Etiology of nephrocalcinosis in preterm neonates: Association of nutritional intake and urinary parameters

Abstract

Etiology of nephrocalcinosis in preterm neonates: AssociationNephrocalcinosis (NC) occurs frequently in preterm of nutritional intake and urinary parameters.neonates. The incidence varies between 17 and 64%, de-Background. Nephrocalcinosis (NC) in preterm neonates pending on different study populations, ultrasonographic has been described frequently, and small-scale studies suggest nates receive a high intake of calcium, phosphorus, and vs. 2.3 mmol/mmol, P Ͻ 0.05) and a lower mean urinary citrate/ vitamin D in the first months of life in order to prevent calcium ratio (1.1 vs. 1.7 mmol/mmol, P ϭ 0.005). rickets of prematurity. In a prospective study, we exam-Conclusions. NC develops as a result of an imbalance beined the association of stone-promoting and stone-inhibtween stone-inhibiting and stone-promoting factors. A high intake of calcium, phosphorus, and ascorbic acid, a low urinary iting factors with the development of NC in preterm citrate/calcium ratio, a high urinary calcium/creatinine ratio, neonates.immaturity, and medication to prevent or treat chronic lung disease with hypercalciuric side effects appear to contribute to the high incidence of NC in preterm neonates. METHODS Patients

Effect of Drugs on Renal Development

“…Third, furosemide is a frequently used diuretic in premature neonates, although chronic treatment of neonates has shifted toward other diuretics because furosemide increases hypercalciuria and is associated with nephrocalcinosis (39). Rats born after maternal treatment with the diuretic furosemide during pregnancy showed a renal concentrating defect that persisted after cessation of nephrogenesis (40).…”

Nutritionally Regulated Hormonal Factors in Prolonged Postnatal Growth Retardation and Its Associated Adverse Neurodevelopmental Outcome in Extreme Prematurity

“…Enteral administration of citrates rather than bicarbonates, when necessary for metabolic acidosis, would be particularly beneficial as citrate, being a buffer, does not alter gastric pH. In addition, when excreted in the urine, citrate increases the solubility of calcium salts through calcium and citrate soluble complex formation, thereby reducing the risk of nephrocalcinosis in situations of hypercalciuria [221]. Based on the estimation that breast milk contains 0.79 mmol/dl of calcium and 0.45 mmol/dl of phosphate, when 2.25 mmol (= 90 mg) of calcium and 1.45 mmol (= 45 mg) of phosphate from a commercial human milk fortifier (e.g., S26 HMF ® , Emfamil HMF ® ) are added to each 100 ml of breast milk to bring the caloric density of the milk feeds up to 81 kcal/dl, infants who are fed fortified breast milk receive approximately 50% more calcium and phosphate than formula-fed infants [222][223][224][225][226].…”

Risk Factors and Outcome of Nephrocalcinosis in Very Low Birth Weight Infants

“…[3][4][5][6][7][8][9] The varying prevalence of NC is considered to be due different study populations and era, development in the sensitivity of ultrasound equipment, and workmanship of the observer. 27 In several reports, the incidence of NC showed a decreasing trend with development in care of preterm infants, 6,20,24 but this study showed an increasing tendency for NC.…”

“…Among different studies, the prevalence of NC ranged from 7 to 41% in very low birth weight (VLBW) infants with a gestational age less than 32 weeks. [3][4][5][6][7][8][9] The etiology of NC is multifactorial including low gestational age and birth weight. Male sex, family history, white race, mechanical ventilation, oxygen therapy, bronchopulmonary dysplasia (BPD), the use of furosemide, methylxanthine, dexamethasone, gentamicin, total parenteral nutrition (TPN), acidosis, hypercalcemia, hypophosphatemia, hypercalciuria, hyperoxaluria, hyperuricuria, and hypocitruria are associated with development of NC.…”