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)

This study was conducted to determine the effect of a high protein diet on calcium metabolism in rat. Wistar strain male rats (50 days old) were divided into 5 groups (day 0): control diet (18% casein); high protein diet (18% casein +20% lactalbumin); high protein and 0.1% sodium bicarbonate diet; high protein and 0.2% sodium bicarbonate diet; and high protein and 0.4% sodium bicarbonate diet. On days 0, 1, 3, 5, 7, 9, urine samples were collected and, at the same time, feces were collected from half of the animals in each group. Urinary titratable acidity (TA-HCO3-), ammonium ion (NH4+), and net acid excretion (NAE) were measured as an index of acid-base balance in rat body. Urinary volume was rapidly increased and the increase of urinary volume continued throughout the study in rats fed the high protein diet. Urinary excretions of calcium and phosphorus were increased after day 3 and day 1, respectively, in rats fed the high protein diet. The high protein diet depressed calcium absorption and elevated phosphorus absorption from the digestive tract in rats fed the high protein diet. The high protein diet decreased TA-HCO3-, which was closely correlated with the decrease of NAE. Sodium bicarbonate supplementation to the high protein diet had little effect on urinary calcium excretion and NAE. This study suggested that there was no relationship between metabolic acidosis and hypercalciuria in rats fed the high protein diet.
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PMID:Effects of high protein diet and sodium bicarbonate supplementation on calcium metabolism in rats. 263 82

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