Renal Concentrating Defect in Sjögren's Syndrome

Abstract

Renal function studies were performed in eight patients with Sjogren''s syndrome. Four of these subjects were shown to have persistent hyposthenuria which was not associated with albuminuria, abnormal urinary sediment, blood electrolyte disturbances, azotemia or hypertension. In one of these patients, studies performed during hydropenia and during water diuresis suggested that the concentrating defect was due to impaired water permeability of the distal convoluted tubules and collecting ducts. The tubular defect was clearly out of proportion to the mild depression of glomerular filtration. There was no evidence of significant impairment of other tubular functions. The probable mechanism of the hyposthenuria is discussed in the context of current concepts of renal physiology. The etiology of the renal defect is discussed in relation to the pathology of Sjogren''s syndrome. Previously described causes of hyposthenuria were ruled out by the appropriate techniques and, although vascular or infiltrative lesions of the kidney may be implicated, final evaluation of the defect must await clinico-pathologic correlation.