Renal Calcification in NICU Patients

Abstract

Sequential renal ultrasonographic studies have shown renal calcifications to be more common in neonatal intensive care unit (NICU) patients than is commonly believed, especially in extremely low-birthweight (ELBW) infants. A family history of kidney stones is an independent risk factor for renal calcifications in ELBW infants. Understanding the role of inhibitors and promoters in crystal formation helps in understanding the pathophysiology of nephrocalcinosis. Identification of the presence or absence of hypercalcemia and hypercalciuria is an effective method of directing the diagnostic evaluation of infants who have nephrocalcinosis. Fortunately, ultrasonographic renal calcifications resolve spontaneously in most NICU patients. Renal calcifications can be associated with persistent abnormalities in renal function if hypercalciuria continues, such as in the rare very low-birthweight (VLBW) infant who receives long-term furosemide therapy after hospital discharge. Only in rare cases, often inborn errors of metabolism, can renal calcifications in NICU patients progress to chronic renal injury, such as in infants who have primary hyperoxaluria that involves persistence of oxalate in the urine, a potent promoter of calcium crystal formation.