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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of NC in VLBW infants appears to be multifactorial. The vulnerability of extreme immaturity and the underdevelopment of renal function may be the most important variables. In some ways, we view this problem as similar to that of retinopathy of prematurity. (Clearly the exposure of the retina to high partial pressures of oxygen contributes to the development of retinopathy of prematurity but other variables--some known, such as an immature retina, and others not yet defined--must be present.) Hypercalciuria is common in the VLBW infant, yet not all develop NC. Decreased glomerular filtration rate, low citrate excretion, and frequently an alkaline urine are in part due to the immaturity of renal function of these infants. The need for prolonged hyperalimentation resulting in increased oxalate excretion and the development of BPD frequently requiring diuretics that may cause phosphaturia and magnesium depletion and that may increase calcium excretion are more common in the smallest and sickest of premature infants. Even transient insults to the kidneys, such as hypoxia or hypotension or the use of nephrotoxic drugs that provoke tubular injury and cell death with the probability of crystal formation and growth by way of heterogeneous nucleation, are likely to occur more frequently in this vulnerable population.
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PMID:Nephrocalcinosis. 157 67

The treatment of premature infants with the diuretic furosemide appears to be a contributory factor in the development of metabolic bone disease presumably because of furosemide-induced hypercalciuria. In this study, we measured calcium and phosphorus balance in furosemide-treated very low birth weight infants (VLBW) infants with bronchopulmonary dysplasia (BPD) who were fed a specialized premature formula containing increased amounts of calcium and phosphorus. Furosemide-treated infants received 166 +/- 37 mg/kg/day and retained 80 +/- 34 mg/kg/day of calcium, and 87 +/- 19 mg/kg/day and retained 52 +/- 14 mg/kg/day of phosphorus. The amounts retained were approximately 65% of the calcium and 72% of the phosphorus requirements for in utero mineral accretion. Compared to a group of similarly fed VLBW infants without BPD and not treated with the diuretic, the furosemide-treated infants excreted a larger percent of the calcium intake in the urine but had similar total urinary calcium and phosphorus losses (mg/kg/day) and serum calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) levels. From the latter two findings, we suggest that the extra mineral content of the formula may have promoted bone mineralization and prevented the occurrence of secondary hyperparathyroidism.
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PMID:Effect of high calcium and phosphorus intake on mineral retention in very low birth weight infants chronically treated with furosemide. 280 41

Nephrolithiasis was present in a 2-month-old premature infant with bronchopulmonary dysplasia who had been receiving furosemide and intravenous (IV) gluconate calcium therapy. This infant was found to be hypercalciuric. Furosemide therapy is known to increase calcium excretion. In the present study, we examined sick infants who were receiving gluconate calcium without furosemide to evaluate the effect of gluconate calcium therapy on urinary calcium excretion. The sick infants receiving gluconate calcium had higher values of urinary calcium than did the well infants taking regular formula feedings. Moreover, the calciuria appeared to increase progressively with continued gluconate calcium therapy. It appears that prolonged use of either furosemide or IV gluconate calcium leads to hypercalciuria, which, in turn, may predispose the premature infant to nephrolithiasis.
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PMID:Gluconate calcium therapy and neonatal hypercalciuria. 678 90

Most of the published studies evaluating renal prognosis of children born very preterm found asymptomatic abnormalities (blood pressure, glomerular filtration rate GFR, hypercalciuria, decreased renal size, microalbuminuria...) during childhood or early adulthood. The objective of this study was to assess renal function (inulin clearance) in a prospective single-center cohort of children born preterm between 1998 and 2001 (< 30 GW,<1000 g) and to identify neonatal risk factors for renal abnormalities during childhood. Fifty children were included in the final part of the study. At a mean age of 7.6 years, no patient had arterial hypertension or chronic kidney disease, but mean centile for diastolic blood pressure was higher than expected and ultrasounds revealed small-sized kidneys compared to controls. The average GFR was 112 ml/min per 1.73 m(2) (91-158). Two children had microalbuminuria, two had hypercalciuria and one had nephrocalcinosis. Children with intra- or extra-uterine growth retardation had an impaired GFR compared to children with appropriate pre- and post-natal growth (107 vs. 110 vs. 125 ml/min per 1.73 m(2), p<0.05). Children with bronchopulmonary dysplasia had a significant higher microalbuminuria. In conclusion, findings of borderline blood pressure and reduced kidney size in children born preterm can be regarded as markers of reduced nephron number. Long term renal follow-up (blood pressure, serum creatinine, urine albumin / creatinine ratio) should be performed in all children born very preterm, with an early referring when abnormalities are highlighted.
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PMID:[Long term renal outcome of children born preterm: a regular follow-up is needed]. 1983 67