When 17 patients with Sjögren's syndrome, without apparent clinical manifestations of renal disease, were examined renal function studies frequently indicated abnormalities in their renal phosphate handling. The percentage tubular reabsorption of phosphate (%TRP) was decreased in six (35.3%), and maximal tubular reabsorption rate for phosphate (TmPO4/GFR) was low in eight (47.1%). In contrast, indices of renal calcium handling and serum parathyroid hormone levels were normal, suggesting that the abnormalities of phosphate metabolism were due not to extrinsic, but rather to intrinsic disease processes occurring in the kidney in Sjögren's syndrome. When the patients were divided into two groups according to the presence or absence of a renal tubular acidification defect (RTAD), patients with RTAD were younger (p less than 0.005), had longer disease duration (p less than 0.01), lower creatinine clearance (p less than 0.05), and higher incidence of low %TRP (p less than 0.05). Thus the patients with lower creatinine clearance generally had disease of longer duration at diagnosis and tended also to have defects in concentrating and acidifying the urine.
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