Lupus Nephritis

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  • The renal manifestation of systemic lupus erythematosus (SLE)
  • American College of Rheumatology (ACR) criteria: persistent proteinuria >500 mg/day or ≥3 on dipstick and/or presence of cellular casts; alternatively, spot urine protein-to-creatinine ratio >0.5 and “active urinary sediment” (>5 RBC/HPF, >5 WBC/HPF in absence of infection, or cellular casts—RBC or WBC casts) (1)
  • Clinical manifestations primarily due to immune complex–mediated glomerular disease. Tubulointerstitial and vascular involvement often coexist. Diagnosis is based on clinical findings, urine abnormalities, autoantibodies, and renal biopsy.
  • Treatment and prognosis depend on International Society of Nephrology/Renal Pathology Society (ISN/RPS) histologic class—risk of end-stage renal disease (ESRD) highest in class IV.
  • Delay in diagnosis/treatment increases risk of ESRD.


  • Peak incidence of SLE is 15 to 45 years of age.
  • Predominant sex: female > male (10:1)
  • Once SLE develops, lupus nephritis (LN) affects both genders equally; it is more severe in children and men and less severe in older adults.

  • SLE: 1.4 to 22/100,000
  • Up to 60% of SLE patients develop LN over time; 25–50% of SLE patients have nephritis as the initial presentation.

Pediatric Considerations
LN is more common and more severe in children: 60–80% of children have LN at or soon after SLE onset.

SLE: 7.4 to 159.4/100,000

Etiology and Pathophysiology

  • Immune complex–mediated inflammation injures glomeruli, tubules, interstitium, and vasculature.
  • Glomeruli: Varying degrees of mesangial proliferation, crescent formation, and fibrinoid necrosis cause reduced glomerular filtration rate (GFR).
  • Persistent inflammation (chronicity) leads to sclerosis and glomerular loss.
  • Tubulointerstitial injury (edema, inflammatory cell infiltrate acutely; tubular atrophy in chronic phase) with or without tubular basement membrane immune complex deposition leads to reduced renal function.
  • Vascular lesions: immune complex deposition and noninflammatory necrosis in arterioles
  • SLE is a multifactorial disease, with multigenic inheritance; exact etiology remains unclear.
  • Defective T-cell autoregulation and polyclonal B-cell hyperactivity contribute to dysregulated apoptosis. Impaired clearance of apoptotic cells inhibits self-tolerance to nuclear antigen.
  • Anti-DNA, anti-C1q, anti–α-actin, and other nuclear component autoantibodies develop.
  • Deposition of circulating immune complexes or autoantibodies attaching to local nuclear antigens leads to complement activation, inflammation, and tissue injury.
  • Interaction of genetic, hormonal, and environmental factors leads to great variability in LN severity.

Multigenic inheritance; clustering in families, ~25% concordance in identical twins

Risk Factors

Younger age, African American or Hispanic race, more ACR criteria for SLE, longer disease duration, hypertension, lower socioeconomic status, family history of SLE, anti-dsDNA antibodies

Commonly Associated Conditions

Skin, hematologic, cerebral, pulmonary, GI, and cardiopulmonary systems are often involved in SLE.

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