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

Increasing urinary net acid (titratable acid + NH4 - HCO-3) excretion is accompanied by an increased urinary Ca excretion because of reduced renal tubular reabsorption of filtered Ca. The relationships between urinary Ca excretion rates and urinary net acid excretion rates are reviewed for data: (1) among healthy adults eating constant diets when net acid excretion is increased by increasing dietary protein, administering NH4Cl, or withdrawal of dietary KHCO3 or reduced by administering KHCO3; (2) among healthy adults eating constant diets providing varying amounts of protein and potassium, and (3) among healthy adults and Ca stone formers with and without idiopathic hypercalciuria eating ad libitum. The results show that urinary Ca excretion varies directly with net acid excretion by 0.035 mmol/mEq. The urinary net acid excretion increases by 0.10-0.15 mEq/mmol urinary urea, and urinary Ca increases by about 0.04 mmol/g dietary protein, while the urinary net acid excretion decreases as the ratio of urinary K/urea, a reflection of the dietary K relative to dietary protein, increases. The relationships between net acid excretion and both urinary urea and K/urea are similar among Ca stone formers without and with idiopathic hypercalciuria, but those with idiopathic hypercalciuria exhibit increased rates of urinary Ca excretion at all levels of net acid excretion.
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PMID:Relationship between urinary calcium and net acid excretion as determined by dietary protein and potassium: a review. 987 10

Population based data on urinary excretion of various metabolites of pathological importance, Calcium, Magnesium, Sodium, Potassium, Oxalates, Citrates, Phosphates, Uric acid and urea have been collected from around three hundred children of the Quetta valley. The body weight was in the range of 11-50 kg and the age was in between 4-16 years. The urine excretion average was 987.5 +/- 452.5 ml per 24 hours. There was 11.5% incidence of hypercalciuria, 8.5% incidence of hyperuricosuria, 2.0% hyperphosphaturia, 2.5% hypomagnesuria, 3.5% hypocitraturia, 6.5% hypernatriuria, 43.5% hypokaliurea and 2.1% hyperoxaluria. Urea excretion average was 23.11 +/- 14.99 g per 24 hours. The study provided the basis for childhood reference pattern in urinary excretion of compounds related to various pathological conditions, in particular stone formation in this region.
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PMID:Population based data on urinary excretion of various metabolites in children of north western region of Pakistan. 1006 40

Biochemical tests by 12 metabolic blood and urine indices reflecting the condition of renal function and metabolism of urolithogenic substances were made in the course of 1-6 year follow-up of 35 and 79 patients (46 females and 68 males aged 18-65 years) with recurrence-free and recurrent urolithiasis, respectively. The risk of recurrence for uric acid urolithiasis in serum concentration of urea 5.67 +/- 0.14 mmol/l and creatinine 0.090 +/- 0.008 mmol/l, in hyperuricemia and hyperuricuria was associated with elevation of renal excretion of total calcium to 5.88 +/- 0.49 mmol/day and ratio of daily renal excretion of sodium to renal daily excretion of potassium to 3.28 +/- 0.08; for calcium-oxalate lithiasis--with a rise in serum concentration of uric acid to 0.310 +/- 0.042 mmol/l and sodium to 114 +/- 0.8 mmol/l in hypercalciuria and hyperuricuria.
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PMID:[Recurrence-free and recurrent urolithiasis: metabolic differences]. 1115 Jan 60

Stone disease is as old as recorded history but despite advances in diagnosis and treatment, it continues to cause significant morbidity. This review summarises the current pharmacologic management of urinary calculi based upon the stone type. All patients with stone disease are advised to increase fluid intake, limit dietary protein and limit sodium. Calcium oxalate stones can be managed on a selective or non-selective basis depending on the cause of the hypercalciuria or hyperoxaluria. Agents currently in use include sodium cellulose phosphate, thiazides, orthophosphates, oral calcium supplements, pyridoxine, cholestyramine, citrate, magnesium and allopurinol. Classically, struvite stones occur in the presence of urea splitting organisms and are composed of magnesium, ammonium phosphate and carbonate apatite. The goal of treatment is to make patients stone free as bacteria retained in stone fragments lead to stone growth. Urease inhibitors, aluminium hydroxide gel, hemiacidrin, and Suby G and M solutions are infrequently used in treatment. Cystine stones are the result of an autosomal recessive disorder. D-Penicillamine, captopril and alpha-mercaptopropionylglycine (MPG) are all oral agents that have proven to be efficacious. As more randomised trials are conducted and the understanding of endogenous stone inhibitors progresses, the medical management of stone disease will continue to improve.
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PMID:Pharmacology for renal calculi. 1124 28

The effect of estrogens on human growth hormone (HGH) and serum sulfation factor was studied in 4 acromegalic and 3 growth hormone-deficient men. Estrogen treatment (.5-1 mg/day) of acromegalic patients for 7-18 days reduced elevated sulfation factor levels, hypercalciuria, and hydroxyprolinuria levels without markedly affecting HGH levels. Increases in blood urea nitrogen and urinary nitrogen reflected the antianabolic effect of estrogen. Subnormal sulfation factor concentrations in HGH-deficient patients were increased to normal or high levels during 4-6 days of HGH administration and returned to pretreatment levels within 2 days of the last treatment. Combined estrogen and HGH treatment inhibited the elevation of serum sulfation factor, urinary calcium, and hydroxyproline excretion, but did not affect the anabolic response to HGH. Urinary calcium and hydroxyproline levels varied in a fashion similar to serum sulfation factor. The response to HGH in estrogen-treated hypopituitary patients seems to indicate that the stimulation of serum sulfation factor is not required for the anabolic action of HGH.
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PMID:Suppression of growth hormone-dependent human serum sulfation factor by estrogen. 1233 22

Annual incidences of kidney stones are about 0.1-0.4% of the population, and lifetime prevalences in the USA and Europe range between 8 and 15%. Kidney stones occur more frequently with increasing age and among men. Within ten years, the disease usually recurs in more than 50% of patients. Nowadays, about 85% of all kidney stones contain calcium salts (calcium oxalate and/or calcium phosphate) as their main crystalline components. Because human urine is commonly supersaturated with respect to calcium salts as well as to uric acid, crystalluria is very common, i.e. healthy people excrete up to ten millions of microcrystals every day. Recurrent stone formers appear to excrete lower amounts or structurally defective forms of crystallization inhibitors which allows for the formation of large crystal aggregates as precursors of stones. Alternatively, crystal adhesion to urothelial surfaces may be enhanced in stone formers. Medical treatment of renal colic is based on nonsteroidal antiinflammatory drugs, because prostaglandins appear to play a crucial role in the pathophysiology of pain during ureteral obstruction. In addition, centrally acting analgesics such as pethidine-HCl may be required in many cases. The administration of high amounts (3-4 liters/day) of intravenous fluids should be abandoned, since it may raise intraureteral pressure whereby pain increases and kidney pelvis or fornices may rupture. All first-stone formers should undergo a simple basic evaluation, including stone analysis (x-ray diffraction or infrared spectrometry), serum values of ionized calcium (alternatively: total calcium and albumin) and creatinine, urinalysis and repeated measurements of fasting urine pH in order to detect urinary acidification disorders or low urine pH. In high-risk patients with as first stone episode (i.e. strongly positive family history, inflammatory bowel disease, short-bowel syndrome, nephrocalcinosis, bilateral stones, hypercalcemia, renal tubular acidosis, airline pilots) as well as in all recurrent stone formers, an extended metabolic evaluation should be performed. Two 24-hurines should be collected on free-choice diet not prior to three months after stone passage or urological intervention. Analysis includes measurements of volume, creatinine, calcium, oxalate, uric acid and citrate; sodium and urea as markers of salt and protein consumption are optional but clinically very helpful. Since hypercalciuria is of much less importance than increases in urinary oxalate, therapeutic efforts should primarily focus on lowering urinary oxalate excretion. Sufficient calcium intake, i.e. 1200 mg per day, is crucial, because it allows for binding of oxalate at the intestinal level whereby increases of urinary oxalate (reciprocal hyperoxaluria) can be avoided. Excess intake of flesh protein (meat, fish, poultry) is lithogenic since it increases urinary calcium, oxalate and uric acid, and lower citrate. On the other hand, a diet rich in alkali (vegetables, fruit) is associated with a lower risk of stone formation. A "common sense diet" containing sufficient amounts of fluids, 1200 mg of calcium per day and reduced amounts of flesh protein as well as salt is able to reduce the 5-year stone recurrence rate in calcium stone formers by 50%. The scientific evidence for drug treatment (thiazides, alkali citrate) is rather poor: the most widely quoted randomized thiazide trial included only 42 patients of whom 36% left the protocol prematurely, whereas 36-48% of patients included in three randomized studies with alkali citrate suffered from undesirable side-effects; nevertheless, citrate therapy reduced the stone recurrence rate by 38%, compared with 22% in patients on placebo treatment (p < 0.0005).
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PMID:[Pathophysiology, diagnosis and conservative therapy in calcium kidney calculi]. 1264 86

The pathogenesis of nephrolithiasis in Cushing's syndrome is still not completely clarified. The current study aimed at investigating prevalence of nephrolithiasis and role of different lithogenic factors in Cushing's disease (CD). Forty-six CD patients (24 with active and 22 with cured disease) and 46 sex- and age-matched controls entered the study. Body mass index, blood pressure, fasting glucose and insulin, serum and urinary creatinine, urea, uric acid, electrolytes, and cystine, urinary volume, pH, oxalate, and citrate levels, and renal ultrasonography (US) were performed in all patients and controls. Nephrolithiasis was found in 50% of active patients, 27.3% of cured patients, and 6.5% of controls (P < 0.001). Compared with controls, patients with active disease had a significantly increased prevalence of obesity, arterial hypertension, diabetes mellitus, hypercalciuria, hypocitraturia, and hyperuricosuria, significantly higher levels of serum and urinary cystine, urinary creatinine, urea, uric acid, potassium, calcium, phosphorus, and oxalate, significantly lower levels of urinary citrate levels. Compared with controls, patients cured from CD had a significantly increased prevalence of obesity, systemic arterial hypertension, and diabetes mellitus, whereas urinary citrate was significantly decreased. At multivariate analysis, a significantly increased risk to develop kidney stones was independently associated with urinary excretion of uric acid (odds ratio = 1.6, confidence interval = 1.0-2.5) and systemic arterial blood pressure (odds ratio = 2.6, confidence interval = 1.1-6.6). In conclusion, patients with active CD have an increased prevalence of nephrolithiasis compared with general population, which decreases but not disappears in patients successfully cured from the disease. This complication is likely caused by the synergic effect of different hypercortisolism-dependent metabolic and hemodynamic abnormalities, among which systemic arterial hypertension and excessive urinary uric acid excretion seem to play a pivotal role.
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PMID:Nephrolithiasis in Cushing's disease: prevalence, etiopathogenesis, and modification after disease cure. 1272 57

Hypercalciuria is an important and common risk factor in the formation of renal stones. In this study we evaluated the incidence and the clinical presentation of hypercalciuria in 75 children over 5 years of age with the diagnosis of recurrent urinary tract infection (UTI). We measured random urinary calcium/creatinine value (three times), 24-h urinary calcium excretion, serum calcium, phosphorus, electrolytes, blood gas, blood urea nitrogen and creatinine levels. Hypercalciuria was found in 32 patients (43%). The mean urinary calcium/creatinine ratio for hypercalciuric patients was 0.50+/-0.21 mg/mg (min: 0.24, max: 2.60). The mean urinary calcium/creatinine ratio for the rest of the study population--those without hypercalciuria--was 0.10+/-0.04 mg/mg (min: 0.01, max: 0.18). Presenting symptoms of the hypercalciuric patients and normocalciuric patients were similar. History of familial urolithiasis was positive in 19 patients (59%). Predisposing urinary tract abnormalities in recurrent UTI was shown in 12 of the hypercalciuric patients (12/32, 37.5%) and 8 of the normocalciuric patients (8/43, 19%) without a statistically significant difference between. We conclude that hypercalciuria is not a rare finding among recurrent UTI cases in Turkish children. Hypercalciuria does not modify the clinical presentation of UTI, and we suggest the investigation of urinary calcium excretion in children with recurrent UTI.
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PMID:Hypercalciuria and recurrent urinary tract infections: incidence and symptoms in children over 5 years of age. 1604 26

Claudins form a family of transmembrane tight junction proteins that play a key role in control and selectivity of paracellular transport. Mutations in claudin-19, which is expressed in kidney, retina, and myelinated peripheral neurons, were identified in familial hypomagnesemia with hypercalciuria and nephrocalcinosis, a hereditary disease causing renal Mg(2+) and Ca(2+) wasting. Here, we studied the distribution and possible functional role of claudin-19 in the renal tubule. By immunofluorescence staining of mouse kidney, claudin-19 was found to be expressed at the tight junction of the thick ascending limb of Henle, the major site of paracellular Mg(2+) reabsorption, where it colocalized with claudin-16, as well as in the thin ascending limb. The role of claudin-19 in paracellular transport was tested by stable transfection into Madin Darby canine kidney II TetOff cells to generate inducible cell lines. Claudin-19 increased the transepithelial electrical resistance and decreased permeability to monovalent and divalent cations, while anion and urea permeability were not affected. Our data suggest that claudin-19 acts as a selective cation barrier at the tight junction. This would be consistent with its physiological role to electrically seal myelinated peripheral neurons. The normal role of claudin-19 in renal tubule function remains to be determined.
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PMID:Renal localization and function of the tight junction protein, claudin-19. 1738 78

Thalassemia is a systematic disease in which the renal involvement has not yet been scrupulously studied. In a cross-sectional study, the renal findings of 50 cases of thalassemia intermedia (group 1) were compared to 58 patients with thalassemia major (group 2). Blood urea nitrogen, serum creatinine, uric acid, calcium, phosphorus, urinalysis, and ultrasonographical findings were evaluated. Mean age was 18 +/- 3.0 in group 1 and 17 +/- 3.5 years in group 2. The mean of serum ferritin levels was 871 +/- 81.8 ng/ml in group 1 vs. 3503 +/- 201 ng/ml in thalassemia major (p > 5) was observed among 19 children (17.6%); 17 of them were in group 1. In contrast, children with thalassemia major had significantly higher serum creatinine (0.89 +/- 0.18 vs. 0.59 +/- 0.37 mg/dl, p < 0.05) and blood urea nitrogen values (12.14 +/- 5.58 vs. 13.85 +/- 3.54 mg/dl, p < 0.05). We conclude that significant renal involvement is not a frequent complication in children and young adults suffering from thalassemia. Hyperuricemia and microscopic hematuria are more common in thalassemia intermedia than thalassemia major. Microscopic hematuria in thalassemia intermedia might be related to either hypercalciuria or hyperuricosuria.
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PMID:Comparative evaluation of renal findings in Beta-thalassemia major and intermedia. 1831 Aug 68


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