Lupus Nephritis



  • Renal disease associated with systemic lupus erythematosus (SLE)
  • A kidney biopsy is necessary to confirm the diagnosis (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 severity of disease.
  • Early diagnosis improves renal outcomes.


  • Peak incidence of SLE is 15 to 45 years of age. Mean age of diagnosis is between 25 and 30 years of age.
  • The lifetime incidence of lupus nephritis (LN) in patients with SLE is 20–60%.
  • Predominant sex: female > male (10:1)
  • Once SLE develops, LN affects both genders equally; it is more severe in children and men and less severe in older adults.
  • More common in African American and Asian populations


  • SLE: 1 to 22/100,000 people
  • 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 to 159/100,000 people

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.


  • Polygenic inheritance; clustering in families, ~25% concordance in identical twins
  • Interaction of general SLE susceptibility genes with more renal-specific genes and epigenetic changes

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, low albumin to globulin ratio

Commonly Associated Conditions

Other organ systems often involved in SLE.

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