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Nephrocalcinosis in neonates

Jodi Smith, MD, MPH
F Bruder Stapleton, MD
Section Editors
Tej K Mattoo, MD, DCH, FRCP
Joseph A Garcia-Prats, MD
Deputy Editor
Melanie S Kim, MD


Nephrocalcinosis is defined as calcium salt deposition in the renal parenchyma including the tubular epithelium and interstitial renal tissue. Nephrocalcinosis occurs more frequently in neonates, especially preterm infants because of their renal tubular immaturity, and administration of medications and nutritional supplements that promote calcium salt deposition.

This topic will review the pathogenesis, etiology, risk factors, and management of neonatal nephrocalcinosis.


The reported incidence of neonatal nephrocalcinosis over the last several decades has varied from 10 to 65 percent. However, subsequent case series in preterm infants who are most susceptible to nephrocalcinosis report a lower but still significant rate of 7 to 41 percent [1-5].


Neonatal nephrocalcinosis is caused by calcium salt crystal formation and aggregation within the renal tubules created by an imbalance that promotes stone producing factors (increased urinary excretion of calcium, oxalate, uric acid) over stone inhibiting factors (decreased urinary excretion of citrate and magnesium) [1,6-13]. Neonates and especially premature infants are at risk for calcium salt crystallization because of renal tubule immaturity, and increased likelihood of hypercalciuria (increased promoting factor) and hypocitraturia (loss of inhibiting factor) as discussed below.


Renal tubular immaturity in preterm infants — Preterm infants are at increased risk for nephrocalcinosis due to renal tubular immaturity, which increases with decreasing birth weight [14]. Nephrogenesis is not completed until 34 to 36 weeks gestation. As a result in the developing kidney, there is continuing proliferation of renal epithelium cells within the renal tubule that are thought to be more susceptible to crystal formation and aggregation [15]. Preterm infants have a markedly low glomerular filtration rate that results in a low fluid flow rate within the tubular lumen [16,17]. This enhances crystal formation and aggregation particularly in the setting of tubular fluid supersaturation, which is promoted by hypercalciuria and hypocitraturia (commonly observed findings in preterm infants).

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Literature review current through: Oct 2017. | This topic last updated: Aug 21, 2017.
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