Magnesium metabolism in chronic renal failure.
Renal excretion is the major route of magnesium elimination from the body and a positive magnesium balance would be expected under conditions of renal insufficiency. However, a compensatory decrease in tubular reabsorption is operating to maintain an adequate urinary magnesium excretion even when glomerular filtration rates are very low. Nevertheless, in end-stage renal disease, the limited ability of the kidney to excrete an increased magnesium load may result in toxic concentrations of the ion in serum. While magnesium intoxication is a real hazard when magnesium-containing drugs are given, magnesium balance may be normal or even decreased in uraemic patients. This is usually due to decreased dietary intake combined with the impaired intestinal magnesium absorption which characterizes chronic renal failure. Impairment of magnesium absorption seems to be related to deficient synthesis of the active metabolite of vitamin D by the non-functioning kidney. Following the institution of chronic haemodialysis or continuous ambulatory peritoneal dialysis (CAPD) treatment, the major determinant of magnesium balance is the concentration of magnesium in the dialysate. Changes in the dialysate magnesium have been used to reduce the incidence of renal osteodystrophy, to alleviate uraemic pruritus, or to retard the development of arterial calcification in chronic renal disease. However, uncertainty about magnesium, calcium and parathyroid hormone relationships in renal failure makes a reasoned approach to such manipulations extremely difficult.
Mountokalakis
T D
TD
Second Medical Department, Athens University, Greece.
D006801:Humans; D007408:Intestinal Absorption; D007676:Kidney Failure, Chronic / Q000378:metabolism*; D008274:Magnesium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D010531:Peritoneal Dialysis, Continuous Ambulatory; D006435:Renal Dialysis; D014018:Tissue Distribution; D014807:Vitamin D / Q000378:metabolism
D014807:Vitamin D; D008274:Magnesium