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The cellular basis of Fanconi syndrome
1Division of Pediatric Nephrology, University of Texas Southwestern Medical Center, Dallas.
Abstract:
In this syndrome, all solutes are prevented from crossing the apical membrane of the proximal renal tubule cell; hence, investigations have focused on generalized transport dysfunction, namely intracellular ATP activity. Experiments suggest that intracellular adenine nucleotide degradation secondary to phosphate depletion causes a decline in ATP.