Kidney And Urinary Tract Pathology
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Direct answer
Renal pathology divides into glomerular, tubulointerstitial and neoplastic disease. Nephritic syndrome presents with haematuria, dysmorphic red cells and red cell casts, hypertension and oliguria; nephrotic syndrome with proteinuria above 3.5 g daily, hypoalbuminaemia, oedema and hyperlipidaemia. Tubulointerstitial disease covers ischaemic and toxic acute tubular injury, drug-induced interstitial nephritis and pyelonephritis, while stones and the three exam tumours — renal cell carcinoma, Wilms tumour and urothelial carcinoma — complete the tract. FMGE rewards the buzzwords: subepithelial humps, spike and dome, tram-track, linear deposits.
What you must remember
- Post-streptococcal glomerulonephritis: children one to three weeks after pharyngitis, low C3, raised ASO; lumpy-bumpy granular deposits with subepithelial humps on electron microscopy; usually self-limiting.
- Other nephritic patterns: IgA nephropathy (Berger) with haematuria one to two days after a cold, the commonest glomerulonephritis worldwide; crescentic rapidly progressive disease — anti-GBM with linear immunofluorescence and lung haemorrhage (Goodpasture), or pauci-immune ANCA-associated; Alport with collagen IV defect, basket-weave basement membrane, deafness and ocular signs.
- Nephrotic syndrome: minimal change disease in children (foot-process effacement, steroid-responsive); membranous in adults (anti-PLA2R, spike-and-dome deposits); focal segmental glomerulosclerosis including the HIV collapsing variant; membranoproliferative with tram-track appearance.
- Systemic renal disease: diabetic nodular glomerulosclerosis (Kimmelstiel-Wilson) with microalbuminuria earliest; lupus with full-house immunofluorescence; amyloid with Congo red apple-green birefringence.
- Tubulointerstitial: acute tubular injury from ischaemia or aminoglycosides, contrast and myoglobin, with muddy brown granular casts; drug-induced interstitial nephritis with fever, rash and eosinophilia; pyelonephritis with white cell casts; papillary necrosis in diabetes, obstruction and sickle disease.
- Stones: calcium oxalate commonest; struvite staghorn from urease-producing Proteus in alkaline urine; uric acid radiolucent; cystine with hexagonal crystals in children.
- Tumours: renal cell carcinoma — clear cells, haematuria-pain-mass triad, left varicocele from renal vein invasion, erythropoietin polycythaemia and PTHrP hypercalcaemia; Wilms tumour — paediatric painless abdominal mass with WAGR and Beckwith-Wiedemann associations; urothelial carcinoma — bladder, painless gross haematuria, linked to smoking, dyes and cyclophosphamide, with schistosomiasis causing squamous cancer.
Common confusion
Nephritic versus nephrotic: abrupt haematuria with casts and hypertension against heavy proteinuria with oedema; membranous disease belongs to adults, minimal change to children. Muddy brown granular casts mark tubular injury, red cell casts glomerulitis. A new left varicocele from renal vein invasion must not be dismissed as the benign adolescent type.
Exam-focused takeaway
FMGE gives a deposition or biopsy phrase and expects the disease: humps (post-streptococcal), spikes (membranous), tram-track (membranoproliferative), linear (anti-GBM), foot-process effacement (minimal change). Scenario stems cover the post-streptococcal child, aminoglycoside injury, staghorn calculi and painless haematuria in a smoker.
Frequently asked questions
Which glomerulonephritis follows streptococcal infection?
Post-streptococcal glomerulonephritis, one to three weeks after pharyngitis, with hypocomplementaemia and subepithelial humps; children usually recover fully.
What is the commonest nephrotic cause in a child?
Minimal change disease, with normal light microscopy and foot-process effacement on electron microscopy, responding to corticosteroids.
Which stain shows renal amyloid?
Congo red with apple-green birefringence under polarised light in mesangium and vessels, causing nephrotic-range proteinuria with chronic inflammation.
Which stone relates to urinary infection?
Struvite, magnesium ammonium phosphate formed by urease-splitting Proteus in alkaline urine, growing into staghorn calculi needing removal plus infection control.
How does renal cell carcinoma present classically?
Haematuria, flank pain and a palpable mass — often late — with paraneoplastic polycythaemia or hypercalcaemia, and renal vein invasion explaining a new left varicocele.
Why does bladder cancer present early?
Even low-grade papillary urothelial tumours bleed, so painless gross haematuria brings early cystoscopy; urothelial field change explains high recurrence demanding surveillance.