ABSTRACT
Glomerulonephritis complicating primary Sjögren's syndrome is extremely rare, with only 3 cases of membranoproliferative glomerulonephritis reported in the literature. We report on a 55-year-old woman with a long-standing history of dryness of the mouth and eyes who was found to have nephrotic syndrome. Extensive investigations indicated primary Sjögren's syndrome. Kidney biopsy revealed a membranoproliferative glomerulonephritis. Treatment with prednisone and cyclophosphamide resulted in complete remission of nephrotic syndrome. The pathogenesis of glomerulonephritis appears to be due to deposition of circulating immune complexes.
Subject(s)
Glomerulonephritis, Membranoproliferative/etiology , Sjogren's Syndrome/complications , Female , Glomerulonephritis, Membranoproliferative/pathology , Humans , Middle AgedSubject(s)
Dental Enamel/ultrastructure , Edetic Acid , Humans , Microscopy, Electron, Scanning , MineralsABSTRACT
This study was undertaken to evaluate the effect of dopamine (D) on renal water excretion. Intravenous (i.v.) infusion of D (7.5 microgram/kg per min) was associated with a significant, reversible increase in free water excretion (CH2O) and a decrease in urinary osmolality (Uosmol). These changes, however, were associated with significant increases in renal blood flow (RBF), glomerular filtration rate (GFR), and urinary sodium excretion (UNaV). These increases could have been responsible for the diuretic response to D. To examine whether D has a direct effect on vasopressin (ADH) release, D was infused into one common carotid artery at a dose equal to one-fourth the i.v. dose. No effects on CH2O and Uosmol were observed. To examine whether D might have an antagonistic effect on ADH a single bolus of ADH (100 mU) was given to the same hypophysectomized dogs with and without D infusion. The antidiuretic response to ADH was the same, whether or not D was given concomitantly. The net changes in Uosmol and CH2O in response to ADH were not significantly different. Taken together, the present results provide no evidence for a direct effect of D on ADH release nor do they indicate an interference with the peripheral action of ADH. The dopamine-induced diuresis is probably the result of increased solute excretion. This, in turn, is the result of the combined effects of dopamine on increasing renal blood flow, GFR, and sodium excretion.
