Calcium and phosphorus metabolism in chronic uremia.
In chronic uremia, the clinical disorders o calcium and phosphorus metabolism are influenced by the following factors: (1) intestinal absorption of calcium and phosphate, resulting in a negative calcium and phosphate balance at normal dietary intakes; (2) renal handling of calcium and phosphate: the fractional transport of calcium (the isoosmotic reabsorption taking place in the proximal tubule) is not affected by GFR modifications, whereas the Tm-limited reabsorption is severely impaired; the external phosphate balance is kept, even in the presence of a reduced nephron population, by means of a proportional reduction in TmPO4 values; (3) physiochemical state and turnover of body calcium and phosphate: in uremic patients, the distribution spaces, turnover rate of calcium, and accretion rate of bones are increased in comparison with the controls; the calcium infusion test in patients with renal osteomalacia is followed by a regular increase in plasma [PO4], whereas a significant decrease is observed in patients with renal osteitis fibrosa, due to the extreme 'avidity' of bones for calcium phosphate; the role of hyperphosphatemia is critical in keeping the plasma [Ca] lower than the expected values for a given metabolic set; moreover, an increased cell uptake of phosphate could counteract to some extent the reduced renal clearance of phosphate; (4) structural and biochemical modifications of bone tissue: uremic osteodystrophy consists mainly of two components: (a) osteomalacia, with osteoid excess, disappearance of the calcification front, and diffuse pathologic mineralization, and (b) osteitis fibrosa, with severe resorption of normally mineralized bone, slight osteoid excess, and almost normal calcification front; (5) hormonal factors: chronic stimulation of parathyroid glands may result in suppressible or even autonomous hyperparathyroidism. As to vitamin D, it has been suggested that the uremic kidney is not able to synthesize the 1,25-di-OH-cholecalciferol, the active metabolite of vitamin D: this results in an impaired intestinal absorption of calcium. On the contrary, the role of calcitonin in chronic uremia is still uncertain, since low values of plasma [Ca] are usually observed.
D002118:Calcium / Q000378:metabolism*; D002908:Chronic Disease; D012080:Chronic Kidney Disease-Mineral and Bone Disorder / Q000378:metabolism; D004100:Dihydroxycholecalciferols / Q000096:biosynthesis; D004351:Drug Resistance; D005919:Glomerular Filtration Rate; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology; D006965:Hyperplasia; D007408:Intestinal Absorption; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D007700:Kinetics; D008659:Metabolic Diseases / Q000209:etiology; D010002:Osteitis Fibrosa Cystica / Q000378:metabolism; D010018:Osteomalacia / Q000378:metabolism; D010280:Parathyroid Glands / Q000473:pathology; D010281:Parathyroid Hormone / Q000378:metabolism; D010710:Phosphates / Q000097:blood; D010758:Phosphorus / Q000378:metabolism*; D014511:Uremia / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D014807:Vitamin D
D004100:Dihydroxycholecalciferols; D010281:Parathyroid Hormone; D010710:Phosphates; D014807:Vitamin D; D010758:Phosphorus; D002118:Calcium