Hypomagnesemia in renal transplant patients: Improvement over time and association with hypertension and cyclosporine levels

Abstract

Hypomagenesemia is frequently encountered early after kidney transplantation, especially in patients receiving cyclosporine (CSA). However, there have been no studies addressing the natural history of this disorder in adult transplant recipients. We conducted this investigation to study the change in the prevalence of hypomagnesemia over time in renal transplant patients as well as to determine the factors associated with this change. Three patient groups were studied: 24 CSA‐treated patients followed longitudinally at 1, 3 and 6 months post‐transplant (Group la, lb, lc); 33 CsA‐treated patients at least 2 years post‐transplant (Group 2; mean follow‐up 55±25 months); and 31 non‐CsA‐treated patients at least 2 years post‐transplant (Group 3; mean follow‐up 132±57 months). The following parameters were monitored: serum and urine magnesium levels; serum potassium; creatinine clearance; fractional excretion of magnesium; and trough CsA levels. In group 1 patients, longitudinal follow‐up showed a significant linear trend for improvement in the serum magnesium over time (1.6±0.3, 1.7±0.2, 1.8±0.2 mg/dl; p=0.0015) as well as a decline in the whole blood CsA level (316±103, 251±82, 194±67 ng/ ml; p=0.0015) at 1, 3 and 6 months, respectively. The serum magnesium was significantly higher in group 2 (1.8±0.2 mg/dl) compared with group la (1.6±0.2 mg/dl; p=0.0024), but did not achieve the level observed in the non‐CsA‐treated group‐3 patients (2.0±0.2 mg/dl; p<0.00004, group 2 vs 3). While the fractional excretion of magnesium showed a decreasing trend over time in CSA‐treated patients, this was not statistically significant. However, the fractional excretion of magnesium was significantly lower in group 3 (6.4±2.4%) compared with groups la (8.7±3.9; p= 0.009) and lb (8.7±3.9; p=0.01). Hypomagnesemia was noted in 11% and 49% (p=0.001) of patients who were normotensive and hypertensive, respectively. Furthermore, of patients requiring 0, 1 or ≥2 antihypertensive medications, 12, 45 and 58% (p=0.001) respectively, were noted to have hypomagnesemia. In our study, hypomagnesemia improves with time in CSA‐treated patients, but not to the level of non‐CsA treated patients. The improvement in the serum magnesium levels in CSA‐treated patients appears to be related to declining CSA levels. The hypomagnesemia is the result of urinary magnesium loss. Finally, hypertension and the severity of hypertension are associated with low serum magnesium levels.