THE MULTIPLE FACES OF SYSTEMIC LUPUS ERYTHEMATOSUS

Systemic lupus erythematosus (SLE), the prototype of systemic autoimmune disorders, has been considered for many years a classic model of immune complex mediated disease. However, earlier data demonstrate that multilevel dysfunction of cellular and humoral immunity underlie the pathophysiology of the disorder.^1,2 The expression and clinical course of SLE vary enormously from very mild, with arthralgias and skin rashes, to life threatening, when the renal and central nervous system function are severely compromised; from complete quiescence to full blown expression of the disease. Coexistence or even evolution into other types of autoimmune disorders, such as Sjögren’s syndrome and mixed connective tissue disease can also occur. Finally, subsets of SLE were early recognised: distinct clinical entities such as antiphospholipid syndrome (APS) or subacute lupus erythematosus are considered to be part of the “SLE” clinical spectrum.¹

RENAL DISEASE IN SLE

Among the various organs affected in SLE, the kidney appears to be one of the most common, and at the same time, more serious complication. In unselected lupus patients, abnormalities in urine or renal function occur in about 25–50% early in the course of the disease.³ In the study of Vlachoyiannopoulos et al renal disease manifested as proteinuria, microscopic haematuria, decreased clearance of creatinine, increased creatinine levels, or the presence of casts was found in about 50% of cases.⁴ In other published series, using similar definitions, the prevalence of renal disease ranged from 29 to 75%.^5,6

Proteinuria is considered the sine qua non of renal disease in lupus. In a comprehensive review on lupus nephritis, proteinuria was reported in 100% of patients, with nephrotic syndrome in 45–65%; microscopic haematuria was found to occur in about 80% of patients during the disease course.³ Evidence of …