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

The clinical peculiarities, and the etiological and pathogenetic factors of urolithiasis in 296 patients suffering from spontaneous stone elimination were studied. It was established that 209 patients eliminated stones consisting of uric acid, sodium salts and ammonium salts. Moderate hypocalcemia and hyperphosphatemia and also hyperuricemia and hyperuricuria were present. There were 39 'eliminators' of calcium stones. Their blood calcium content was higher, hypercalciuria, inorganic phosphorus and normal uric acid, were noted. Compound stones were present in 48 observations. When carrying out additional biochemical tests in 57 patients with calcium and compound stones, primary hyperparathyroidism was diagnosed in 34 observations; and parathyroidectomy was successfully performed.
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PMID:On the pathogenesis of stone formation in stone-eliminating patients. 42 6

The effects of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone (iPTH) were studied. Acute metabolic acidosis induced by administration of ammonium chloride (NH4Cl) produced a barely detectable increase in serum iPTH. Chronic NH4Cl administration produced a marked elevation of serum iPTH that was well correlated with the magnitude of acid-induced hypercalciuria but not with the degree of acidosis. Acetazolamide administration produced an equivalent degree of acidosis, but hypercalciuria was minimal and iPTH increased only marginally. Methionine administration caused moderate hypercalciuria and a significant but moderate increase in iPTH. Chronic NH4Cl-induced acidosis produced no hypercalciuria when dietary sodium intake was rigidly restricted, and under these conditions serum iPTH remained normal. When sodium intake was suddenly increased while maintaining the acid load, hypercalciuria appeared and was followed by progressive rise in serum iPTH equivalent to that observed during chronic NH4Cl-induced acidosis in subjects consuming salt ad lib. These results indicate that chronic acidosis elevates iPTH mainly by producing hypercalciuria and that acidosis itself is not a primary stimulus to PTH secretion.
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PMID:Effect of acute and chronic metabolic acidosis on serum immunoreactive parathyroid hormone in man. 120 55

Our primary objective was to test the hypothesis that a defect in acidification is more common in patients who have idiopathic calcium phosphate kidney stones than in those whose stones are formed mainly of calcium oxalate. Additionally, other risk factors might differ for these 2 stone types. Urine pH was measured serially over 24 hours, and along with ammonium and titratable acid, it was measured before and serially after ingestion of ammonium chloride in 3 groups of subjects: 24 patients with predominantly calcium phosphate stones, 30 patients with calcium oxalate stones, and 15 health non-stone-formers. Twenty-six parameters potentially related to stone formation and acidification were assayed on urines collected over 24 hours, and 15 parameters on blood. The data base was a computerized list of 5900 analyses of stones from patients living in Newfoundland. Patients not known by their physician to have had urinary tract infection, anatomical abnormality, hyperparathyroidism, or renal tubular acidosis were asked to participate in the study. Differences between means were considered significant if p values were less than 0.05 for F by analysis of variance and also less than 0.01 by t-test. In all patients with calcium oxalate stones and all non-stone-formers, urine acidified to pH less than 5.25, but in 8 of the 23 phosphate stone formers who completed the ammonium chloride study urine failed to acidify to pH less than 5.25. As all 8 had normal values for venous pH, total CO2, and chloride, they were considered to have incomplete renal tubular acidosis (IRTA). The 8 phosphate stone formers with IRTA had greater mean values for urine pH on all 9 specimens collected serially over 24 hours (all means greater than 6.2), and after administration of ammonium chloride (p less than 0.01), as well as lower mean values for urine titratable acid excretion (p less than 0.01), both after administration of ammonium chloride and in 24-hour urine samples, compared with the remaining phosphate stone formers whose urine acidified and the oxalate and non-stone-forming control groups. Nearly all the phosphate stone formers had 1 or more risk factors for stone formation, but with frequencies not significantly higher than those found in the oxalate group. Hypercalciuria and hypocitruria were the commonest, but increased oxalate or urate also occurred. Thus, idiopathic calcium phosphate stone formation can be associated with 1 or more of several risk factors, and, with the possible exception of those with IRTA, treatment should be similar to that given to patients with calcium oxalate stones.
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PMID:Comparison of patients with idiopathic calcium phosphate and calcium oxalate stones. 195 78

Nephrolithiasis is a heterogeneous disorder, with varying chemical composition and pathophysiologic background. Although kidney stones are generally composed of calcium oxalate or calcium phosphate, they may also consist of uric acid, magnesium-ammonium phosphate, or cystine. Stones develop from a wide variety of metabolic or environmental disturbances, including varying forms of hypercalciuria, hypocitraturia, undue urinary acidity, hyperuricosuria, hyperoxaluria, infection with urease-producing organisms, and cystinuria. The cause of stone formation may be ascertained in most patients using the reliable diagnostic protocols that are available for the identification of these disturbances. Effective medical treatments, capable of correcting underlying derangements, have been formulated. They include sodium cellulose phosphate, thiazide, and orthophosphate for hypercalciuric nephrolithiasis; potassium citrate for hypocitraturic calcium nephrolithiasis; acetohydroxamic acid for infection stones; and D-penicillamine and alpha-mercaptopropionylglycine for cystinuria. Using these treatments, new stone formation can now be prevented in most patients.
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PMID:Etiology and treatment of urolithiasis. 196 46

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

Adult cats with normal renal function were fed a nutritionally balanced, vitamin A-replete, experimental dry diet with or without ammonium chloride (NH4Cl) for 6 mo to study the effects of chronic dietary acidification on acid-base parameters and the metabolism of selected minerals. Dietary balance studies were performed monthly. Blood and urine samples were collected monthly to evaluate acid-base parameters, plasma parathyroid hormone (PTH) and 1.25-dihydroxycholecalciferol levels. Ammonium chloride-treated cats had significantly lower blood and urinary pH, and lower blood bicarbonate concentrations. Treated cats also had higher blood ionized calcium concentrations, hypercalciuria and lower intestinal calcium absorption relative to baseline (prior to feeding the experimental diet) and to control cats. This resulted in the development of lower calcium balance in the first several months. PTH levels were unaffected by dietary acidification; however, 1.25-dihydroxycholecalciferol levels were significantly decreased in treated cats. Treated cats had negative potassium balance during 5 mo of dietary acidification. Magnesium, sodium, and phosphorus balances were lower, but positive, in treated cats compared to control cats. Cats consuming the NH4Cl-supplemented diet had increased chloride balance. Thus, chronic dietary acidification with 1.5% NH4Cl produced chronic metabolic acidosis and lower or negative, calcium and potassium balance.
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PMID:The effect of chronic dietary acidification using ammonium chloride on acid-base and mineral metabolism in the adult cat. 274 72

A 41-year-old man with acromegaly was suffering from chronic, progressive backache and aware of reduction in his body height. Endocrine studies revealed increased glucose non-suppressible serum growth hormone (GH) and serum prolactin (PRL). Pituitary microadenoma was detected by a computerized axial tomogram and subsequently resected by trans-sphenoidal adenomectomy. The tumor proved to be a mixed GH- and PRL-secreting adenoma by electron microscopy and immunoperoxidase staining. Concurrent investigation of backache and reduced height disclosed markedly reduced radiodensity of the spinal bones, bilateral nephrocalcinosis, and hypercalciuria, which were ascribed to renal tubular acidosis (RTA) demonstrated by reduced urinary excretion of acids and insufficient reduction of urinary pH following oral administration of ammonium chloride. From the analogy to certain endocrinopathies, it appears likely that enhanced calcium metabolism and resultant hypercalciuria due to excess GH and PRL have led to the development of RTA, which further enhanced calciuria. Such enhanced calcium metabolism and consequent hypercalicuria conceivably led to accelerated demineralization of the spine and resulted in the reduced height of this patient in his early forties.
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PMID:A case of active acromegaly with reduced height and type 1 renal tubular acidosis. 289 4

Calcium metabolism and renal acidification ability were examined in renal stone patients. On a random diet 33 of 52 patients excreted more than 4 mg. per kg. body weight per day of urinary calcium and were entered into a second study on a 300 mg. calcium diet. Absorptive and renal hypercalciuria was differentiated by fasting urinary calcium (mg. per 100 ml. glomerular filtration). Every absorptive hypercalciuria patient tested and 5 renal hypercalciuria patients had a normal renal acidification ability, and the serum parathyroid hormone and urinary cyclic adenosine monophosphate levels were normal. By calcium restriction urinary calcium decreased more in absorptive hypercalciuria than in renal hypercalciuria (2.48 +/- 0.14 versus 3.34 +/- 0.27 mg. per kg. body weight per day, p less than 0.05). However, urinary calcium remained high in 76 per cent of the patients with absorptive hypercalciuria. Nine patients had a defect in renal tubular acidification and the calcium metabolism was similar to those with renal hypercalciuria. Present studies show that renal hypercalciuria and renal tubular acidification defect cannot be differentiated without an ammonium chloride test.
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PMID:Renal hypercalciuria and acidification defect in kidney stone patients. 292 70

Acidosis induced increase in renal calcium excretion was produced by means of ammonium chloride load in 12 control persons and in 76 patients with recurrent oxalate lithiasis. This increase is more marked in stone patients - even in those with normocalciuria - than in control persons. The calcium excretion is especially increased in patients with renal hypercalciuria. This might result from the primary nature of the renal defect. The acid load did not prove useful in the diagnosis of hyperparathyroidism.
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PMID:[Calcium excretion in patients with calcium oxalate calculi in acid administration]. 360 99

The increasing incidence of urolithiasis makes it important to report about 34 children with urolithiasis seen between 1976 and 1986 at the Department of Pediatrics, University Medical School Vienna. At the time of the first diagnosis 59 percent of the patients were less than 7 years of age; 62 percent of our patients were males. Recurrent chronic urinary tract infection in 32 percent, metabolic disorder (secondary hyperoxaluria 5, idiopathic hypercalciuria 3, cystinuria 2, hyperuricuria 2) in 27 percent were evaluated; in 13 patients the origin of calculi was idiopathic. Most infectious stones contained magnesium ammonium phosphate, most idiopathic stones calcium oxalate. In 21 patients (62%) surgical treatment, in one patient extracorporal shock wave lithotripsie was realized. Adequate metaphylaxis (general, dietetic, medicementous) can lower the rate of occurrence of stone formation.
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PMID:[Urolithiasis in pediatrics: analysis of 34 patients]. 368 52


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