Supplemento S71 - Editorial

Nephrocalcinosis in children


Nephrocalcinosis (NC) is a renal disease characterized by  deposition of calcium salts into the renal medulla. There are several causes, organic, iatrogenic, hereditary and sometimes related to extrarenal diseases. We studied 34 children affected by  NC, 21 M and 13 F (average age at diagnosis 7.8 months), with the aim of analyzing the associated diseases, clinical manifestations, metabolic abnormalities, growth and renal function at onset and after follow-up. At onset 70% of patients were asymptomatic and diagnosis was occasional. Renal function was normal in 33 patients. The most frequent clinical symptoms were: failure to thrive (9%), abdominal pain (6%), proteinuria/hematuria (7%). The associated diseases  were: tubulopathies (8 pcs – tubular acidosis, Dent, Bartter and Lowe Syndromes), medullary sponge kidney, policalicosis (3 pcs ), Short bowel Syndrome (3 pcs), hyperparathyroidism, hypothyroidism (2 pcs), thalassemia (1pc), tyrosinemia (1 pc.). We recognized two forms of hypervitaminosis D. In a pc NC would be correlated with prematurity, another one with lipid necrosis. Among the metabolic abnormalities, observed in 25% of pcs, hyperoxaluria is the most frequent (47%), hypercalciuria (20%), hypercalcemia (15%). In some cases we found endocrine non pathogenic alterations: hypovitaminosis D (2 pcs) and hypoparathyroidism (6 pcs). During follow-up  the growth was normal in 87% of cases and glomerular function was stable in 90% of pcs; IRC developed in 3 cases. From our analysis, it appears that the treatment of the underlying condition of NC is associated with catch-up growth and stabilization of renal function in most patients, but not with the reduction of the degree of the NC.

Keywords: nephrocalcinosis, tubulopathies, hyperoxaluria, ultrasound, growth, renal function

Sorry, this entry is only available in Italian.


La nefrocalcinosi (NC) è un quadro morfologico renale caratterizzato da aumentato deposito di calcio a livello del parenchima renale, più spesso a carico della midollare o della giunzione cortico-midollare, con accumuli di materiale cristallino all’apice delle piramidi renali che possono coinvolgere le cellule tubulari, l’interstizio o il lume tubulare (1). Le cause possono essere associate a: iperparatiroidismo, iper- ed ipotiroidismo, acidosi tubulare distale, iperossaluria ; S. di Bartter, S. di Dent, S. di Lowe, Rene a spugna midollare, M. di Wilson, tirosinemia, fibrosi cistica, anemia mediterranea, S. di Cushing, anemia falciforme, Ipomagnesiemia familiare con ipercalciuria; patologie iatrogene (diuretici, intossicazione da Vitamina D, Nutrizione parenterale , amfotericina B, Sindrome da intestino corto);  necrosi corticale renale e miscellanea di altre patologie che non sempre riguardano il rene. 

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