Renal function in experimental cystic disease of the rat.
The administration of diphenylamine to rats induces an acquired form of cystic disease. In order to examine the early changes in this model of experimental cystic disease prior to the development of the more severe structural alterations, clearance, micropuncture, and morphologic studies were performed in rats fed DPA for 3 to 6 weeks. A significant defect in maximal urine concentrating ability (Umax) was manifest by the second week and averaged 50% of control values. Further studies were undertaken to examine the cause of the defect in Umax. Whole-kidney glomerular filtration rate (GFR), single-nephron GFR, end-proximal TF/Pinulin, glucose and bicarbonate reabsorption were all normal, indicating normal function of the proximal tubule. Free water clearance and free water reabsorption were not significantly different in DPA-treated rats as compared to controls, suggesting normal function of the ascending limb of the loop of Henle and collecting duct. Morphologic examination revealed gross cysts in less than 10% of the kidneys but structural changes were consistently demonstrated in the collecting ducts of DPA-treated rats. These studies indicate that the decrease in Umax in DPA-treated animals is the result of a defect located at the terminal portion of the collecting duct.
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D004159:Diphenylamine / Q000009:adverse effects; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D007671:Kidney Concentrating Ability / Q000187:drug effects; D007684:Kidney Tubules / Q000378:metabolism / Q000648:ultrastructure; D007690:Polycystic Kidney Diseases / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D014867:Water / Q000378:metabolism
D001639:Bicarbonates; D014867:Water; D004159:Diphenylamine; D005947:Glucose