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)

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44

There is a consensus that adequate calcium intake during bone development, and possibly in adulthood and senescence, helps to prevent bone resorption and osteoporosis. The uptake of dietary calcium should be sufficient to maintain both normal serum calcium concentrations and parathyroid hormone levels in the low normal range throughout the day, otherwise, increased bone resorption occurs. Calcium intake varies with race and with environmental and dietary conditions. Estimating the appropriate amount of calcium to be added to dietary sources for an optimal supplementation regimen is therefore difficult. Few intervention studies have evaluated the dose-effect relationship for calcium supplementation conclusively. The mechanisms regulating fractional calcium absorption as a function of intake suggest that very high daily doses are probably useless. They may be unsafe in the long term because of the risks of hypercalciuria and kidney stones, and of an imbalance in the ratio of calcium to magnesium. Concomitant supplementation with limited amounts of magnesium may reduce this risk and improve mineralization. Dietary intake is 500-600 mg/day in most studies, making 400 mg/day an appropriate supplementary dose for most premenopausal women (RDA 1000 mg/day). After the menopause and during lactation (RDA 1200-1500 mg/day), 800 mg/day is probably appropriate, particularly if low doses of vitamin D are taken concomitantly.
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PMID:Dietary calcium and mineral/vitamin supplementation: a controversial problem. 1041 56