Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020438 (hypercalciuria)
 2,502 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sodium chloride deficiency (SCD) was observed within the 1st year of life in 12 of 46 cystic fibrosis (CF) patients between July 1989 and September 1992. All patients showed sweating, loss of appetite, fever, vomiting, irritation, dehydration, weakness, and cyanosis during an attack. Mean plasma sodium, potassium and chloride levels were 122.9 (range 106-135), 2.5 (range 1.6-3.5), and 73.3 (range 60-90) mEq/l respectively. Alkalosis and elevated plasma renin activity were detected in all patients. Of the patients, 50% showed microscopic haematuria, and hypercalciuria was detected in two out of four patients. Low urinary sodium and high urinary potassium were observed in the four examined patients. Increased creatinine, BUN and uric acid values returned to normal with treatment. All the patients were treated initially with intravenous fluids and electrolyte solutions. All patients were less than 7 months of age during the first attack, five received only breast milk and the others breast milk with formula milk. Their oral salt supplement was 2-4 mEq/kg per day, which is recommended for CF patients, but could be deficient in excessively sweating infants. The genotype of these patients might be cause of high salt losses. F508 is the most common mutation with the frequency of 38% in our CF patients with SCD, but the frequency of unknown mutations is high (54%).
 ...
PMID:Sodium chloride deficiency in cystic fibrosis patients. 784 98

Recent studies have shown that, not only in hypertensive animals but even in normotensive rats, dietary salt (sodium chloride) produces a dose-related increase in the left ventricular and renal mass. In the present study the effects of the angiotensin converting enzyme inhibitor (ACEI) enalapril and the thiazide-type diuretic, hydrochlorothiazide, on the development of the salt-induced left ventricular and kidney hypertrophy were examined in normotensive Wistar-Kyoto and Wistar rats. A high intake of sodium chloride (6% of the dry weight of the chow to mimic the level found in many human food items) during eight weeks produced a marked increase in the mass of the left ventricle and the kidneys in both rat strains with little or no effect on blood pressure. The cardiac hypertrophy correlated strongly with the renal hypertrophy. These salt-induced changes in the heart and in the kidneys were completely blocked by hydrochlorothiazide, while enalapril was devoid of any significant effects during the high-salt diet. However, during a low-salt diet enalapril, but not hydrochlorothiazide, effectively lowered the blood pressure and decreased the left ventricular mass of the normotensive rats. There was a 3- to 4-fold increase in the urinary excretion of calcium during the high intake of sodium chloride. Hydrochlorothiazide decreased the urinary excretion of calcium even during the low salt diet, and it completely blocked the salt-induced hypercalciuria. Enalapril had no significant effect on the urinary calcium excretion. During the low-salt diet hydrochlorothiazide increased the calcium and decreased the potassium concentration in the heart while enalapril increased the phosphorus concentration. In conclusion, a high intake of sodium chloride produced hypertrophy both in the heart and in the kidneys, even in the absence of a rise in blood pressure. Salt also remarkably increased the urinary calcium excretion. These harmful effects of salt were blocked by the thiazide diuretic hydrochlorothiazide but not by the ACEI enalapril. However, this study does not allow to make any direct comparison between the effects of enalapril and hydrochlorothiazide.
 ...
PMID:Effects of enalapril and hydrochlorothiazide on the salt-induced cardiac and renal hypertrophy in normotensive rats. 784 79

Kidney stone patients with hypercalciuria type I are treated with an oral calcium binder. Lower intakes of calcium (Ca) in the range of 0-1500 mg/day have been associated with an increased incidence of colorectal cancer. The aim of this study is to analyze the effects of feeding ethylene diamine tetraacetic acid sodium salt (EDTA), a strong, non-absorbable binder of Ca, on the solubility of bile acids (BA) and long chain fatty acids (LCFA) in the large intestine of the rat. We have shown that the concentrations of soluble BA and LCFA in the large intestine contents remained constant while the concentration of total BA and LCFA decreased. Therefore, lowering the amount of Ca available for binding BA or LCFA is unlikely to increase the risk of colorectal cancer by that method.
 ...
PMID:Effects of a calcium binder on the solubility of bile acids and fatty acids in the large intestine of the rat. 801 91

The effects of dietary sodium and potassium, given as salts of chloride or bicarbonate, on theophylline-induced hypercalciuria in the rat were investigated. In experiment 1, rats fed diets containing 0.3 mmol/g diet NaCl, KCl, NaHCO3, or KHCO3 exhibited a calciuria of NaCl > KCl > controls = NaHCO3 = KHCO3. This study indicated that cation effects were dependent on the accompanying anion, however the dose of added salt was inadequate to produce a consistent, significant salt effect. A second experiment was run in which animals were given salts at 0.4 mmol/g diet; the salt-induced pattern of calciuria was similar. After one week of salt pretreatment, rats were given diets containing theophylline (7.72 mumol/g diet), which induced calciuria all groups regardless of salt pretreatment. Urinary volume and urinary phosphate changes were parallel to each other and not to the changes in urinary calcium induced by salt or theophylline. Changes in urinary excretion of prostaglandin E2 were directly proportional to changes in urinary calcium. In the rat, pretreatment with sodium bicarbonate or sodium chloride reduces the extent of theophylline-induced diuresis, but does not reduce theophylline-induced hypercalciuria. Further, potassium chloride increases and potassium bicarbonate does not reduce urinary calcium excretion. Theophylline-induced calciuria is correlated with prostaglandin E2 excretion rates.
 ...
PMID:Effect of diets high in sodium and potassium on the magnitude of theophylline-induced hypercalciuria in the rat. 840 66

Abnormalities in renal handling of calcium, magnesium, or phosphate have been implicated in the development and/or maintenance of human hypertension. We have shown recently that renal excretion of these ions is correlated to blood pressure in Dahl salt-sensitive as well as salt-resistant rats. The present study was designed to determine whether renal perfusion pressure per se could affect excretion of these ions. Urinary excretion of calcium, magnesium, and phosphate was studied in anaesthetized Sprague-Dawley rats under basal conditions and during an intravenous infusion of angiotensin II (ANG II), vasopressin (AVP) or phenylephrine (PE). A cuff, placed around the aorta between the two renal arteries, allowed maintenance of normal perfusion pressure in the left kidney, while that in the right kidney was allowed to rise. Infusion of pressor agents raised mean arterial blood pressure to comparable levels (means +/- SE): ANG II (n = 7), before = 102 +/- 4, during = 133 +/- 3 mmHg, AVP (n = 8), before = 110 +/- 7, during = 136 +/- 5 mmHg, PE (n = 6), before = 111 +/- 6, during = 141 +/- 6 mmHg. Although there was no difference in excretion of calcium, magnesium and phosphate between the two kidneys under basal conditions, infusion of ANG II or PE induced hypercalciuria, hypermagnesiuria and hyperphosphaturia in the right kidney which was exposed to the increased arterial pressure. Such effects did not appear in the pressure-controlled left kidney. Infusion of AVP was associated with reduced excretion of calcium and magnesium, and increased excretion of phosphate, in the normotensive kidney. The response to the similarly increased renal perfusion pressure in this group was also reduced for calcium and magnesium, and enhanced for phosphate. The results indicate (1) renal excretion of calcium, magnesium and phosphate is renal perfusion pressure-dependent; the higher the renal perfusion pressure, the greater the excretion of these ions. (2) Independently of perfusion pressure, AVP can inhibit phosphate reabsorption and stimulate divalent cation reabsorption.
 ...
PMID:Effect of renal perfusion pressure on excretion of calcium, magnesium, and phosphate in the rat. 856 1

Mutations in the Na-K-2Cl cotransporter (NKCC2), a mediator of renal salt reabsorption, cause Bartter's syndrome, featuring salt wasting, hypokalaemic alkalosis, hypercalciuria and low blood pressure. NKCC2 mutations can be excluded in some Bartter's kindreds, prompting examination of regulators of cotransporter activity. One regulator is believed to be ROMK, an ATP-sensitive K+ channel that 'recycles' reabsorbed K+ back to the tubule lumen. Examination of the ROMK gene reveals mutations that co-segregate with the disease and disrupt ROMK function in four Bartter's kindreds. Our findings establish the genetic heterogeneity of Bartter's syndrome, and demonstrate the physiologic role of ROMK in vivo.
 ...
PMID:Genetic heterogeneity of Bartter's syndrome revealed by mutations in the K+ channel, ROMK. 884 Nov 84

The differential effects of sodium-induced renal hypercalciuria on the biochemical markers of bone metabolism and calcium homeostasis were studied in oophorectomized (Oophx) and sham-operated rats. The rats consuming a normal (0.4%) calcium semisynthetic diet were randomly allocated to either 0, 0.4, 0.6, 0.9, or 1.25% NaCl in their drinking water for 7 days. At that time fasting blood and urine specimens were collected and analyzed for bone-related biochemical variables. The urinary calcium/creatinine ratio was increased with increasing urinary sodium (p < 0.01) in both sham and Oophx animals. The hydroxyproline/creatinine ratio was elevated as a result of Oophx (p < 0.001) and was raised with increasing urinary sodium in both sham (p = 0.012) and Oophx animals (p = 0.007). Serum osteocalcin and alkaline phosphatase were elevated in Oophx rats (p < 0.02). While serum osteocalcin was raised with increasing urinary sodium in Oophx rats (p = 0.035), there was no effect on osteocalcin levels in sham-operated rats. This study demonstrates that sodium-induced renal hypercalciuria potentiates bone turnover in Oophx rats as compared with ovary-intact rats and indicates important implications for the effect of dietary salt on bone turnover with ovarian hormone deficiency.
 ...
PMID:Increased urinary calcium excretion potentiates bone turnover in oophorectomized rats. 905 68

Several studies have reported that high sodium (Na) intake increases not only urinary Na but also urinary calcium (Ca), suggesting that high Na intake could be involved in the pathogenesis of hypercalciuria. No research data are available on the relationship of Na intake to the prevalence of hypercalciuria within the general population. Moreover, it is not clear if Na intake relates only to urinary Ca or also to other indices of Ca homeostasis, including intestinal Ca absorption. In the present paper, two distinct studies addressed these points using 24-hour urinary Na as an index of salt intake in individuals on their habitual unrestricted free diet. Study 1 analyzed the relationship between 24-hour urinary Na and hypercalciuria (24-hour urinary Ca > or = 7.5 mmol in men, > or = 6.25 mmol in women) in a population sample of 203 men and women, aged 20-59 years. Study 2 analyzed the relationship between 24-hour urinary Na and intestinal strontium (Sr) absorption, used as an index of intestinal Ca absorption, urinary (24-hour and fasting) and plasma Ca, and plasma parathyroid hormone in 36 healthy men and women, aged 18-65 years. Within the population sample (study 1), 24-hour urinary Na was directly and significantly correlated with prevalence of hypercalciuria when controlling for gender, age, weight, and urinary creatinine: the relationship was continuous and linear for urinary Na ranging between 40 and 200 mmol/24 h. In the 36 volunteers (study 2), 24-hour urinary Na was related to 24-hour and fasting urinary Ca (p < 0.001) but not to intestinal Sr absorption: the relationship between 24-hour urinary Na and urinary Ca (both 24 h and fasting) was also significant, controlling for other variables. The results indicate that in adults on their habitual diet, urinary Na, which reflects dietary salt intake, correlates with the prevalence of hypercalciuria independently of intestinal Ca absorption and mainly via renal mechanisms.
 ...
PMID:Salt intake, urinary sodium, and hypercalciuria. 938 30

The calcium (Ca)-restricted diet of urolithiasis patients with absorptive hypercalciuria type II may decrease Ca excretion but increase biochemical markers of risk for osteopenia. We randomly allocated 25 patients from six hospitals into an experimental group (Ca restriction to 500 mg/day, oxalate-rich products discouraged and normalization of animal protein and sodium) and a control group (no restrictions) for one month. The urinary Ca excretion did not decrease significantly, but the oxalate excretion decreased, although not significantly. The hydroxyproline:creatinine ratio in fasting urine seemed to increase and the calcium:creatinine ratio to decrease. The deoxypyridinoline:creatinine ratio in fasting urine did not change. We conclude that our Ca-restricted diet, which is lower in Ca, animal protein and table salt due to the omission of dairy products, may be of benefit for absorptive hypercalciuria type II patients without enhancing the risk for osteopenia. However, a long-term clinical trial is required.
 ...
PMID:The effects of the calcium-restricted diet of urolithiasis patients with absorptive hypercalciuria type II on risk factors for kidney stones and osteopenia. 953 99

The Na-K-Cl cotransporters are a class of membrane proteins that transport Na, K, and Cl ions into and out of a wide variety of epithelial and nonepithelial cells. The transport process mediated by Na-K-Cl cotransporters is characterized by electroneutrality (almost always with stoichiometry of 1Na:1K:2Cl) and inhibition by the "loop" diuretics bumetanide, benzmetanide, and furosemide. Presently, two distinct Na-K-Cl cotransporter isoforms have been identified by cDNA cloning and expression; genes encoding these two isoforms are located on different chromosomes and their gene products share approximately 60% amino acid sequence identity. The NKCC1 (CCC1, BSC2) isoform is present in a wide variety of tissues; most epithelia containing NKCC1 are secretory epithelia with the Na-K-Cl cotransporter localized to the basolateral membrane. By contrast, NKCC2 (CCC2, BSC1) is found only in the kidney, localized to the apical membrane of the epithelial cells of the thick ascending limb of Henle's loop and of the macula densa. Mutations in the NKCC2 gene result in Bartter's syndrome, an inherited disease characterized by hypokalemic metabolic alkalosis, hypercalciuria, salt wasting, and volume depletion. The two Na-K-Cl cotransporter isoforms are also part of a superfamily of cation-chloride cotransporters, which includes electroneutral K-Cl and Na-Cl cotransporters. Na-K-Cl cotransporter activity is affected by a large variety of hormonal stimuli as well as by changes in cell volume; in many tissues this regulation (particularly of the NKCCI isoform) occurs through direct phosphorylation/dephosphorylation of the cotransport protein itself though the specific protein kinases involved remain unknown. An important regulator of cotransporter activity in secretory epithelia and other cells as well is intracellular [Cl] ([Cl]i), with a reduction in [Cl]i being the apparent means by which basolateral Na-K-Cl cotransport activity is increased and thus coordinated with that of stimulated apical Cl channels in actively secreting epithelia.
 ...
PMID:The Na-K-Cl cotransporters. 967 38


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>