureters, and bladder (CT KUB).
What type of renal stone is associated with Proteus infections?
Struvite stones (magnesium ammonium phosphate).
What inherited condition leads to cystine stones?
Cystinuria.
What is the hallmark histological feature of clear cell renal carcinoma?
Tumor cells with clear cytoplasm due to lipid and glycogen accumulation.
What is the most common type of bladder cancer?
Transitional (urothelial) cell carcinoma.
What is the first-line imaging for evaluation of AKI?
Renal ultrasound to assess for obstruction.
What causes anemia in chronic kidney disease?
Reduced erythropoietin production by the kidneys.
What is the primary cause of CKD-MBD (mineral bone disorder)?
Phosphate retention and reduced calcitriol synthesis leading to secondary hyperparathyroidism.
What are key lab features of CKD-MBD?
High phosphate, low calcium, high PTH.
What urinary cast is most specific for pyelonephritis?
White blood cell casts.
What organism most commonly causes UTIs?
Escherichia coli.
What structure prevents vesicoureteral reflux?
Oblique entry of ureters into the bladder wall.
Which nerve provides voluntary control of the external urethral sphincter?
Pudendal nerve.
What bladder condition involves detrusor overactivity and urgency?
Urge incontinence.
What is the first-line treatment for minimal change disease?
High-dose corticosteroids (prednisolone).
What is the mainstay of treatment for membranous nephropathy with nephrotic syndrome?
ACE inhibitors/ARBs for proteinuria; immunosuppressants if severe.
What medication class is used to reduce proteinuria in nephrotic syndrome?
ACE inhibitors or ARBs.
How is edema managed in nephrotic syndrome?
Loop diuretics (e.g., furosemide).
What is the general treatment approach for focal segmental glomerulosclerosis (FSGS)?
ACEi/ARB, corticosteroids, possible immunosuppressants.
What is the management of IgA nephropathy with persistent proteinuria?
ACE inhibitors or ARBs; corticosteroids if proteinuria >1 g/day.
What is the treatment for post-streptococcal glomerulonephritis?
Supportive: manage hypertension, fluid overload; antibiotics if infection persists.
How is acute kidney injury (AKI) managed initially?
Identify and treat the underlying cause, fluid resuscitation, and stop nephrotoxins.
What is the management of hyperkalemia in AKI?
IV calcium gluconate, insulin with glucose, beta-agonists, and potassium binders.
What therapy is used if AKI progresses to severe acidosis or volume overload?
Renal replacement therapy (dialysis).
What is the first-line management of pre-renal AKI?
Volume repletion with IV fluids.
What is the mainstay of treatment for acute tubular necrosis (ATN)?
Supportive care: fluids, avoid nephrotoxins, manage electrolytes.
What is the key management strategy in chronic kidney disease (CKD)?
Control underlying cause (e.g., diabetes, hypertension), ACEi/ARB, lifestyle modification.
What is used to manage hypertension in CKD?
ACE inhibitors or ARBs.
How is anemia of CKD treated?
Erythropoiesis-stimulating agents (e.g., EPO), iron supplementation.
What medications manage mineral bone disorder in CKD?
Phosphate binders, active vitamin D analogs (calcitriol), cinacalcet.
What dietary advice is given in advanced CKD?
Restriction of sodium, phosphate, potassium, and fluid depending on stage.
When is dialysis indicated in CKD?
When GFR <15 or in presence of refractory symptoms like fluid overload, hyperkalemia, or uremia.
What are the two main types of dialysis used in renal replacement therapy?
Hemodialysis and peritoneal dialysis.
What is the definitive treatment for end-stage renal disease (ESRD)?
Renal transplantation.
How are uncomplicated UTIs treated?
Oral antibiotics: nitrofurantoin or trimethoprim.
How is pyelonephritis treated?
Broad-spectrum IV antibiotics initially (e.g., ceftriaxone), then step down to oral.
What is the prophylactic treatment for recurrent UTIs?
Low-dose nightly antibiotics or post-coital prophylaxis.
How are urinary tract stones managed acutely?
NSAIDs for pain, hydration, and alpha-blockers (e.g., tamsulosin) for stone passage.
What is the intervention for large or obstructive renal stones?
Shock wave lithotripsy, ureteroscopy, or percutaneous nephrolithotomy.
What medication reduces calcium stone recurrence?
Thiazide diuretics.