Glomerular diseases overview

Glomerular diseases overview

Glomerular diseases overview

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Glomerular Anatomy - The Kidney's Sieve

Renal Corpuscle: Glomerulus and Glomerular Capsule

  • Glomerular Filtration Barrier (GFB): A three-layered sieve controlling passage from blood to urine.
    • 1. Fenestrated Capillary Endothelium: First layer; blocks cells but allows plasma through.
    • 2. Glomerular Basement Membrane (GBM): Middle layer; with Type IV collagen and negatively charged heparan sulfate.
    • 3. Podocyte Foot Processes: Outer layer with slit diaphragms between them.
  • Selective Permeability:
    • Size Barrier: Prevents passage of molecules > 70 kDa.
    • Charge Barrier: Anionic heparan sulfate in the GBM repels negatively charged molecules like albumin.

High-Yield Fact: Podocyte effacement (flattening of foot processes) is the characteristic finding in Minimal Change Disease, leading to selective albuminuria.

Nephritic vs. Nephrotic - A Clinical Duel

  • Nephritic Syndrome: "Inflammation"

    • Pathophysiology: Immune complex deposition → glomerular inflammation (hypercellularity).
    • Hallmarks: Hematuria (dysmorphic RBCs, RBC casts) & Azotemia (↑ BUN/Cr).
    • Clinical: Abrupt onset of oliguria, hypertension, and mild periorbital edema from salt/water retention.
    • Proteinuria: Mild to moderate, always < 3.5 g/day.
  • Nephrotic Syndrome: "Podocyte Damage"

    • Pathophysiology: Podocyte effacement → loss of negative charge barrier → massive protein leak.
    • Hallmarks: Heavy proteinuria (> 3.5 g/day) & severe hypoalbuminemia (< 3.0 g/dL).
    • Clinical: Insidious onset of anasarca (pitting edema, ascites), hyperlipidemia (fatty casts, oval fat bodies), and frothy urine.
    • 📌 PALE Mnemonic: Proteinuria, HypoAlbuminemia, HyperLipidemia, Edema.

⭐ Loss of antithrombin III in nephrotic syndrome urine creates a hypercoagulable state, predisposing patients to thrombosis, particularly renal vein thrombosis.

  • Nephrotic Syndrome: Massive proteinuria (>3.5 g/day), hypoalbuminemia, edema, hyperlipidemia/uria.
    • 📌 PALE: Proteinuria, Albuminemia (hypo), Lipidemia (hyper), Edema.
    • Minimal Change (MCD): #1 in kids. LM normal; EM shows podocyte effacement.
    • FSGS: #1 in adults (esp. Black). LM shows sclerosis; EM effacement.
    • Membranous Nephropathy: #2 in adults. LM thick GBM; IF granular; EM "spike & dome."
  • Nephritic Syndrome: Inflammation. Hematuria (RBC casts), HTN, oliguria, azotemia.
    • Post-strep (PSGN): LM hypercellular glomeruli; IF "starry sky"; EM subepithelial humps.
    • IgA Nephropathy (Berger): Most common cause worldwide. Episodic hematuria post-URI/GI infection.
    • RPGN: Crescents on LM. Poor prognosis.

⭐ Subepithelial "humps" on EM are characteristic of PSGN, representing immune complex deposition.

Post-streptococcal glomerulonephritis: EM, IF, and PAS

High‑Yield Points - ⚡ Biggest Takeaways

  • Nephritic syndrome: Inflammatory process causing hematuria (RBC casts), oliguria, and hypertension.
  • Nephrotic syndrome: Massive proteinuria (>3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia.
  • Linear IF is pathognomonic for Goodpasture syndrome; most others are granular.
  • Podocyte effacement on EM is the hallmark of Minimal Change Disease.
  • Look for "spike and dome" in Membranous Nephropathy and "tram-tracks" in MPGN.
  • FSGS is the most common cause of nephrotic syndrome in adults.
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Practice Questions: Glomerular diseases overview

Test your understanding with these related questions

A 43-year-old man comes to the physician for a 1-week history of swelling around his eyes and decreased urination. His pulse is 87/min, and blood pressure is 152/95 mm Hg. Physical examination shows 1+ periorbital and pretibial edema. Serum studies show a urea nitrogen concentration of 21 mg/dL and a creatinine concentration of 1.4 mg/dL. Urinalysis shows 3+ blood and 1+ protein. Further evaluation of this patient is most likely to show which of the following?

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Flashcards: Glomerular diseases overview

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Circulating _____ deposition causes glomerular damage and subsequent nephritic syndrome in Post-strep glomerulonephritis

TAP TO REVEAL ANSWER

Circulating _____ deposition causes glomerular damage and subsequent nephritic syndrome in Post-strep glomerulonephritis

immune complex

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