Hypomagnesemia as a reversible complication of cyclosporine in pediatric nephrotic syndrome: a case report

Abstract

Calcineurin inhibitors remain a cornerstone in the treatment of steroid-resistant nephrotic syndrome (SRNS) in pediatric patients. Hypomagnesemia, a clinically relevant yet frequently neglected complication of calcineurin inhibitors like cyclosporine, may exacerbate hypokalemia and induce neuromuscular symptoms such as tetany, challenging patient management. However, serum magnesium is not routinely monitored in many clinical settings. A 46-month-old girl with SRNS had been receiving highdose cyclosporine for over 1 year. She was admitted with vomiting, diarrhea, generalized edema, and hypovolemic shock. After stabilization, she developed persistent hypokalemia refractory to supplementation, despite normal renal function and basic electrolyte panel. On hospital day 10, carpal-type tetany prompted the first measurement of serum magnesium, revealing severe hypomagnesemia (0.14 mmol/L). Cyclosporine was temporarily withheld, and intravenous then oral magnesium was administered. Tetany resolved within 48 hours, and both serum magnesium and potassium levels normalized. This case highlights the risk of delayed recognition of symptomatic hypomagnesemia during prolonged cyclosporine therapy in children. Tetany was the first neurological manifestation of a preventable complication. Current guidelines lack clear recommendations regarding magnesium surveillance in pediatric SRNS receiving cyclosporin. This case underscores a critical gap in practice and calls for the integration of magnesium monitoring into standard care for this vulnerable population.