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RESPONSE OF GENETIC HYPERCALCIURIC RATS TO A LOW CALCIUM DIET
Author(s): KIM M, SESSLER NE, TEMBE V, FAVUS MJ, BUSHINSKY DA
Source: KIDNEY INTERNATIONAL    Volume: 43    Issue: 1    Pages: 189-196    Published: JAN 1993  
Times Cited: 38     References: 49     
Abstract: A fundamental mechanism for hypercalciuria in genetic hypercalciuric rats appears due to a primary increase in intestinal calcium absorption. However previous studies could not exclude additional mechanisms to account for the hypercalciuria. To determine if enhanced bone mineral dissolution either as a primary abnormality or secondary to a defect in renal tubule calcium reabsorption is responsible for a component of the augmented calcium excretion we studied rats continually inbred for hypercalciuria. Nineteenth generation adult female idiopathic hypercalciuric (IH) and non-inbred control (Ctl) rats were fed 13 g/day of a normal calcium diet (0.6% calcium, NCD) for 10 days. Urine calcium excretion over the last seven days was greater in IH (34 +/- 2 mg/7 day) than in Ctl (2.9 +/- 0.3, P < 0.01) rats. Some rats in each group were continued on the same diet while others were fed a low calcium diet (0.02% calcium, LCD) for an additional 10 days; balance measurements were made over the final seven days. With LCD, urine calcium excretion was approximately 8-fold higher in IH compared to Ctl (13 +/- 2 mg/7 day vs. 1.6 +/- 0.1, IH vs. Ctl, respectively, P < 0.01). In IH rats percent calcium absorption was greater (59 +/- 3% vs. 45 +/- 3, IH vs. Ctl, P < 0.01), however calcium retention was negative (-1.9 +/- 2.0 mg/7 day vs. 6.5 +/- 0.5, IH vs. Ctl, P < 0.01) compared to Ctl rats. The fall in urine calcium excretion when IH rats are fed LCD indicates that enhanced intestinal calcium absorption is a primary mechanism of the hypercalciuria. However, the continued hypercalciuria and negative calcium retention during LCD indicates that an additional mechanism of hypercalciuria leads to a loss of bone mineral. Whether this additional mechanism is a primary bone resorptive process or due to an inability to conserve urinary calcium remains to be determined.
Document Type: Proceedings Paper
Language: English
Addresses:
1. UNIV ROCHESTER, SCH MED & DENT, DEPT MED, 601 ELMWOOD AVE, BOX 675, ROCHESTER, NY 14642 USA
2. UNIV CHICAGO, ENDOCRINOL & NEPHROL SECT, CHICAGO, IL 60637 USA
Publisher: BLACKWELL SCIENCE INC, 238 MAIN ST, CAMBRIDGE, MA 02142
Subject Category: Urology & Nephrology
IDS Number: KC891
ISSN: 0085-2538
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