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A Clinical Approach of Lupus Nephritis Associated with Catastrophic Antiphospholipid-Antibody Syndrome Review and Case Report

Glomerulonephritis is a major cause of morbidity in systemic lupus erythematosus (SLE). In fact, immune complex formation and deposition in the kidney results in intraglomerular inflammation with recruitment of leukocytes, and activation and proliferation of resident renal cells. Intense injury may destroy resident renal cells by necrosis or apoptosis resulting in fibrinoid necrosis. When injury is less intense, endocapillary cells respond by proliferating and production of extracellular matrix (proliferative lesions). Renal biopsy, examination of urine sediment and measurement of C3 levels (and to less anti-DNA titers) are essential for the management of lupus nephritis. Treatment depends on the severity of the lupus nephritis. Disease severity depends on the presence or absence of high-risk factors. These include demographic (male gender, black race), clinical (failure to achieve response or marked delay in response, multiple relapses, pregnancy), laboratory (impaired renal function, severe anemia with hematocrit less than 26%) and histologic features (mixed membrane- proliferative or proliferative nephritis; cellular crescents and/or fibrinoid necrosis; cellular crescent and/or fibrinoid necrosis; and moderate to high degrees of interstitial fibrosis and/or tubular atrophy).