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- Title
Intestinal phosphate absorption in a model of chronic renal failure.
- Authors
Marks, J.; Churchill, L. J.; Srai, S. K.; Biber, J.; Murer, H.; Jaeger, P.; Debnam, E. S.; Unwin, R. J.
- Abstract
Hyperphosphatemia is an important consequence of chronic renal failure (CRF). Lowering of the plasma phosphate concentration is believed to be critical in the management of patients with CRF, especially those on dialysis. Reports of the effect of CRF on the intestinal handling of phosphate in vitro have been conflicting; but what happens in vivo has not been studied. What effect a reduction in the dietary phosphate intake has on intestinal phosphate absorption in CRF in vivo is unclear. In this study, we have used the in situ intestine loop technique to determine intestinal phosphate absorption in the 5/6-nephrectomy rat model of CRF under conditions of normal and restricted dietary phosphate intake. In this model of renal disease, we found that there is no significant change in the phosphate absorption in either the duodenum or jejunum regardless of the dietary phosphate intake. There was also no change in the expression of the messenger RNA of the major intestinal phosphate carrier the sodium-dependent-IIb transporter. Furthermore, we found no change in the intestinal villus length or in the location of phosphate uptake along the villus. Our results indicate that in CRF, unlike the kidney, there is no reduction in phosphate transport across the small intestine. This makes intestinal phosphate absorption a potential target in the prevention and treatment of hyperphosphatemia.Kidney International (2007) 72, 166–173. doi:10.1038/sj.ki.5002292; published online 25 April 2007
- Subjects
CHRONIC kidney failure; KIDNEY diseases; MESSENGER RNA; NUCLEIC acids; SMALL intestine; JEJUNUM
- Publication
Kidney International, 2007, Vol 72, Issue 2, p166
- ISSN
0085-2538
- Publication type
Article
- DOI
10.1038/sj.ki.5002292