Journal
CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION
Volume 22, Issue 4, Pages 481-487Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MNH.0b013e3283621310
Keywords
chronic kidney disease; intestine; NaPi-IIb; phosphate toxicity
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Funding
- Kidney Research UK
- St Peter's Trust for Kidney, Bladder and Prostate Research
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Purpose of reviewFor a number of years, there has been increasing interest in the concept of directly targeting intestinal phosphate transport to control hyperphosphatemia in chronic kidney disease. However, progress has been slow due to the paucity of information on the mechanisms involved in intestinal phosphate absorption. This editorial highlights the most recent developments in our understanding of this process and the role of the intestine in the maintenance of phosphate balance.Recent findingsRecent studies in NaPi-IIb knockout mice have confirmed that this transport protein plays a significant role in intestinal phosphate absorption and is critical in the proposed feed-forward mechanism between the small intestine and kidney, which helps to maintain normal phosphate balance and steady-state plasma phosphate concentrations. In addition, renal failure-induced hyperphosphatemia is attenuated in NaPi-IIb knockout mice, confirming that NaPi-IIb is a suitable target in the prevention and treatment of hyperphosphatemia.SummaryRecent findings suggest that consumption of processed foods containing phosphate preservatives may lead to excessive phosphate exposure (if not overload), toxicity, and cardiovascular disease in the general population, as well as in patients with declining renal function. Therefore, establishing more effective ways of targeting the intestine to limit dietary phosphate absorption could have wide-reaching health benefits.
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