Publication | Closed Access
Renal Involvement in Patients with Primary Sjögren's Syndrome
28
Citations
8
References
1989
Year
Glomerular DiseaseBicarbonate ExcretionSecondary SsVasculitisRenal PathologyRenal InflammationPathologyGlomerulonephritisRenal FunctionIga GlomerulonephritisChronic Kidney DiseasePrimary SjögrenRheumatologyAutoimmune DiseaseLupus NephritisRenal ManifestationsUrologyRenal DiseaseSjögren’s SyndromeNephritic SyndromeGlomerulopathyMedicineNephrologyKidney Research
Among the renal manifestations of Sjogren’s syndrome (SS), chronic tubulointerstitial nephritis (CTN) is the most common histopathological lesion. It presents clinically as renal tubular acidosis (RTA) and hyposthenuria (1-3). In contrast to the tubular changes, glomerulonephritis is a rare complication of the disease (4). Most published studies discuss the kidney involvement in primary and secondary SS together. In two studies, renal lesions were revealed in about a quarter of patients with primary SS (5, 6). We present here our observations on the renal manifestations in our primary SS patients. PATIENTS AND METHODS Sixty-five primary SS patients with extraglandular symptoms (63 women and 2 men) were followed up for a mean period of 6.2 years. All of them met the criteria for primary SS. They came from an area with I .9 million inhabitants. For the diagnosis of keratoconjunctivitis sicca and xerostomia, the Copenhagen criteria (7) were used with two modifications: parotid gland flow rate stimulated with 2% citric acid solution (abnormal if 61.5 mVlO min) was measured, and parotid gland scintigraphy or sialography was performed. Throughout the follow-up period, serum electrolytes, urea nitrogen, creatinine, urine analysis and urine cultures in the case of leukocyturia were tested in all patients. In the presence of proteinuria, with or without haematuria or systemic acidosis, further examinations were carried out. An acute oral ammonium chloride loading test with 0.1 g NH4Cl/kg body weight was carried out on 10 patients with acidaemia, and on I5 patients without evidence of renal involvement as controls (8). Urinary pH (electric pH meter), ammonia excretion (direct Berthelot method, normal range: -1 OOO md24 h) and titratable acidity (normal range: 2040 mmH+/24 h) were measured. Before and 5 h after the ingestion of the drug, blood gasometric analysis was carried out. To determine the RTA type, a bicarbonate loading test was applied and 0.125 g NaHCO,/kg body weight was given in infusion for 2 h. Venous bicarbonate concentrations were determined at the beginning and IS, 45, 75, 105 and 180 min after the beginning of the infusion. Urinary pH and bicarbonate excretion were measured at the beginning and 30, 60, 90, 120 and 180 min later (9, 10). Statistics The results were evaluated statistically by the two-tailed Student’s t-test.
| Year | Citations | |
|---|---|---|
Page 1
Page 1