PE20.1-9 | Genito-Urinary System — Practice Quiz

Escherichia coli accounts for 75–85% of all urinary tract infections in children due to its uropathogenic virulence factors (P-fimbriae, haemolysin).

E. coli is the most common uropathogen across all paediatric age groups. A midstream clean-catch urine culture (significant growth ≥10⁵ CFU/mL for spontaneous void) remains the gold standard for diagnosis.

Klebsiella is second most common but much less frequent; Pseudomonas is seen mainly in catheterised/immunocompromised patients; S. saprophyticus is a cause in adolescent females, not toddlers.

Current guidelines (NICE/IAP) recommend renal ultrasound (acute phase), then MCU to grade VUR and DMSA scan 4–6 months post-infection to detect renal scarring.

After a first febrile UTI in children <2 years, the recommended imaging is: renal USG acutely, MCU to grade VUR (I–V), and DMSA scan at 4–6 months to assess renal scarring.

CT urogram carries unnecessary radiation; ultrasound alone misses VUR and cortical scars; IVU is now rarely used in children.

APSGN presents with the nephritic syndrome (haematuria, hypertension, oligoedema) typically 1–2 weeks after pharyngitis (or 3–6 weeks after pyoderma), with LOW C3 and elevated ASO/anti-DNase B.

APSGN has a latent period of 1–2 weeks post-pharyngitis (or 3–6 weeks post-pyoderma). Serum C3 is LOW at presentation and normalises by 6–8 weeks; failure to normalise should prompt search for other diagnoses. ASO titre is elevated in post-pharyngitis cases; anti-DNase B is more sensitive for post-pyoderma APSGN.

Nephrotic syndrome has massive proteinuria, hypoalbuminaemia, and normal C3; IgA nephropathy presents with synpharyngitic haematuria (concurrent, not 1–2 weeks later); HUS features microangiopathic anaemia + thrombocytopenia.

Nephrotic syndrome in a school-age child with the classic presentation (nephrotic-range proteinuria, hypoalbuminaemia, oedema, normal C3) is treated with oral prednisolone 2 mg/kg/day (max 60 mg/day) for 4 weeks, then tapering.

Childhood nephrotic syndrome in a school-age child with selective proteinuria and normal complement is most likely minimal-change disease (MCNS), which is steroid-sensitive in ~90% of cases. First-line: prednisolone 2 mg/kg/day (max 60 mg/day) for 4 weeks, then alternate-day for 4 weeks (ISKDC/IAP protocol).

Cyclophosphamide is reserved for steroid-resistant or frequently-relapsing nephrotic syndrome; furosemide alone does not address the underlying glomerular leak; ACE inhibitors reduce proteinuria but are not the primary treatment for acute nephrotic syndrome.

Red cell casts are pathognomonic of glomerular bleeding. Cola-coloured (tea-coloured) urine without clots is characteristic of glomerular haematuria; RBC casts form in the renal tubules from RBCs + Tamm-Horsfall protein.

Red cell casts on urine microscopy are pathognomonic of glomerular haematuria. Dysmorphic RBCs and proteinuria (nephrotic-range or sub-nephrotic) further support glomerular origin. Non-glomerular haematuria (calculus, tumour, UTI) typically shows isomorphic RBCs without casts.

Renal calculus causes colicky pain with haematuria; UTI-associated haematuria rarely produces RBC casts; Wilms tumour presents with an abdominal mass and less frequently with gross haematuria — RBC casts would not be present.

Antibiotics are CONTRAINDICATED in EHEC-associated HUS because they trigger bacterial lysis and massive Shiga toxin release, worsening the endothelial injury and accelerating HUS progression.

HUS (triad: microangiopathic haemolytic anaemia + thrombocytopenia + AKI) is most commonly caused by EHEC O157:H7 in children. Antibiotics are CONTRAINDICATED as they increase Shiga toxin release. Management is supportive: fluid balance, dialysis when needed, and red cell transfusion for severe anaemia.

Dialysis is indicated for refractory AKI in HUS; antihypertensives are used for hypertensive crisis; red cell transfusion is given for haematocrit <18% or severe symptomatic anaemia.

In CKD, impaired 1,25-dihydroxyvitamin D synthesis leads to hypocalcaemia, secondary hyperparathyroidism, hyperphosphataemia, and renal osteodystrophy. Combined with GH-IGF-1 axis resistance, these are the primary drivers of linear growth failure.

Paediatric CKD causes growth failure through: 1) renal osteodystrophy (low calcitriol → secondary hyperparathyroidism → bone disease), 2) GH-IGF-1 resistance, and 3) metabolic acidosis. Management includes phosphate binders, calcitriol, correction of acidosis, and recombinant growth hormone.

Anaemia contributes to fatigue but is not the main driver of growth failure; hypertension per se does not directly stunt growth; dietary protein restriction is guided carefully in CKD and is not the primary cause.

Wilms tumour (nephroblastoma) in a young child requires urgent CT abdomen for staging (NWTS staging I–V) and surgical referral. The capsule must NOT be palpated repeatedly as this risks tumour rupture and upstaging.

Wilms tumour (nephroblastoma) is the most common renal malignancy in children (peak age 3–4 years). DO NOT palpate repeatedly — rupture upstages the tumour. NWTS staging (I–V) guides management. Distinguish from neuroblastoma: Wilms is intrarenal (displaces kidney but stays contained), crosses midline rarely; neuroblastoma often crosses midline, encases vessels.

Vigorous palpation risks tumour rupture; chemotherapy is staged after histological confirmation; a renal mass in a young child must never be dismissed.

Granular casts represent degenerated cellular casts and indicate tubular injury accompanying glomerulonephritis; the combination of haematuria, proteinuria, WBCs, and granular casts defines an active nephritic sediment.

On urine microscopy: normal <5 RBCs/HPF and <5 WBCs/HPF; RBC casts = glomerular; WBC casts = pyelonephritis/interstitial nephritis; granular casts = tubular injury; hyaline casts = normal in small numbers. Dipstick blood positive with abundant RBCs = haematuria; positive without RBCs = haemoglobinuria or myoglobinuria.

This is clearly abnormal and requires urgent evaluation; secondary UTI is possible but not the primary interpretation; haemoglobinuria shows dipstick blood with no/few RBCs on microscopy — here RBCs are abundant.

Calcium oxalate (and calcium phosphate) stones are radio-opaque on plain KUB X-ray because calcium is radiopaque; they account for the majority (~75%) of urinary calculi in children.

On plain KUB: calcium oxalate/phosphate stones = radio-opaque (most common, 75%); cystine = faint ground-glass opacity; uric acid/matrix = radiolucent. Ultrasound detects all stone types (including radiolucent) and is first-line in children. KUB X-ray helps in monitoring known calcium stones.

Uric acid stones are radiolucent (not visible on plain X-ray); cystine stones are faintly opaque (ground-glass); matrix stones are radiolucent.