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  • Management of disturbed calcium metabolism in uraemic patients: 1 Use of vitamin D metabolites
  • Schomig M; Ritz E
  • Nephrol Dial Transplant 2000[]; 15 Suppl 5 (): 18-24
  • Chronic renal failure is characterized by diminished synthesis of, and resistance to, the active vitamin D metabolite 1,25-dihydroxy-vitamin D3 (1,25(OH)2D3, calcitriol). Calcitriol results from the biotransformation of the precursor 25-hydroxy-vitamin D3 (25(OH)D3) to 1,25(OH)2D3. 25(OH)D3 is synthesized in the liver, and 1alpha-hydroxylase, the rate-limiting enzyme for its biotransformation into the most active metabolite, 1,25(OH)2D3, is located in the kidney. The regulation of 1alpha-hydroxylase in renal failure is not well known. Recent work indicates that, in contrast to previous opinion, 1alpha-hydroxylase is predominantly expressed not in the proximal tubule but in the distal tubule [1]. In vivo, the main stimulatory signal is presumably parathyroid hormone (PTH) and the main inhibitory signal hyperphosphataemia. Both signals are altered in renal failure. There is also evidence that the renal 1alpha-hydroxylase becomes substrate-dependent in patients with renal failure. This means that a higher concentration of the precursor 25(OH)2D3 will result in a higher rate of transformation into the active metabolite 1,25(OH)2D3 in renal patients. Calcitriol is not exclusively synthesized in the kidney, but may also be synthesized in extra-renal tissues, e.g. activated monocytes/macrophages [2], particularly in granuloma [3] as shown by anephric uraemic patients who develop hypercalcaemia and elevated calcitriol concentrations when sarcoidosis [4] or tuberculosis [5] supervenes. On the other hand, calcitriol is less effective in uraemia. This may be to some extent due to diminished expression of vitamin D receptors [6], particularly in parathyroid glands when they undergo nodular transformation [7], but there may also be resistance to calcitriol at the post-receptor level [8]. In a series of elegant experiments [9,10], calcitriol resistance has been related to disturbed genomic effects of active vitamin D because the interaction of the vitamin D receptor ligand complex with vitamin D-responsive elements (VDREs) upstream of vitamin D-regulated genes was disturbed by the action of low molecular weight substances in uraemia, which have not been completely characterized. The role of genetically determined polymorphisms of the vitamin D receptor in the genesis of disturbed calcium metabolism of renal failure is currently unclear.
  • |Animals[MESH]
  • |Biomarkers/blood[MESH]
  • |Calcitriol/*therapeutic use[MESH]
  • |Calcium Channel Agonists/*therapeutic use[MESH]
  • |Calcium/*blood[MESH]
  • |Cholecalciferol/*therapeutic use[MESH]
  • |Humans[MESH]
  • |Hypercalcemia/blood/*drug therapy/etiology[MESH]
  • |Hyperparathyroidism, Secondary/blood/complications[MESH]
  • |Hypocalcemia/blood/*drug therapy/etiology[MESH]
  • |Parathyroid Hormone/blood[MESH]
  • |Uremia/blood/*complications[MESH]

  • *{{pmid11073270}}
    *<b>[ Management of disturbed calcium metabolism in uraemic patients: 1 Use of vitamin D metabolites ]</b> Nephrol Dial Transplant 2000; 15 Suppl 5() ; 18-24 Schomig M; Ritz E


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    Nephrol Dial Transplant

    18 .15 Suppl 5 2000