The effect of decreased renal function with and without reduction in renal mass on 1,25-dihydroxycholecalciferol production in rats.
Decreased production of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) by the kidney may be responsible for vitamin D resistance in renal failure and contribute to renal osteodystrophy. The present studies investigate the effect of reduced renal mass and reduced renal function on conversion of 3H-25-hydroxycholecalciferol to 3H-1,25-(OH)2D3 in vitamin D-deficient rats. Renal mass was reduced by partial or total nephrectomy. Renal function was reduced by ureteral ligation. At comparable degrees of renal function, reducing renal mass decreased 1,25-(OH)2D3 formation approximately proportional to the amount of renal tissue removed. Ureteral ligation without reduction of renal mass also reduced production within the first 24 hours. This may have been caused by the marked hyperphosphatemia which occurred with ureteral ligation. When partial nephrectomy and ureteral ligation were done together the results were additive. The decreased 1,25-(OH)2D3 formation produced by unilateral nephrectomy was not improved 4 weeks after surgery, although renal function had returned to normal.
D058186:Acute Kidney Injury / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D004100:Dihydroxycholecalciferols / Q000096:biosynthesis*; D006887:Hydroxycholecalciferols / Q000096:biosynthesis*; D006984:Hypertrophy / Q000378:metabolism / Q000473:pathology; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D007677:Kidney Function Tests; D009392:Nephrectomy; D009929:Organ Size; D051381:Rats; D014808:Vitamin D Deficiency / Q000378:metabolism
D004100:Dihydroxycholecalciferols; D006887:Hydroxycholecalciferols