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)

The selective determination of mid-C-regional parathyroid hormone (mid-C-PTH) in combination with other laboratory parameters is a reliable tool for diagnosis and treatment of extra-renal (primary) and renal (secondary) hyperparathyroidism. Early stages, which show either high-to-normal serum calcium and elevated mid-C-PTH or increased serum calcium but normal mid-C-PTH, can be distinguished from overt hyperparathyroidism. Alkaline phosphatase (AP) activity and mid-C-regional PTH provide biochemical confirmation of histologically classified renal osteodystrophy. Since the index AP X PTH signifies osseous changes in dialysis patients at an early stage, therapeutic regimens may be altered without additional invasive procedures. After renal transplantation mid-C-PTH normalizes and serum creatinine decreases. Increased mid-C-PTH in patients with normal renal graft function reflects autonomous PTH secretion, which requires careful monitoring to prevent PTH-induced hypercalciuria.
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PMID:[Mid C regional parathyroid hormone in the clinical workup: diagnostic value in extrarenal (primary) and renal (secondary) hyperparathyroidism]. 352 Jan 30

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

Growth retardation is a cardinal feature of children with renal tubular acidosis. This is reversible by correcting the non-uremic acidosis with alkali therapy. Sodium bicarbonate solutions or citrate solutions have been used for this purpose. However, the odious taste of these medications almost invariably causes medical noncompliance. The persistent and often profound metabolic acidosis from medical noncompliance, precipitates hypercalciuria and hypocitraturia, and increases the risk of nephrocalcinosis. The mechanism of the growth retardation in renal tubular acidosis is thought to be related to a blunting of anterior pituitary growth hormone secretion. In experimental metabolic acidosis, the growth hormone secretory pulse areas are reduced. Just as importantly, hepatic growth hormone receptor expression and IGF-I mRNA were blunted in metabolic acidosis. In uremia, growth retardation is secondary to a host of factors including metabolic acidosis, renal osteodystrophy, and the side effects of treatment such as corticosteroids, which compound the growth retardation. Growth hormone secretion by individual pituitary cells was stimulated by corticosteroids but, paradoxically, the total number of somatotropes was suppressed. In uremia, the secretion of growth hormone was not different from controls at any level of growth-hormone-releasing hormone challenges. Hepatic IGF-I mRNA was markedly reduced in uremic rats. Growth hormone receptor expression was significantly reduced in uremic acidotic rats. The growth hormone and IGF-I expression on the growth plate of the long bone of uremic rats was reduced. IGF-I immunoreactivity was present in both the hypertrophic and proliferative zones. The lack of growth of the proliferative zones suggested growth hormone and IGF-I resistance in uremic chondrocytes.
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PMID:Growth hormone and insulin-like growth factor in non-uremic acidosis and uremic acidosis. 906 56