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1 Department of Medicine, University of Maryland, School of Medicine, Baltimore, MD, USA; Department of Physiology, University of Maryland, School of Medicine, Baltimore, MD, USA; Medical Service, Department of Veterans Affairs Medical Center, Baltimore, MD, USA
2 Harbor Hospital Center, Brooklyn, MD, USA
3 Department of Medicine, University of Maryland, School of Medicine, Baltimore, MD, USA
4 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA
* To whom correspondence should be addressed. E-mail: eweinman{at}medicine.umaryland.edu.
NHERF-1 binds numerous renal protein targets, including the proximal tubule transporters NHE3 and Npt2a. Young NHERF-1-/- male mice display defective targeting of Npt2a to apical membranes in the renal proximal tubule and manifest hypophosphatemia and increased urinary excretion of phosphate. The present studies describes the changes in the urinary excretion of phosphate, calcium, uric acid, and sodium in male and female wild-type and NHERF-1 null mice over a time period from 12 to 54 weeks of age. Young male and female NHERF-1-/- mice demonstrated increased urinary excretion of phosphate and urine phosphate/creatinine ratios. There was an age related decline in the phosphate/creatinine ratio in mutant mice such that there were no differences between wild-type and NHERF-1-/- by 24 to 30 weeks of age despite the continued presence of hypophosphatemia. Male and female NHERF-1 null mice also demonstrate increased urine calcium/creatinine and uric acid/creatinine ratios compared to wild-type controls. These studies indicate defects in the renal tubule transport of phosphate, calcium and uric acid in NHERF-1-/- male and female mice that could account for the increased deposition of calcium in the papilla of null mice.
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