Posterior reversible encephalopathy syndrome in children with kidney disease
A five-year-old-male child weighing 14 kg was admitted with ARF and serum creatinine of 6.4 mg/dl, and respiratory acidosis. He was prepared by acute peritoneal dialysis for PCN diversion of obstructed solitary functioning kidney. Postoperatively after 12 h of diversion child developed convulsion. Clinically, his pulse and hydration was normal and BP was 130/90 mmHg (grade 2 HT) which was controlled with oral nifedipine. Biochemically, electrolytes were normal except for ionized serum calcium which was 2.26 mg/dl, phosphate 5.4 mg/dl, Magnesium 1.77 mg/dl, pH of 7.32 and serum bicarbonate level was 17.5 meq/L. Patient was treated by sodium bicarbonate drip in one IV line and calcium gluconate drip in another IV line. In first 12 h the child received 15 ml of calcium gluconate and 10ml in next 12 h. He was given 0.5 ml of magnesium sulphate (i.e., 250 mg; 25% w/v) intramuscularly. The child's venous blood gas and electrolytes were studied every 6 hours and child persisted to be severely hypocalcemic though he received 15 ml of calcium gluconate on second day and 10 ml for further two days. So in total 50 ml of calcium gluconate was given in three days of PCN diversion in a 14 kg child. Childs hypocalcemia was within normal range on fourth day only when we reduced 24 h calcium dose in stepwise fashion. His BP was well controlled with oral nifedipine. Throughout the course, his urine output, serum urea, and serum creatinine were improving day by day after diversion. We measured 24 h urinary calcium also on 2nd day after diversion which was 30 mg/24 h which was high in face of very low ionized serum calcium level. The amount of calcium gluconate the child required parenterally to correct hypocalcemia was surprisingly high which we have observed first time in such a setting. His iPTH, five days after PCN diversion was 408 pg/ml which was 540 pg/ml when he presented with ARF. Logically, we hypothesized that calcium gluconate given iv was increasingly being taken up by bone due to decreasing hyperparathyroidism in association with improving renal function and it was wasted to some extent in urine also because of defect in tubular reabsorption leading to persistent hypocalcemia. Calcium has unique intracellular messanger role and it is complexed with numerous ligands in cytosol, including adenosine and vitamin D dependent calcium binding protein, calmodulin.[] Persistent hypocalcemia may be expected to affect directly or indirectly mechanisms involved in autoregulation and endothelial function.