Renal leak; mechanism of hypercalciuria in short-term immobilization.

Dear Editor,

Hypercalciurai is daily urine excretion of calcium beyond 4 mg/kg or calcium to creatinine excretion over 0.21 randomly.[1] Hypercalciuria incidence in healthy children varied.[2] immobilization is a common cause of hypercalciuria.[3] We studied 40 critically ill children were immobilized and starved for their disease. In short term (5 days), their serum calcium in both total (8.4 ± 0.8 vs 8.6 ± 0.6 mg/dl) and ionized (4.1 ± 0.4 vs 4.2 ± 0.3 mg/dl) was not changed while serum phosphor decreased significantly, it was 0.5 mg/dl in average (4 ± 1 vs 3.5 ± 0.8, P 0.02). Calcium excretion in 1st day in compared to control was (0.31 ± 0.3 vs 0.1 ± 0.08, P 0.03). This measure in 5th day of observation was (0.37 ± 0.4 vs 0.1 ± 0.08, P 0.003) Hypercalciuria occurs in 10% of control group and 51% in 1st day (0.001) and 54% in 5th day. Urinary sodium excretion in cases with hypercalciuria was higher but the excretion rate was more significant in 1st day compared to 5th day. In contrast to 1st day of observation in 5th day, hypercalciuria occurred more significant in lower age [Table 1]. Resorptive hypercalciuria in immobilization may happens due to parathyroid and 1-25 dihydroxyvitamin D axis mechanism.[4] The time for hypercalciuria evolving is short because in a case report in a 10-year-old boy nephrolithiasis was observed after immobilization for 8 days.[3] As our study in critical ill child hypercalciuria occurs so soon in 1st days of disease in near half of cases while the serum calcium both total and free part were not differed in both hypercalciuric and normal calcium excreted groups. In fact, this show that mechanisms of hypercalciuria in immobilized ill children is a common and complex matter beyond that theories which suggested earlier, it may be due to increase serum cytokine levels which derange calcium metabolism in inflammatory conditions by secretion of interleukin1 and tumor necrosis factor–α which play role in bone resorption in special conditions like as malignancies.[5] Other studies in adults describe hypercalciuria starts at 4th week of immobilization the mechanism of hypercalciuria in this group people are attributed to resorptivehypercalciuria which lead to hypercalcemia, hyperphosphatemia beside to renal phosphor threshold and in prolonged time with decrease renal function calcium filtration decreases which aggrevate hypercalcemia.[4] We show hypercalciuria appear short term after immobilization and serum calcium both total and free not changed. Serum phosphor also drops 0.5 mg/dl in 5 days without effecting in hypercalciuria incidence or severity which is not related to reabsortive phenomena because all patients were starved or resorptive as serum calcium was not changed and activation of parathyroid axis activity takes time to activate while renal leak hypercalciuria mechanism by act of unknown mechanism like as cytokines similarly to what occur in malignancies[5] can be involve in this phenomena which lower age are more vulnerable to hypercalciuria in longer immobilization 5 days as our study.

Table 1

Laboratory tests in children with and without hypercalciuria in 1st and 5th day of immobilization