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)

Fifteen cases of hypervitaminosis D in childhood are reviewed. In all of them, vitamin D was given following medical prescription. In four occasions, excessive dosage of vitamine D impaired the evolution of a previous nephropathy. The clinical, analytical, radiological and histological findings as well as the therapeutical aspects are commented. Hypercalcemia, hypercalciuria, polyuria with hypostenuria, renal failure, bone lesions and nephrocalcinosis are the most prominent features of the picture. Occasionally, arterial hypertension and glycosuria were found. Prednisone, thyrocalcitonine and phosphates were used as therapeutical means. In spite of nephrocalcinosis and renal failure generally present at diagnosis, the clinical course was rather good.
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PMID:[Hypervitaminosis D. Review of fifteen cases]. 44 41

The management of 78 children with upper urinary calculi is described. Boys outnumbered girls by a ratio of 2 to 1. Two-thirds of the patients had identifiable metabolic causes, while the remaining third had infected renal lithiasis. In this latter group, all patients had had multiple urologic procedures, urinary infection, and stasis with diversionary and indwelling drainage devices. Contrary to earlier views, idiopathic renal lithiasis with or without hypercalciuria was the most common metabolic form of nephrolithiasis in children. Sixty-seven patients (86 per cent) were followed for an average of 7 1/2 years. With appropriate therapy, stone disease became inactive in 70 per cent of the children. The remaining 30 per cent continued with active disease--5 died of renal failure and 1 has received a renal allograft. Stone formation may be regarded as a solitary complication or one of several manifestations of a large number of underlying disorders. Along with a thorough search for etiologic factors there must be an equally aggressive therapeutic effort. Because the disease is ofter sporadic, careful long-term followup of the patients with active as well as those with inactive stone disease is mandatory.
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PMID:Pediatric nephrolithiasis. 111 31

Renal failure was found in a five-year-old patient who had been treated with insulin since he was diagnosed as having insulin dependent diabetes mellitus (IDDM) at 3 years of age. Laboratory data showed that his renal failure was caused by a renal tubular dysfunction. The autopsy findings of his pancreas were compatible with those of IDDM. The kidneys were atrophied with an innumerable number of crystals in the proximal tubuli. Staining by Kossa indicated that the crystals contained calcium salt. The calcium content of his kidneys was significantly higher than that of control. The nephrocalcinosis seems to be caused by hypercalciuria associated with IDDM.
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PMID:Insulin dependent diabetes mellitus accompanied by nephrocalcinosis and renal failure. 144 54

Variants of renal damage in sarcoidosis demonstrate the diversity of clinical manifestations common to this systemic disease and serve distinctive reference points in the choice of the treatment policy. A well-defined relationship between hypercalciuria associated with sarcoidosis and risk of calcium nephropathy development is, one the one hand, a reliable criterion for the disease activity and, on the other one, the basis for administration of drug the therapy permitting one to control its level (corticosteroids and drugs of the 4-aminoquinoline series). Other variants of renal damage in sarcoidosis, excluding amyloidosis, form the basis for corticosteroid administration even in cases of the presence of renal failure, demonstrating that so-called "dramatic therapy" produces a remarkable beneficial effect characterized by the disappearance of the signs of renal failure.
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PMID:[Kidney involvement in sarcoidosis]. 194 30

Advances in the understanding of amino acid metabolism and of the interaction of amino acids with skeletal muscle, liver, brain, and other tissues have led to refinements of parenteral amino acid solutions. Clinical situations may dictate the use of specific amino acid formulations. Branched-chain amino acid (BCAA) solutions may normalize aberrant amino acid profiles in patients with hepatic encephalopathy; however, controlled trials demonstrate little effect on clinical outcome, and the effectiveness in patients with acute liver failure or undergoing orthotopic liver transplantation is unproved. BCAA solutions have also been tried in septic and severely stressed patients with equivocal results. Renal failure has been treated with essential amino acid solutions, yet low-dose standard amino acid formulations are probably equally effective. Pediatric preparations have been tailored to "normalize" amino acid profiles to those of healthy term, breast-fed neonates. Recent studies suggest that premature infants receiving these formulations may achieve intrauterine growth rates, although the effect on long-term outcome is unknown. Glutamine may be essential for the preservation of intestinal mucosal structure and function; further study is indicated to determine the necessity of adding glutamine to parenteral amino acid solutions. Recently, amino acid infusions have been associated with enhanced ventilatory drive, possibly via stimulation of central ventilatory mechanisms. A variety of other side effects have been documented, including acidosis, hyperammonemia, hypercalciuria, and possibly bone disease and hepatotoxicity. Further understanding of the metabolism of intravenous infusion of amino acids is necessary to provide optimal nutritional protein support. Because full information regarding the complex effects of intravenous substrates is lacking, special amino acid formulations must be used with caution.
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PMID:General and specialized parenteral amino acid formulations for nutrition support. 210 46

Home parenteral nutrition has prevented malnutrition in patients who cannot maintain adequate nutrition by enteral feedings alone. The risk of bone and mineral abnormalities in these patients is significant for several reasons. Pre-existing skeletal disease can occur from factors known to affect the population at large as well as from malnutrition, malabsorption, and corticosteroid use related to the underlying disease process. Long-term use of infused nutrients and potential toxins can further alter bone turnover. Hypercalciuria is frequently present during HPN, yet its etiology is poorly defined. Parenteral nutrition admixture concentrations of calcium, phosphorus, protein, sodium, and dextrose may all play a role. Any development of acidosis can certainly aggravate hypercalciuria, which may be an indirect marker of abnormal bone turnover. Although increased protein intake can promote the development of acidosis-induced calciuresis, infused phosphorus and acetate can help reduce calcium excretion. Parenteral nutrition contamination by aluminum can cause a spectrum of osteomalacic bone disease similar to aluminum-associated changes seen in renal failure patients. Even with recent attempts to remove aluminum from the parenteral admixture, low-turnover bone disease can still occur. At present, HPN-related bone disease is a poorly understood entity because of its multifaceted nature. Patients receiving long-term parenteral nutrition should be considered to have an increased risk for the development of metabolic bone disease. Early monitoring for and treatment of bone disease should be considered in all patients receiving HPN.
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PMID:Long-term parenteral nutrition and metabolic bone disease. 211 69

The clinical and laboratory findings in 14 infants, 2 children and 42 adults with RTA-1 have been retrospectively analyzed and the patients classified as having the hereditary (14%), acquired (31%), or idiopathic (55%) form. In 7 of the 8 hereditary cases, RTA-1 appeared to be a complication of hereditary hypercalciuria. The majority of acquired cases (61%) were secondary to immune-mediated diseases. All of the 14 infants with RTA-1 were classified as idiopathic. All of the idiopathic cases in children and adults were associated with nephrolithiasis and/or nephrocalcinosis, 33% of which had a family history of nephrolithiasis. The 14 infants presented with failure to thrive. Seventy-seven percent of children and adults with RTA-1 had nephrolithiasis and/or nephrocalcinosis and usually presented with symptoms related to this problem. Adults without nephrolithiasis or nephrocalcinosis usually presented with electrolyte disturbances or acidosis. Hypokalemia, the most common electrolyte disturbance, was present in 28% of the entire series. Acidosis was present in all infants and in 70% of children and adults. Clinically apparent bone disease was observed in 3 infants, and in 1 adult with nephrolithiasis. Glomerular function was normal in infants and in the 2 children, but depressed in 40% of adults. Recurrent urinary tract infection was a contributing factor but was not the sole cause of renal failure. Surprisingly, kidney stone number, the number of surgical procedures, and the presence of nephrocalcinosis had no apparent effect on the development of renal failure. Glomerular filtration rate was significantly higher in patients with incomplete RTA-1, and serum total CO2 was significantly correlated with creatinine clearance and minimum urinary pH. Hypercalciuria was present in 32% of patients with nephrolithiasis and/or nephrocalcinosis, and urinary citrate excretion was low in all of 16 patients in whom it was measured. Hypocitraturia appeared to be due in most cases to potassium depletion and renal failure, but may have occurred as a primary defect in 1 patient with hereditary RTA. Urinary uric acid excretion was elevated in 23% of patients with stones in whom it was measured. The mean number of stone-forming events was 51 +/- 14. Although a weak correlation between urinary calcium excretion and stone number was observed, the cause for prodigious stone formation could not be explained. This series emphasizes the variable degree to which the common clinical manifestations of RTA-1 (metabolic acidosis, hypercalciuria, nephrolithiasis, nephrocalcinosis, and potassium depletion) are expressed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The syndrome of distal (type 1) renal tubular acidosis. Clinical and laboratory findings in 58 cases. 312 50

Mild hypercalciuria has been observed in hypertension, but it is not yet established whether the prevalence of urinary stone disease is increased as well. Data from the cross-sectional phase of the Gubbio Study--a population-based survey on hypertension involving 5376 subjects (84% response rate)--have been analysed to address this issue, defining as hypertensive those subjects with diastolic pressure falling within the fifth quintile for each sex- and age-specific category, and/or under regular antihypertensive treatment. The prevalence of a positive history for urinary stone (radiographic and/or surgical evidence, and/or stone excretion) was increased by over 50% (P less than 0.01) in treated and untreated hypertensives. None of the 136 subjects with a positive urinary stone history were hypercalcaemic and none had renal failure.
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PMID:Elevated blood pressure and positive history of kidney stones: results from a population-based study. 324 Dec 40

The results are presented of an oral calcium tolerance test with 1,000 mg calcium in 20 patients with recurrent renal calcium calculosis, a woman with primary hyperparathyroidism and incipient renal failure (serum creatinine 1.8 mg%), creatinine clearance 55 ml/min) and 9 healthy persons as controls. The serum osteocalcin level was determined before and after the oral test. The results show that the serum osteocalcin level alone is of no differential diagnostic value for differentiation of the various types of hypercalciuria in patients with recurrent renal calcium calculosis. As a marker of osteoblasts functional state however the determination of serum osteocalcin level is of great importance for the early diagnosis of osteoporosis. In 3 patients with renal hypercalciuria, often leading to general osteoporosis, an acute rise of serum osteocalcin level was found after the oral calcium tolerance test. High osteocalcin level was also found in the patient with primary hyperparathyroidism and incipient renal failure.
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PMID:[Serum osteocalcin level as a marker of the functional state of osteoblasts after oral calcium tolerance test]. 326 44

Distal RTA is characterized by decreased distal renal tubular hydrogen ion secretion, decreased ability to acidify urine, hypercalciuria, hyperphosphaturia, hypocitraturia, and metabolic acidosis. Because of the resulting alterations in urine composition and pH, patients with distal RTA are predisposed to urolithiasis and renal calcification. Diagnosis of distal RTA is important because it is a potentially reversible disorder that, left untreated, may cause nephrocalcinosis, recurrent urolith formation, moderate to severe metabolic acidosis, and renal failure.
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PMID:Canine distal renal tubular acidosis and urolithiasis. 348 13


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