Glomerular and Tubulointerstitial Disease
Glomerular and Tubulointerstitial Disease
This domain tests pattern recognition: separating nephritic from nephrotic syndromes, linking serology and biopsy findings to a diagnosis, and choosing initial management. Expect questions on complement levels, immunofluorescence patterns, and drug-induced tubulointerstitial disease.
Core rules
- Nephritic syndrome: hematuria with dysmorphic RBCs and RBC casts, hypertension, oliguria, and falling GFR. Nephrotic syndrome: proteinuria >3.5 g/day, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.
- IgA nephropathy causes synpharyngitic gross hematuria 1–2 days after a URI with normal complement and mesangial IgA deposits. Post-infectious GN follows 1–3 weeks after strep infection with low C3 and subepithelial humps.
- Anti-GBM disease gives linear IgG on immunofluorescence; ANCA vasculitis is pauci-immune; membranous nephropathy shows subepithelial spikes and anti-PLA2R antibodies.
- Minimal change disease shows podocyte effacement and is steroid-responsive; FSGS shows segmental sclerosis. MPGN often has low C3 and tram-track appearance.
- Acute interstitial nephritis: drugs such as NSAIDs, antibiotics, and PPIs; fever, rash, eosinophilia, WBC casts, and eosinophiluria; stop the drug and consider steroids.
Worked example
A 28-year-old develops gross hematuria two days after a sore throat. Complement C3 is normal. Biopsy shows mesangial IgA deposits. The timing and normal complement point to IgA nephropathy, not post-infectious GN, which typically has a latent period and low C3. Management is supportive; ACE inhibitors reduce proteinuria in persistent disease.
Traps
- Calling RBC casts a lower urinary tract finding; they indicate glomerular bleeding.
- Forgetting that complement levels narrow the differential.
- Treating rapidly progressive GN before biopsy confirmation.
- Missing drug-induced AIN because fever and rash are absent.