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Research Article Free access | 10.1172/JCI106285

Micropuncture studies of the recovery phase of myohemoglobinuric acute renal failure in the rat

Donald E. Oken, Gerald F. DiBona, and Franklin D. McDonald

Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

Find articles by Oken, D. in: PubMed | Google Scholar

Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

Find articles by DiBona, G. in: PubMed | Google Scholar

Department of Medicine, Peter Bent Brigham Hospital, Boston, Massachusetts 02115

Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115

Find articles by McDonald, F. in: PubMed | Google Scholar

Published April 1, 1970 - More info

Published in Volume 49, Issue 4 on April 1, 1970
J Clin Invest. 1970;49(4):730–737. https://doi.org/10.1172/JCI106285.
© 1970 The American Society for Clinical Investigation
Published April 1, 1970 - Version history
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Abstract

Micropuncture studies of the recovery phase of glycerol-induced myohemoglobinuric acute renal failure were performed in rats whose blood urea nitrogen (BUN) had fallen at least 20% below its peak value. The glomerular filtration rate (GFR) of individual nephrons in a single kidney in the recovery period generally either was in the normal range or minimal. Each animal's BUN concentration at the time of the study was inversely related to the proportion of functioning surface nephrons, but did not correlate with individual nephron GFR values. Proximal tubule fractional water absorption was significantly depressed as manifested by both depressed inulin (TF/P) values and supernormal volumes of collections, a finding which, in the absence of a urea-induced osmotic diuresis, suggests impaired sodium transport by the damaged nephron. The mean proximal tubule hydrostatic pressure in recovery was normal and there was little variation in pressure among functioning nephrons. It is concluded that recovery from this model of acute renal failure reflects the progressive recruitment of increasing numbers of functioning nephrons. The recovery of individual nephron glomerular filtration, once begun, was rapid and complete. No evidence could be adduced that the gradual return of renal function towards normal reflects a slow release of tubular obstruction or repair of disrupted tubular epithelium. Rather, recovery appeared to be directly attributable to the return of an adequate effective glomerular filtration pressure. Significant limitation in proximal tubule water absorption persisted after individual nephron GFR had returned to normal or supernormal values in this model of experimental acute renal failure in the rat, a finding which readily accounts for the diuresis associated with the recovery phase of this syndrome.

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