[Studies on cultured rat mesangial cells using cyclosporin A and magnesium--is magnesium nephroprotective in cyclosporin A therapy?].

One serious side effect of Cyclosporine A therapy is its acute nephrotoxicity characterized by a marked decrease in the glomerular filtration rate. A main determinant of the glomerular filtration rate is the ultrafiltration coefficient which is thought to be regulated by the contractile state of the cells of the mesangium. Cyclosporine A enhances contractions of mesangial cells elicited with angiotensin II. By way of lowered ultrafiltration coefficient this effect of Cyclosporine A may be partly responsible for its acute nephrotoxicity. Hypomagnesaemia is often associated with Cyclosporine A therapy. Profound tubular magnesium wasting by Cyclosporine A has been claimed its cause. We have investigated the effect of low and high magnesium concentration on the contractility of mesangial cells pretreated with Cyclosporine A. Without magnesium 80% of the cells contracted upon addition of angiotensin II. A marked decrease in the contractility was seen when the magnesium concentration was elevated to 2 mmol/l (34%). From these observations we conclude that magnesium serum levels even in the high normal range might be protective against the decrease of the glomerular filtration rate seen with CsA therapy.