Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The risk of nephrocalcinosis in preterm infants is considerable, but conflicting numbers are given for the actual incidence (10-65%). Furosemide induced hypercalciuria is said to be the main risk factor. We examined retrospectively the incidence, causes and outcome of nephrocalcinosis in preterm infants born in our hospital from 1988 to 1998 ( n=2190). An abnormal renal echogenicity or nephrocalcinosis was seen in 31 infants (29.7+/-3.3 weeks gestational age; 1307+/-690 g birth weight). Nephrocalcinosis was diagnosed in 16, hyperechoic kidneys (HK) in 10 and Tamm-Horsfall kidneys in 5 infants. Main risk factors were low gestation age and birth weight, length of hospitalization, variations in acid-base status, length of assistant ventilation and hypercalciuria at diagnosis. The incidence of nephrocalcinosis was 0.73% [1.7% for low birth weight infants (VLBW)]. Taking the cases of nephrocalcinosis and HK together, incidence was calculated to be 1.2% overall and 2.5% for VLBW infants, but increased to 7% in 1998. The follow-up showed persisting nephrocalcinosis or hyperechoic kidneys in 8/26 preterm infants. In conclusion, the incidence of nephrocalcinosis was lower in our population than is usually reported. The numbers have, however, increased over the past few years. From the follow-up it was obvious that long-term observation of preterm infants is necessary and that complications might arise in the long run.
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PMID:Nephrocalcinosis in preterm infants: a single center experience. 1195 79

Furosemide is a loop diuretic agent that has been used to treat hypercalcemia because it increases renal calcium excretion. The effect of furosemide on calcium transport molecules in distal tubules has yet to be investigated. We conducted studies to examine the effects of furosemide on renal calcium excretion and expression of calcium transport molecules in mice. Mice were administered with a single dose of furosemide (15 mg/kg) and examined 4 h later or were given twice-daily furosemide injections for 3 days. To evaluate the effects of volume depletion, drinking water was supplemented with salt. Our results showed that, in acute experiments, furosemide enhanced urinary calcium excretion, which was associated with a significant increase in mRNA levels of TRPV5, TRPV6, and calbindin-D28k but not calbindin-D9k as measured by real-time PCR (TRPV5 and TRPV6 are transient receptor potential vanilloid 5 and 6). Chronic furosemide administration induced three- to fourfold increases in urinary calcium excretion and elevated mRNA levels of TRPV5, TRPV6, calbindin-D28k, and calbindin-D9k without or with salt supplement. Similar upregulation of calcium transport molecules was observed in mice with gentamicin-induced hypercalciuria. Coadministration of chlorothiazide decreased furosemide-induced calciuria, either acutely or chronically, although still accompanied by upregulation of these transport molecules. Immunofluorescent staining studies revealed comparably increased protein abundance in TRPV5 and calbindin-D28k. We conclude that furosemide treatment enhances urinary calcium excretion. Increased abundance of calcium transport molecules in the distal convoluted tubule represents a solute load-dependent effect in response to increased calcium delivery and serves as a compensatory adaptation in the downstream segment.
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PMID:Effects of furosemide on renal calcium handling. 1765 76


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