9.3 Nephritic Syndromes, RPGN & Indications for Renal Replacement Therapy

ABIM Internal Medicine Exam

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9.3 Nephritic Syndromes, RPGN & Indications for Renal Replacement Therapy

Key Takeaways Explain This Topic AI

Nephritic syndrome features hematuria with dysmorphic red cells and red cell casts, hypertension, edema and a rising creatinine.

Linear IgG staining along the glomerular basement membrane establishes anti-glomerular basement membrane disease, treated with plasmapheresis plus immunosuppression.

Low complement narrows the nephritic differential to postinfectious, lupus, membranoproliferative and cryoglobulinemic disease.

IgA nephropathy classically produces synpharyngitic hematuria within days of an upper respiratory infection, unlike the weeks-long latency of postinfectious disease.

Refractory hyperkalemia, acidosis, volume overload, uremic pericarditis and certain intoxications are the accepted indications for emergent dialysis.

Last updated: August 2026

1. Nephritic Syndromes & Rapidly Progressive Glomerulonephritis (RPGN)

Nephritic conditions are characterized by inflammatory disruption of the glomerular capillary wall, leading to hematuria with dysmorphic RBCs and RBC casts, variable sub-nephrotic proteinuria, oliguria, hypertension, and azotemia.

Classification by Serum Complement Levels

Diagnostic evaluation of suspected nephritic syndrome begins with testing serum complement levels (C3 and C4): ┌─────────────────────────────────────────┐

• │ Suspected Nephritic Syndrome │
• └────────────────────┬────────────────────┘
• │
• Check Serum C3 & C4
• │
• ┌────────────────────────┴────────────────────────┐
• ▼ ▼
• ┌─────────────────────────┐ ┌─────────────────────────┐
• │ Low Serum C3/C4 │ │ Normal Serum C3/C4 │
• │ (Hypocomplementemic) │ │ (Normocomplementemic)│
• └────────────┬────────────┘ └────────────┬────────────┘
• │ │
• ┌─────────────┼─────────────┐ ┌─────────────┼─────────────┐
• ▼ ▼ ▼ ▼ ▼ ▼
• Post-Strept. Lupus Cryo- IgA Anti-GBM ANCA
• (PSGN) Nephritis globulinemia Nephropathy (Goodpasture) Vasculitis
• (Low C3, (Low C3 & (Low C4 >> C3, (Berger) (Linear IgG) (Pauci-immune)
• Norm C4) Low C4) Hep C +) (Normal C3/C4) (Normal C3/C4) (Normal C3/C4)
• Clinical Profiles of Major Nephritic Disorders

IgA Nephropathy (Berger Disease):

Epidemiology: The most common primary glomerulonephritis worldwide; prominent in East Asian and young adult Caucasian populations.

Clinical Presentation: Synpharyngitic macroscopic hematuria occurring concurrently or 1 to 2 days following an upper respiratory tract infection or vigorous exercise. Characterized by normal serum complement (C3/C4 normal).

Comparison with Post-Streptococcal GN (PSGN):

IgA Nephropathy: Hematuria occurs 1–2 days after URI; serum C3 is normal ; recurrent episodic hematuria is common.

Post-Streptococcal GN: Hematuria occurs 1 to 3 weeks after streptococcal pharyngitis (or 3 to 6 weeks after streptococcal impetigo); serum C3 is markedly low (normalizes in 6–8 weeks); positive ASO or anti-DNase B titers; subepithelial "humps" on EM.

Histopathology: Mesangial proliferation with intense mesangial IgA and C3 deposition on immunofluorescence.

Systemic Counterpart: IgA Vasculitis (Henoch-Schönlein Purpura) : IgA nephropathy plus palpable purpura (buttocks/lower extremities), non-deforming arthralgias, and colicky abdominal pain / GI bleeding.

Treatment:

Conservative First-Line: Maximum tolerated ACE inhibitor or ARB to achieve BP <120 mmHg and proteinuria <0.5–1.0 g/day; add SGLT2 inhibitor (Dapagliflozin / Empagliflozin).

Targeted Disease-Modifying Agents: Targeted-release oral Budesonide (Tarpeyo) 16 mg daily (acts on mucosal Peyer's patches in the terminal ileum to reduce galactose-deficient IgA1 production; NefIgArd trial); or Sparsentan (dual endothelin-angiotensin receptor antagonist; PROTECT trial).

Systemic Immunosuppression: Systemic corticosteroids reserved for rapidly progressive crescentic variants.

Anti-Glomerular Basement Membrane (Anti-GBM) Disease / Goodpasture Syndrome:

Pathophysiology: Circulating autoantibodies directed against the non-collagenous domain of the alpha-3 chain of Type IV collagen in the glomerular and alveolar basement membranes.

Clinical Presentation: Rapidly progressive glomerulonephritis (RPGN) with acute oliguric renal failure combined with diffuse alveolar hemorrhage (hemoptysis, dyspnea, new alveolar infiltrates on chest imaging, iron-deficiency anemia, elevated DLCO >130% due to intra-alveolar RBC uptake of carbon monoxide).

Renal Biopsy: Diagnostic hallmark is smooth, continuous, linear deposition of IgG (and C3) along the glomerular capillary loops on immunofluorescence, accompanied by extensive cellular crescent formation (>50% of glomeruli).

Therapeutic Emergency:

Immediate Plasma Exchange (Plasmapheresis) daily or every other day for 14 days to remove circulating anti-GBM antibodies.

High-Dose Corticosteroids: IV Methylprednisolone 500–1000 mg daily for 3 days, followed by oral Prednisone 1 mg/kg/day.

Cyclophosphamide: Oral (2 mg/kg/day) or IV pulsed monthly for 3 to 6 months to arrest autoantibody production.

ANCA-Associated Vasculitis (Pauci-Immune RPGN):

Definition: Necrotizing crescentic glomerulonephritis with absence or paucity of immunoglobulin and complement staining (Pauci-Immune) on immunofluorescence.

Phenotypes:

Granulomatosis with Polyangiitis (GPA, Wegener): Associated with c-ANCA (anti-proteinase 3 [PR3]) . Triad of upper airway disease (chronic sinusitis, bloody nasal crusting, saddle-nose deformity, subglottic stenosis), lower respiratory involvement (pulmonary nodules with central cavitation, alveolar hemorrhage), and necrotizing crescentic GN.

Microscopic Polyangiitis (MPA): Associated with p-ANCA (anti-myeloperoxidase [MPO]) . Rapidly progressive crescentic GN and pulmonary capillaritis without granulomatous inflammation or upper airway destructive lesions.

Eosinophilic Granulomatosis with Polyangiitis (EGPA, Churg-Strauss): Associated with p-ANCA (MPO) in ~40–50% ; severe asthma, marked peripheral blood eosinophilia (>1500/µL or >10%), migratory pulmonary infiltrates, mononeuritis multiplex, and necrotizing vasculitis.

Treatment Strategy:

Induction Therapy: Rituximab (375 mg/m2 weekly x 4 or 1000 mg q2 weeks x 2) is preferred first-line, or IV Cyclophosphamide, combined with high-dose corticosteroids.

Targeted Complement Inhibition: Avacopan (oral C5a receptor antagonist, 30 mg PO BID via ADVOCATE trial) allows significant corticosteroid reduction/tapering while achieving equivalent remission rates and improved renal recovery.

Maintenance Therapy: Rituximab 500 mg IV every 6 months for 2 years, or Azathioprine / Mycophenolate Mofetil.

Lupus Nephritis (Systemic Lupus Erythematosus):

Pathophysiology: Deposition of circulating and in situ DNA/anti-DNA immune complexes activating classical complement pathway.

ISN/RPS Classification:

Class I: Minimal mesangial lupus nephritis.

Class II: Mesangial proliferative lupus nephritis.

Class III: Focal proliferative lupus nephritis (<50% of glomeruli involved).

Class IV: Diffuse proliferative lupus nephritis (>=50% of glomeruli involved) . Most common and most severe form; demonstrates subendothelial deposits, "wire-loop" lesions on LM, marked endocapillary proliferation, and crescents.

Class V: Membranous lupus nephritis (subepithelial deposits, severe nephrotic proteinuria).

Class VI: Advanced sclerosing lupus nephritis (>90% global sclerosis).

Biopsy Hallmark: "Full-House" Immunofluorescence positive for IgG, IgA, IgM, C3, and C1q .

Laboratory Profile: Hypocomplementemia (profoundly low C3 and low C4 ), elevated anti-double-stranded DNA (anti-dsDNA) titers, positive ANA.

Treatment for Proliferative Lupus Nephritis (Class III / IV +/- V):

Induction: Mycophenolate Mofetil (MMF) (2–3 g/day; preferred in non-white patients) OR IV Cyclophosphamide (low-dose Euro-Lupus or high-dose NIH regimen), combined with pulse IV glucocorticoids tapered to low-dose oral prednisone.

Add-On Biologics / Novel Regimens: Belimumab (BLyS inhibitor, added to MMF/corticosteroids) OR Voclosporin (novel calcineurin inhibitor added to MMF/corticosteroids) significantly improves complete renal response rates.

Background Therapy: Hydroxychloroquine for all SLE patients unless strictly contraindicated (reduces flares, renal damage accrual, and thrombosis).

Maintenance: MMF (1–2 g/day) or Azathioprine for >=3–5 years.

2. Indications for Emergent Renal Replacement Therapy

When acute medical management fails, emergent initiation of dialysis is lifesaving. The indications are summarized by the classic mnemonic AEIOU :

Indicator Clinical Definition & Thresholds Critical Management Pearls

A — Acidosis Severe metabolic acidosis with arterial pH < 7.10–7.15 or serum HCO3- < 10 mEq/L refractory to medical therapy Avoid aggressive IV sodium bicarbonate in oliguric patients with volume overload, as the massive sodium load precipitates flash pulmonary edema.

E — Electrolytes Severe hyperkalemia (serum K+ > 6.5 mEq/L) or rapidly rising K+ refractory to medical shifting/elimination therapies or accompanied by ECG changes Medical therapies (Calcium, Insulin/D50, Albuterol) are temporary bridges; hemodialysis is the definitive clearance modality.

I — Ingestions Ingestion of dialyzable toxins (Mnemonic SLIME ): S alicylates, L ithium, I sopropanol, M ethanol, E thylene glycol Dialyze for: Ethylene glycol/Methanol with high osmolar gap/acidosis or visual changes; Lithium >4.0 mEq/L (or >2.5 with neurotoxicity/renal failure); Salicylates >80–100 mg/dL or altered mental status.

O — Overload Refractory volume overload / acute pulmonary edema unresponsive to maximal IV loop diuretics (e.g., Furosemide 160–200 mg IV +/- thiazide synergy) Hypoxemic respiratory failure due to volume overload in oliguric AKI mandates emergent ultrafiltration / hemodialysis.

U — Uremia Symptomatic uremic organ dysfunction: Uremic Pericarditis (pericardial friction rub), Uremic Encephalopathy (asterixis, lethargy, confusion, seizures), Uremic Coagulopathy / Bleeding Uremic pericarditis is an absolute indication for urgent hemodialysis; avoid therapeutic pericardiocentesis and systemic anticoagulation if possible due to extreme risk of converting to hemorrhagic tamponade.