Page 28 of 30
PE20.1-9 | Genito-Urinary System — Graded Quiz
Click any question card to reveal the correct answer.
A 2-year-old girl has her second febrile UTI in 6 months. MCU shows bilateral VUR grade III. DMSA scan reveals a cortical scar on the right upper pole. Which long-term complication is most important to monitor?
Reflux nephropathy (VUR + recurrent UTIs → cortical scarring) is the leading cause of hypertension and CKD in young adults. Bilateral scars significantly increase this risk.
Reflux nephropathy from recurrent febrile UTI + VUR is a leading preventable cause of hypertension and CKD in children. Annual BP measurement and eGFR monitoring are mandatory in children with bilateral renal scarring.
Calculi are not the primary complication of VUR; bladder neck obstruction is a cause, not a complication; isolated haematuria from chronic cystitis is not the major long-term concern.
Click to reveal answer
A 9-year-old boy had APSGN 6 weeks ago with low C3 at presentation. His repeat C3 is still low and he has ongoing haematuria and deteriorating renal function. What does this suggest?
In APSGN, C3 should normalise within 6–8 weeks. Persistent low C3 beyond 8 weeks should prompt investigation for other complement-consuming nephritides such as MPGN or lupus nephritis.
APSGN: C3 normalises by 6–8 weeks. Persistent low C3 + ongoing nephritis = investigate for MPGN, lupus nephritis, or chronic GN. A renal biopsy is indicated when the clinical course deviates from expected APSGN resolution.
Normal APSGN resolves with C3 normalisation by 6–8 weeks; empirical steroids without a biopsy are inappropriate for persistent nephritis; prophylactic penicillin is for prevention of recurrent streptococcal infections, not for persistent low C3.
Click to reveal answer
A 6-year-old boy presents with periorbital and scrotal oedema, urine protein 4+, serum albumin 1.6 g/dL, cholesterol 450 mg/dL, and no haematuria. C3 is normal. He is diagnosed with minimal-change nephrotic syndrome and started on prednisolone 2 mg/kg/day. Which is the MOST dangerous immediate complication?
Nephrotic syndrome causes urinary loss of IgG and alternative-pathway complement factors, severely impairing opsonisation. Spontaneous bacterial peritonitis from encapsulated organisms (S. pneumoniae) is a life-threatening emergency requiring prompt diagnosis and antibiotics.
The most dangerous immediate complications of nephrotic syndrome are: 1) bacterial peritonitis/sepsis (pneumococcal — due to IgG and opsonin loss), 2) thrombosis (urinary loss of antithrombin III + hyperfibrinogenaemia), and 3) hypovolaemia. Prophylactic penicillin V and pneumococcal vaccine are recommended.
Hyperkalaemia is not a feature of nephrotic syndrome (oedema causes dilutional hyponatraemia, not hyperkalaemia); hypernatraemia does not typically occur; polycythaemia is not a complication.
Click to reveal answer
A 7-year-old girl presents with painless gross haematuria. Urine microscopy shows dysmorphic red cells but no casts and no proteinuria. Blood pressure, serum creatinine, and C3 are normal. Which is the most appropriate initial investigation?
Isolated asymptomatic glomerular haematuria (dysmorphic RBCs, no proteinuria, normal function and BP) in a child most likely represents thin basement membrane nephropathy or IgA nephropathy. The initial workup includes renal USG, urine culture, and family screening for haematuria (TBM disease is autosomal dominant).
Isolated microscopic haematuria without proteinuria, hypertension, or renal impairment: workup includes USG and family screening for haematuria. Thin basement membrane nephropathy (autosomal dominant) and IgA nephropathy are common causes; most children have a benign course with normal long-term renal function.
Biopsy is not indicated initially for isolated haematuria with normal function and BP; CT urogram carries radiation and is not indicated over USG; cystoscopy is used for lower urinary tract evaluation, not glomerular haematuria.
Click to reveal answer
A 5-year-old develops oliguria, vomiting, and drowsiness 3 days after profuse bloody diarrhoea. Investigations: Hb 6.2 g/dL, platelets 35,000/µL, creatinine 5.1 mg/dL, blood smear shows schistocytes. What is the MOST appropriate supportive measure to restore haematological recovery?
In EHEC-HUS, management is supportive: packed red cells for haematocrit <18% or symptomatic severe anaemia; peritoneal/haemodialysis for AKI; strict fluid and electrolyte management. FFP, platelet transfusion, and antibiotics are not indicated (platelet transfusion can worsen microthrombi).
Typical EHEC-HUS: management is entirely supportive. Avoid antibiotics (worsen Shiga toxin release), avoid platelet transfusion (worsen thrombotic microangiopathy), avoid FFP. Packed RBCs for haematocrit <18%; dialysis for fluid overload/hyperkalaemia/uraemia. Plasmapheresis is for atypical HUS/TTP.
FFP is not indicated in typical HUS (not DIC); platelet transfusion may worsen thrombotic microangiopathy; plasmapheresis is the treatment for atypical HUS (complement-mediated) and TTP, not typical EHEC-HUS.
Click to reveal answer
A 12-year-old with CKD stage 4 (eGFR 18 mL/min/1.73 m²) develops metabolic acidosis (HCO₃⁻ 14 mEq/L). What is the PRIMARY reason to correct this acidosis promptly?
Metabolic acidosis in CKD accelerates CKD progression (through ammoniogenesis and complement activation), promotes protein catabolism and muscle wasting, worsens renal osteodystrophy, and further impairs linear growth. Oral sodium bicarbonate supplementation to maintain HCO₃⁻ ≥22 mEq/L is recommended.
Metabolic acidosis in CKD is a major cause of growth retardation, protein catabolism, bone disease, and accelerated CKD progression. Target: HCO₃⁻ ≥22 mEq/L with oral sodium bicarbonate. Also correct: hyperphosphataemia, anaemia (EPO), and hypertension in paediatric CKD.
Acidosis causes hyperkalaemia (not hypokalaemia — H⁺/K⁺ exchange); it does not directly treat hypertension; anaemia is from EPO deficiency, not acidosis.
Click to reveal answer
A Wilms tumour is staged as Stage III. Which feature is MOST likely responsible for this staging?
NWTS Stage III = residual non-haematogenous tumour confined to the abdomen: tumour rupture (iatrogenic or spontaneous), peritoneal implants, biopsy before nephrectomy, incomplete excision, or positive abdominal lymph nodes. This is why avoiding pre-operative palpation and biopsy is critical.
NWTS Wilms tumour staging: I = confined + complete excision; II = extends beyond kidney but complete excision; III = rupture/biopsy/residual/positive nodes (abdominal); IV = haematogenous metastases (lung/liver); V = bilateral. Tumour rupture from examination or biopsy converts Stage I/II → Stage III, mandating radiation and more intensive chemotherapy.
Stage I = confined kidney + complete excision; Stage II = extends beyond kidney but completely excised; Stage V = bilateral renal involvement.
Click to reveal answer
Urine microscopy from a child shows WBC casts and numerous polymorphonuclear leucocytes. Urine culture grows >10⁵ colony-forming units (CFU) of E. coli per mL. Which segment of the urinary tract is MOST likely involved?
WBC casts form when white cells aggregate within the renal tubular lumen and are incorporated into a Tamm-Horsfall protein matrix — they are pathognomonic of upper UTI (pyelonephritis) or acute interstitial nephritis.
WBC casts = pathognomonic of pyelonephritis (or acute interstitial nephritis). RBC casts = glomerular disease. Granular casts = tubular injury. Hyaline casts = physiological (exercise, fever). Fatty casts = nephrotic syndrome. Always examine casts under the microscope to localise the segment involved.
Urethritis and cystitis show pyuria without casts; glomerulonephritis shows RBC casts (not WBC casts).
Click to reveal answer
A plain X-ray KUB of a 8-year-old with right flank pain shows a faint calcification projected over the right ureter at the level of L3–L4. A small calcification is also noted at the right vesico-ureteric junction (VUJ). Ultrasound shows mild right hydronephrosis. What is the MOST appropriate next step in management?
Non-contrast CT KUB is the most sensitive imaging for urolithiasis (detects all stone types including radiolucent) and provides exact stone size, location, and density (Hounsfield units). Metabolic work-up (urine calcium, oxalate, citrate, uric acid, cystine screen) is mandatory in paediatric stone disease to identify the cause.
Paediatric urolithiasis management: USG first (no radiation); non-contrast CT KUB for precise characterisation; metabolic work-up in all children (high recurrence risk). KUB X-ray helps monitor known calcium stones. Conservative management (hydration, analgesia) for stones <5 mm; SWL/URS for larger or obstructing stones.
Discharge with analgesia alone misses the hydronephrosis and metabolic cause; immediate open surgery is not indicated for uncomplicated urolithiasis; IVU is an older technique with high radiation that has been superseded by CT.
Click to reveal answer
A 4-year-old develops the nephrotic syndrome and is started on prednisolone 2 mg/kg/day. After 4 weeks of daily steroids, urine protein is still 4+. He is declared steroid-resistant. What is the MOST important next investigation?
Steroid-resistant nephrotic syndrome (defined as persistent nephrotic-range proteinuria after 4 weeks of daily prednisolone at 2 mg/kg/day, per ISKDC) requires renal biopsy to identify the histological subtype (FSGS, mesangial proliferative, MCD) before choosing second-line immunosuppression.
Steroid-resistant nephrotic syndrome (SRNS) = no remission after 4 weeks of prednisolone 2 mg/kg/day (ISKDC criterion). Renal biopsy is mandatory. FSGS is the most common histology in SRNS. Second-line options: calcineurin inhibitors (cyclosporine/tacrolimus) ± ACE inhibitor.
Empirical IV pulses without biopsy are not standard; cyclosporine/tacrolimus dosing and choice depend on biopsy findings; repeating the same course without biopsy is not evidence-based for steroid-resistant nephrotic syndrome.
Click to reveal answer