Nephrotic vs Nephritic

Who: Children (2-6 yo). Also: NSAIDsNSAIDs reduce prostaglandin-mediated blood flow to the glomerulus. The resulting ischemia can trigger podocyte injury → minimal change pattern., Hodgkin lymphomaHodgkin releases cytokines (IL-13) that damage podocyte foot processes. If an adult presents with MCD, screen for lymphoma..

Biopsy: Light microscopy is normal (that's the "minimal change"). EM shows foot process effacement — the podocytes flatten out.

Treatment: Steroids — responds dramatically. If it doesn't, rethink the diagnosis.

Board clue: Kid + nephrotic + responds to steroids = MCD until proven otherwise.

Who: African Americans (#1 cause of nephrotic in AA), HIV, heroin use, obesity, sickle cell.

Biopsy: Focal (some glomeruli) + segmental (part of a glomerulus) sclerosis on LM. EM shows foot process effacement (like MCD but with sclerosis).

Why boards test it: It's the most common primary nephrotic syndrome in African American adults. HIV-associated nephropathy = FSGS.

Response to steroids: Poor (unlike MCD). This is a key differentiator.

Who: #1 nephrotic in adults overall. Associations: HBVHepatitis B antigens deposit in the subepithelial space, forming immune complexes that thicken the basement membrane., SLE (class V), solid tumors, anti-PLA2R antibodiesPhospholipase A2 receptor antibodies — present in ~70% of primary membranous. The target antigen sits on podocytes. This is the diagnostic serologic marker..

Biopsy: "Spike and dome" pattern on silver stain. Subepithelial deposits (between podocyte and GBM). Diffuse thickening of GBM.

Board clue: Adult + nephrotic + subepithelial deposits = membranous. If they mention anti-PLA2R, it's basically free points.

Who: Long-standing diabetes (type 1 or 2). Most common cause of nephrotic syndrome AND ESRD in the US.

Biopsy: Kimmelstiel-Wilson nodulesNodular glomerulosclerosis — round, acellular, eosinophilic nodules in the mesangium. Pathognomonic for diabetic nephropathy. Named after the two pathologists who described them in 1936. (nodular glomerulosclerosis). Diffuse GBM thickening + mesangial expansion.

Progression: Microalbuminuria → overt proteinuria → nephrotic syndrome → ESRD. ACE inhibitors slow progression (reduce intraglomerular pressure).

Board clue: Diabetic for 15+ years + proteinuria = diabetic nephropathy. Don't overthink it.

What: Misfolded proteins (amyloid) deposit in the kidney (and other organs). AL (primary, from plasma cells) or AA (secondary, from chronic inflammation like RA).

Biopsy: Congo red stain → apple-green birefringence under polarized light. That's the pathognomonic finding.

Board clue: Nephrotic syndrome + multiple organ involvement (big tongue, carpal tunnel, heart failure) + Congo red positive = amyloidosis.

Key fact: Most common glomerulonephritisGlomerulonephritis = inflammation of the glomeruli. All nephritic diseases are forms of GN. The "-itis" suffix = inflammation = blood getting through. worldwide. Usually young adults.

Presentation: Gross hematuria DURING or within days of a URI (synpharyngitic — happens simultaneously, NOT weeks later).

Biopsy: Mesangial IgA depositsIgA is the mucosal antibody (gut, respiratory). During infection, IgA production surges. Abnormal IgA1 isn't cleared → deposits in the mesangium → inflammation → hematuria. on immunofluorescence.

Complement: Normal (not consumed in this process).

HSP connection: Henoch-Schonlein PurpuraHSP is the systemic form of IgA nephropathy. Same IgA deposits, but also in skin vessels (purpura), joints, GI tract. Think: IgA nephropathy is Berger disease (kidney only), HSP is Berger disease + everything else. = systemic IgA vasculitis. Same kidney findings, but add purpura + arthritis + abdominal pain.

Who: Kids (6-10 yo), 2-4 weeks AFTER Group A Strep pharyngitis or skin infection.

Key timing: AFTER, not during. This is the #1 differentiator from IgA (which is during/synpharyngitic).

Biopsy: "Lumpy bumpy" subepithelial depositsImmune complexes (antibody-antigen from the strep infection) deposit on the outer surface of the GBM. They're irregular = lumpy bumpy on immunofluorescence. Granular pattern. on IF. Enlarged, hypercellular glomeruli on LM.

Labs: Low C3 (complement consumed), elevated ASO/anti-DNase BASO (anti-streptolysin O) rises after pharyngitis. Anti-DNase B rises after skin infections. These confirm prior strep infection, not active infection..

Prognosis: Kids almost always recover fully. Adults have worse outcomes.

What: Rapid loss of kidney function (days to weeks). The most aggressive form of GN.

Biopsy: Crescents on light microscopy — proliferating parietal cells and macrophages in Bowman's space.

Three types:

• Type I — Anti-GBM (GoodpastureAnti-GBM antibodies attack type IV collagen in the glomerular AND alveolar basement membranes. Kidney + lungs. Linear IF pattern. Young men who smoke are classic.): Linear IF pattern. Lungs + kidneys.
• Type II — Immune complex: Granular IF pattern. Caused by SLE, IgA, post-strep going bad.
• Type III — Pauci-immune (ANCA-associatedPauci-immune = few/no immune deposits on IF. The damage is from neutrophils activated by ANCA antibodies (c-ANCA in GPA, p-ANCA in MPA/EGPA). "Pauci" = the IF is deceptively quiet while the kidney is being destroyed.): Negative/few deposits on IF. GPA (c-ANCA), MPA (p-ANCA).

Board clue: Rapidly worsening renal function + crescents on biopsy = RPGN. Then use IF pattern to identify the type.

What: Defective type IV collagenType IV collagen is the structural protein of ALL basement membranes — kidney, eye, ear. That's why Alport hits all three. The mutation makes the GBM progressively thin → split → fail. — the stuff basement membranes are made of.

Inheritance: Most commonly X-linked (boys hit harder, carrier moms may have mild hematuria).

Triad: Nephritis + sensorineural hearing loss + eye abnormalities (anterior lenticonus).

EM: "Basket-weave" splitting of the GBM.

Board clue: Young male + hematuria + hearing loss = Alport. Don't overthink it.