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Research Article Free access | 10.1172/JCI106733

Renal handling of phosphorus in oliguric and nonoliguric mercury-induced acute renal failure in rats

Mordecai M. Popovtzer, Shaul G. Massry, Mario Villamil, and Charles R. Kleeman

Cedars-Sinai Medical Research Institute and Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048

Cedars-Sinai Medical Research Institute and Department of Medicine, University of California Medical School, Los Angeles, California 90048

Find articles by Popovtzer, M. in: PubMed | Google Scholar

Cedars-Sinai Medical Research Institute and Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048

Cedars-Sinai Medical Research Institute and Department of Medicine, University of California Medical School, Los Angeles, California 90048

Find articles by Massry, S. in: PubMed | Google Scholar

Cedars-Sinai Medical Research Institute and Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048

Cedars-Sinai Medical Research Institute and Department of Medicine, University of California Medical School, Los Angeles, California 90048

Find articles by Villamil, M. in: PubMed | Google Scholar

Cedars-Sinai Medical Research Institute and Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048

Cedars-Sinai Medical Research Institute and Department of Medicine, University of California Medical School, Los Angeles, California 90048

Find articles by Kleeman, C. in: PubMed | Google Scholar

Published November 1, 1971 - More info

Published in Volume 50, Issue 11 on November 1, 1971
J Clin Invest. 1971;50(11):2347–2354. https://doi.org/10.1172/JCI106733.
© 1971 The American Society for Clinical Investigation
Published November 1, 1971 - Version history
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Abstract

The renal handling of phosphorus was evaluated in rats with acute renal failure (ARF) induced by injection of mercuric chloride (HgCl2). Clearances of endogenous creatinine (Ccr) and of phosphorus (Cp) were measured in the following groups: 1. Intact animals (control); 2. Parathyroidectomized rats (PTX) with normal kidney function (PTX control); 3. Animals with mercury-induced acute renal failure (Hg-ARF); 4. PTX rats with Hg-ARF; 5. Rats with Hg-ARF maintained normophosphatemic with dietary phosphate restriction; 6. Animals with oliguric ARF following renal artery constriction; 7. Rats with unilateral Hg-ARF. In addition, radioinulin clearances were measured in 6 normal and in 14 azotemic animals and correlated with simultaneously recorded endogenous Ccr. Radioinulin clearance was also used as an estimate of GFR (glomerular filtration rate) in the animals of group 7.

The Cp/GFR in the intact animals (group 1) was 0.25 ±0.06 (mean ±SD). PTX (group 2) caused a subsequent decrease in Cp/GFR to 0.11 ±0.04 P < 0.0005. The ARF animals in group 3 were classified either as oliguric (Uvol [urine volume] <2 ml/24 hr, Ccr 0.008 ±0.005 ml/min) or nonoliguric (Vvol >2 ml/24 hr, Ccr 0.136 ±0.12). The Cp/GFR in the oliguric animals (0.16 ±0.09) was lower than that in group 1, P < 0.0005, and failed to increase following administration of exogenous parathyroid hormone. The Cp/GFR in the oliguric animals in groups 5 and 7 was also lower than the clearance ratio in group 1, 0.030 ±0.08 and 0.077 ±0.006, respectively. In the nonoliguric ARF animals of group 3 the Cp/GFR (0.94 ±0.29) was higher than that in group 1, P < 0.0005. In the nonoliguric ARF animals of group 4 the Cp/GFR 0.27 ±0.08 did not differ from the clearance ratio in group 1, however it was higher than that in the PTX animals (group 2) P < 0.0005. Cp/GFR in the nonoliguric animals of group 5 was not different from that in the nonoliguric rats of group 3. In the animals with nonoliguric unilateral Hg-ARF Cp/GFR on the affected side 0.51 ±0.16 was higher than that on the control (contralateral) side, 0.23 ±0.07, P < 0.0005. These results indicate that the low Cp/GFR observed in the oliguric ARF animals was not related to the level of circulating parathyroid hormone nor to the presence or absence of azotemia but probably was due to a reduced renal cortical perfusion. The high Cp/GFR in the nonoliguric ARF animals could be explained by secondary hyperparathyroidism and impaired phosphorus reabsorption due to tubular injury.

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