Glomerular Diseases — Nephritic vs Nephrotic

Nephritic: hematuria + HTN + low GFR. Nephrotic: proteinuria + edema + hyperlipidemia.

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◆Diagnostic clues / contrasts

•Cola-colored urine + RBC casts + dysmorphic RBCs = NEPHRITIC
•Frothy urine + edema + hyperlipidemia + lipiduria (Maltese cross) = NEPHROTIC
•Synpharyngitic (DAYS after URI) = IgA. Post-pharyngitic (1–4 WEEKS after) = PSGN
•Low C3 + C4 = lupus, MPGN. Low C3 only = PSGN, endocarditis-associated GN
•Hemoptysis + GN: Goodpasture (linear IgG) or GPA (c-ANCA)
•Nephrotic + hepatitis B = membranous; nephrotic + HIV/Black = FSGS; nephrotic + child = minimal change

•Hypercoagulability (loss of antithrombin III) → renal vein thrombosis (esp. membranous); flank pain + sudden ↓ renal function
•Infection (loss of IgG) → encapsulated organisms
•Hyperlipidemia → atherosclerosis
•Hypocalcemia (vit D binding protein loss)

Disease	Features	Complement	Light micro / IF / EM	Treatment
Post-streptococcal GN	1–4 weeks after pharyngitis/impetigo (kids); cola urine + edema + HTN	↓ C3	Hypercellular glomeruli; 'lumpy bumpy' IgG/C3; subepithelial 'humps'	Supportive; usually self-resolves
IgA nephropathy (Berger)	Synpharyngitic hematuria (within DAYS of URI, not weeks)	Normal	Mesangial IgA + C3	ACEi; steroids if severe
Anti-GBM (Goodpasture)	Hemoptysis + glomerulonephritis (pulmonary-renal)	Normal	Linear IgG on IF	Plasmapheresis + steroids + cyclophosphamide
Rapidly progressive GN (crescentic)	Renal failure in days–weeks; crescents on biopsy	Variable	Crescents = subdivisions: type I anti-GBM, II immune complex (lupus, PSGN, IgA), III pauci-immune (ANCA — GPA, MPA, EGPA)	Aggressive immunosuppression
Lupus nephritis	Lupus + hematuria/proteinuria	↓ C3, ↓ C4	Class IV diffuse proliferative most common/severe; full-house IF (IgG, IgM, IgA, C3, C1q)	Steroids + cyclophosphamide or MMF
MPGN	Mixed nephritic/nephrotic; HCV + cryoglobulinemia association	↓ C3, ↓ C4	Tram-track BM splitting; subendothelial deposits	Treat underlying
Alport syndrome	Hereditary; sensorineural hearing loss + lens dislocation + hematuria	Normal	Type IV collagen mutation; basket-weave EM	ACEi; eventual transplant

Disease	Demographics	Features	Biopsy	Treatment
Minimal change disease	Most common in CHILDREN; after URI/vaccine/Hodgkin	Selective albuminuria	Light micro normal; EM podocyte foot process effacement	Steroids (highly responsive)
FSGS	Most common in ADULTS (Black, HIV, heroin, obesity, sickle cell)	Non-selective proteinuria	Segmental sclerosis	Steroids ± immunosuppression; poor response often
Membranous nephropathy	Adults — primary (anti-PLA2R antibody) or secondary (hepatitis B, SLE, malignancy, drugs — gold, penicillamine, NSAIDs)	Hypercoagulable (renal vein thrombosis)	Spike and dome subepithelial deposits; granular IF	ACEi + immunosuppression
Diabetic nephropathy	Long-standing DM; hyperglycemia → mesangial expansion → Kimmelstiel-Wilson nodules	Microalbuminuria earliest	GBM thickening, mesangial expansion	ACEi/ARB + SGLT2; tight glycemic control
Amyloidosis	Multiple myeloma (AL), chronic inflammation (AA)	Restrictive cardiomyopathy + nephrotic + macroglossia	Apple-green birefringence under polarized light with Congo red	Treat underlying

◆Mnemonic for nephritic: hematuria + HTN + Oliguria + RBC casts (cola urine)
◆Mnemonic for nephrotic: massive Proteinuria + edema + hypoalbumin + hyperlipidemia
◆Acute interstitial nephritis (AIN): triad of fever + rash + eosinophilia after drug (PPI, NSAID, β-lactam, sulfa); WBC casts + eos in urine — stop drug
◆ATN: muddy brown casts (covered in S2 renal note)

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