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Kidney diseases

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Glomerular Diseases - The Great Filter Failure

  • Core Pathophysiology: Damage to the glomerular filtration barrier (endothelium, GBM, podocytes) dictates the clinical syndrome.
  • Nephrotic Syndrome: Podocyte damage leads to massive protein loss.

    • Features: Pitting edema, hypoalbuminemia, hyperlipidemia, lipiduria (oval fat bodies).
    • Key Causes: Minimal Change Disease (kids), FSGS, Membranous Nephropathy, Diabetic Nephropathy.
  • Nephritic Syndrome: Inflammation-driven damage.

    • Features: Hypertension, oliguria, hematuria (RBC casts are pathognomonic), mild proteinuria.
    • Key Causes: Post-streptococcal GN, IgA Nephropathy (Berger disease), Lupus Nephritis.

Exam Favorite: Subepithelial immune complex "humps" on electron microscopy are classic for Post-Streptococcal Glomerulonephritis.

Post-streptococcal glomerulonephritis: Light, IF, EM

Tubulointerstitial Disease - When Pipes Go Bad

  • Inflammation or fibrosis of tubules & interstitium, initially sparing the glomeruli.

  • Acute Interstitial Nephritis (AIN):

    • Type IV hypersensitivity, often drug-induced (NSAIDs, penicillins, PPIs).
    • Presents with fever, rash, arthralgias, and acute kidney injury (↑ creatinine).
    • Urinalysis: Sterile pyuria (WBC casts), eosinophiluria.
    • 📌 Mnemonic (Causes): The "P" drugs - Pee (diuretics), Pain-free (NSAIDs), Penicillins, PPIs.
  • Chronic Interstitial Nephritis:

    • Prolonged inflammation leads to interstitial fibrosis, tubular atrophy, & progressive CKD.
    • Key causes: Analgesic abuse, lead, reflux nephropathy.

⭐ The classic triad of fever, rash, and eosinophilia for drug-induced AIN is present in only 10-15% of patients. Suspect it in any patient with AKI after starting a new medication.

Acute interstitial nephritis with eosinophilic infiltrates

Vascular & Cystic Diseases - Plumbing & Pockets

  • Hypertensive Nephrosclerosis: Arteriolosclerosis (hyaline or hyperplastic "onion-skinning") → glomerulosclerosis & atrophy.
  • Renal Artery Stenosis (RAS): Due to atherosclerosis or fibromuscular dysplasia. Causes ↑renin & secondary hypertension.
  • Autosomal Dominant Polycystic Kidney Disease (ADPKD): Adult onset. Mutations in PKD1 or PKD2. Bilateral, massive cystic kidneys.
  • Autosomal Recessive (ARPKD): Infancy/childhood. PKHD1 mutation. Associated with hepatic fibrosis.

ADPKD vs. ARPKD: Kidney Morphology & Clinical Features

⭐ Patients with ADPKD have an increased risk of intracranial berry aneurysms.

Renal Neoplasia - Unwanted Growths

  • Renal Cell Carcinoma (RCC): Most common renal malignancy in adults. Classic triad (hematuria, flank pain, mass) is uncommon. Associated with paraneoplastic syndromes (EPO, PTHrP). Clear cell type linked to VHL gene mutation.
  • Wilms Tumor (Nephroblastoma): Most common renal tumor in children (age 2-5). Associated with WAGR syndrome.
  • Benign Tumors:
    • Angiomyolipoma: Hamartoma; linked to tuberous sclerosis.
    • Oncocytoma: Eosinophilic cells; may have a central stellate scar.

Clear Cell Renal Carcinoma Histopathology Diagram

⭐ RCC has a propensity to invade the renal vein and inferior vena cava (IVC), leading to hematogenous spread.

  • Nephrotic syndrome is marked by >3.5 g/day proteinuria and edema, while nephritic syndrome features hematuria and RBC casts.
  • Minimal change disease is the leading cause of nephrotic syndrome in children, showing podocyte effacement.
  • Membranous nephropathy is the most common primary cause in adults, with a characteristic "spike and dome" appearance.
  • Post-streptococcal GN presents as a nephritic syndrome with subepithelial "humps" after infection.
  • Acute Tubular Necrosis (ATN) is the #1 cause of AKI, identified by muddy brown casts.

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