Should We Screen Preterm Infants for Nephrocalcinosis? An Evidence-based Decision

Shahirose S Premji; Majeeda Kamaluddeen


Pediatr Health. 2010;4(1):24-35. 

In This Article

Etiology & Pathogenesis

The etiology of nephrocalcinosis is multifactorial and those at higher risk for developing nephrocalcinosis include infants with low gestational age, LBW[3,16,17] and severe respiratory disease.[17] Furosemide has not been consistently identified as a contributing factor to early development of nephrocalcinosis[7] as preterm infants who never received furosemide have still developed nephrocalcinosis.[3,18] Furosemide-induced hypercalciuria may not be the predominant factor in the etiology of nephrocalcinosis, which may involve a complex interaction of risk factors including: LBW; short gestational age; medication treatment (e.g., corticosteroids; xanthenes; gentamicin and furosemide); and nutrition (e.g., high intake of calcium, phosphorus and ascorbic acid).[2,6,16,17,19] These risk factors contribute to an imbalance between stone-inhibiting (e.g., low urinary citrate excretion) and stone-promoting factors (e.g., hypercalciuria and hyperoxaluria), thereby leading to nephrocalcinosis.[6,17,20] Hypocitraturia has been documented in several studies[6,21] and lung disease and metabolic acidosis may explain the pathogenesis of lower citrate excretion.[21,22] Calcium oxalate deposits are a type of renal calcification commonly found in autopsies of infants and neonates who received intensive care.[14,23] It is asserted that the pathogenesis of nephrocalcinosis includes hyperoxaluria, defined as elevated urine oxalate excretion, since LBW infants have been reported to have a high urine oxalate:creatinine ratio.[23,24] Hypercalciuria, which may be related to factors such as the drug furosemide, acidosis or nutrition, may play a role in nephrocalcinosis.[3,6,19,25] In preterm infants, metabolic acidosis (pH < 7.25) is due to multiple etiological factors including: patent ductus arteriosus; physiological proximal tubular dysfunction; dehydration; sepsis; necrotizing enterocolitis and so on. However, metabolic acidosis was more common in the first week of life or primary hospital stay in those preterm infants who developed nephrocalcinosis[4,26] and was also reported to be more severe and prolonged.[2] Although the etiology of nephrocalcinosis is multifactorial, the common pathway is the formation of crystals in the immature kidney, which provides an ideal milieu to promote crystalization given the deep and well developed medullary nephrons, the longer loop of Henle in the juxtamedullary nephrons, and the lower urine velocity secondary to low glomerular filtration rate (GFR).[6,25]


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