Nephritic syndrome

Nephritic Essentials - Inflamed & Leaky Filters

• Pathophysiology: Glomerular inflammation (proliferative changes) damages the capillary wall, creating pores that allow RBCs and some protein to leak into the urine.
• Clinical Hallmarks:
  • Hypertension (salt/water retention)
  • Oliguria (↓ GFR)
  • Hematuria (cola-colored urine)
  • Edema (periorbital)
• Urinalysis: The key diagnostic finding is RBC casts. Also shows dysmorphic RBCs and hematuria. Proteinuria is present but sub-nephrotic (< 3.5 g/day).

⭐ Post-streptococcal glomerulonephritis (PSGN) is the classic example, typically developing 1-3 weeks after a streptococcal pharyngitis or impetigo. Look for low C3 levels.

Etiology - A Cast of Characters

• Post-Infectious Glomerulonephritis (PIGN)

  • Most common: Post-streptococcal (PSGN), typically 1-3 weeks after pharyngitis or impetigo.
  • Others: Endocarditis, shunt nephritis, abscesses.

• IgA Nephropathy (Berger's Disease)

  • Most common primary glomerulonephritis worldwide.
  • Often follows URI/GI infection (synpharyngitic).

• Rapidly Progressive Glomerulonephritis (RPGN) - Crescentic

  • Type I (Anti-GBM): Goodpasture's syndrome.
  • Type II (Immune Complex): Complication of PIGN, IgA, Lupus Nephritis, MPGN.
  • Type III (Pauci-Immune): ANCA-associated vasculitis (GPA, MPA).

• Hereditary Nephritis

  • Alport Syndrome: Defect in Type IV collagen.

⭐ Exam Favorite: PSGN classically shows a "lumpy-bumpy" granular pattern on immunofluorescence due to subepithelial immune complex deposits.

Workup & Dx - The Clinical Detective

• Urinalysis (UA) First:
  • Hematuria (>3 RBCs/hpf)
  • RBC casts & dysmorphic RBCs are hallmark findings.
  • Sub-nephrotic proteinuria (<3.5 g/day)
• Bloodwork:
  • ↑ BUN & Creatinine (azotemia)
  • ↓ Complement levels (C3, C4) suggest post-strep, lupus, or MPGN.
  • Serology: ASO (post-strep), anti-dsDNA (SLE), ANCA (vasculitis).
• Kidney Biopsy: Gold standard for definitive diagnosis & guiding therapy.

⭐ RBC casts are pathognomonic for glomerular hematuria, essentially confirming glomerulonephritis as the cause of bleeding.

Management - Damage Control

• Goal: Control hypertension, edema, and hypervolemia to prevent immediate complications (e.g., hypertensive encephalopathy, pulmonary edema).
• Core Interventions:
  • Salt & Water Restriction: Foundational first step.
  • Loop Diuretics: Furosemide is first-line for managing volume overload and hypertension.
  • Vasodilators: Add if blood pressure remains uncontrolled (e.g., CCBs, hydralazine).
• Severe/Refractory Cases:
  • Dialysis for unresponsive fluid overload, severe hyperkalemia, or uremic symptoms.

⭐ In rapidly progressive glomerulonephritis (RPGN), treatment is urgent: initiate high-dose pulse corticosteroids (e.g., methylprednisolone) ± cyclophosphamide or rituximab.

High-Yield Points - ⚡ Biggest Takeaways

• Nephritic syndrome is an inflammatory process causing hematuria (RBC casts), oliguria, azotemia, and hypertension.
• Post-streptococcal glomerulonephritis (PSGN) is the classic prototype, typically affecting children 1-3 weeks after a GAS infection.
• Key labs show low C3 levels and elevated anti-streptolysin O (ASO) or anti-DNase B titers.
• Biopsy in PSGN reveals "lumpy-bumpy" granular immunofluorescence and characteristic subepithelial humps on electron microscopy.
• Management is primarily supportive.