INNER MEDULLARY COLLECTING DUCT FUNCTION IN ISCHEMIC ACUTE RENAL-FAILURE

  • 1 June 1988
    • journal article
    • research article
    • Vol. 11  (3) , 157-166
Abstract
The purpose of this study was to determine the role of the medullary collecting duct in the increased urine sodium concentration, decreased urine osmolality, and altered potassium excretion with hyperkalemia which are characteristic of ischemic acute renal failure. Microcatheterization of the inner medullary collecting duct (0.1 to 5 mm from papillary tip) was carried out in rats 24 h after bilateral renal artery clamping for 45 min (n = 8) or sham-operated (n = 8). In ischemic acute renal failure (ARF), tubular fluid osmolality did not increase significantly along their inner medullary collecting duct (IMCD). Tubular fluid sodium concentration was similar to controls at the beginning of IMCD but was significantly higher at the papillary tip. Tubular fluid to plasma potassium concentration ratio (TF/PK) increased to a greater extent along the IMCD in ischemic ARF than in controls. During acute KCl loading in two additional groups, tubular fluid potassium concentration and TF/PK were much lower at the beginning of the IMCD in ischemic ARF than in controls but increased similarly along the IMCD. In ischemic ARF, with or without KCl loading, renal tissue electrolytes showed reduced potassium concentration in the outer medullary region. The results indicate that impaired IMCD function contributes significantly to the increase in urine sodium concentration and the decrease in urine osmolality which are characteristic of ischemic acute renal failure. In ischemic ARF with mild hyperkalemia, an adaptive increase in K secretion occurred in the IMCD. Severe hyperkalemia and decreased potassium excretion during acute potassium loading in ischemic ARF were determined in more proximal nephron segments and were associated with decreased outer medullary tissue potassium, presumably due to tubular necrosis. Decreased outer medullary tissue potassium could contribute to hyperkaelmia by diminishing K secretion in the pars rectae and descending limbs or in the cortical and outer medullary collecting ducts.