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)

A statistical association between arterial hypertension and kidney stone disease has been observed in three retrospective epidemiological surveys: the first was conducted in the early 1960s on 895, 50-year-old men living in Goteborg, Sweden; the second on 3,431 in-wall residents of the ancient town of Gubbio in central Italy, and the third on 688 workers (88% of the male work force) of the Olivetti factory in Pozzuoli, Naples, Italy. In all three studies, the participants in the upper part of the respective blood pressure distributions, or on long-term treatment for arterial hypertension had a significantly higher frequency of a positive history of nephrolithiasis compared with normotensives. This statistical association was independent of age, body mass, and biochemical indicators of renal function. The aim of this article is to review the evidence provided by these epidemiological surveys and to discuss a few pathogenetic hypotheses with special reference to the role of hypercalciuria and other alterations of calcium metabolism commonly found in patients with essential hypertension. The higher risk of calcium nephrolithiasis in hypertensive patients has obvious clinical and public health implications, given the large diffusion of both conditions in the population and the elevated social costs of their complications and sequelae. Several nutritional measures are known to be effective for the prevention and treatment of both hypertension and nephrolithisis, and therefore, there is attention in this article to the important role of the micronutrients sodium, potassium, and calcium and to their biological relationships.
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PMID:Hypertension and kidney stones: hypotheses and implications. 858 12

Hypercalciuria has been observed in human and experimental hypertension. The distal convoluted tubule (DCT) is the site of fine regulation for Ca2+ excretion. We assessed the cellular factors responsible for Ca2+ reabsorption in the DCT of spontaneously hypertensive rats (SHR). Vitamin D3 dependent Ca-binding protein 28k (CaBP28k), a factor involved in Ca2+ influx, and plasma membrane Ca ATPases (PMCA), a factor involved in Ca2+ efflux, were studied in hypertensive 16-week-old SHR and normotensive Wistar-Kyoto rats (WKY). mRNA levels for CaBP28k, PMCA 2 and PMCA 4 were not different in the two strains. However, CaBP28k protein was more abundant, and PMCA protein was less abundant in SHR than in WKY. PMCA antibody recognized only DCT in the two strains. In conclusion, decreased PMCA in DCT may be responsible for the hypercalciuria in SHR.
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PMID:Renal abnormality of calcium handling in spontaneously hypertensive rats. 874 45

In a prospective study of idiopathic glomerulonephritis we determined the natural history of 49 adult patients (12 primary IgA nephropathy, 13 thin GBM nephropathy, 20 normal renal tissue and 4 miscellaneous nephropathies) who presented with idiopathic non-proteinuric non-azotemic hematuria of at least six months duration, in the absence of hypertension and with a negative urological work-up. The median follow-up was 11 years with a range of 8 to 14 years. At the end of the follow-up, renal function had remained stable in all subsets except for those with miscellaneous disease. Hematuria was still present in all patients with thin GBM nephropathy, in all but two patients with IgA nephropathy who went into immunopathological remission, in three out of four miscellaneous nephropathies, and in seven out of 20 patients with normal renal tissue. Of the latter patients five had a history suggestive of urolithiasis at follow-up, which was in the absence of hypercalciuria and hyperuricosuria. Seven thin GBM patients, five IgA nephropathy patients and three miscellaneous nephropathies developed hypertension; the incidence of hypertension in each subset was significantly higher than in patients with normal renal tissue. This study shows that in young adults with idiopathic chronic non-proteinuric hematuria of four years duration, renal biopsy will give a definite diagnosis in 86% of the patients, and that those patients with so-called minor glomerular diseases are at high risk for hypertension. Those patients with normal renal tissue have a high incidence of urolithiasis and should have a urological follow-up.
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PMID:A prospective study of the natural history of idiopathic non-proteinuric hematuria. 877 Sep 71

The prevalence of arterial hypertension (HT) was investigated in 258 patients (171 m, 87 f, 22-68 years) with a history of primary stone disease. HT was detected in 64 patients (24.8%), with no difference between males (25.7%) and females (23.0%). The prevalence of HT by age was very similar to that of a general population, especially in the calcium stone group. The discriminant analysis demonstrated that the composition of stones, other than the age and body weight of the patients, were the main factors associated with HT. As far as the different kind of stone is concerned, the prevalence of HT was higher in patients with uric acid (17/37, 45.9%) and struvite stones (11/27, 40.7%) than in calcium stone formers (35/188, 18.6%) (chi 2 16.31, p < 0.001). The prevalence of hypercalciuria was higher in the calcium stone group than in uric acid or struvite stone patients (36.4 vs. 9.7 vs. 13.7%; chi 2 10.35, p < 0.01). Furthermore, the hypercalciuria showed a trend to be more prevalent in the untreated (47.0%) than in the treated (31.2%) hypertensives, or normotensives (35.1%). Uric acid stone formers were older, heavier and with higher triglycerides and uric acid plasma levels than calcium or struvite patients. Also the struvite stone formers were older than the calcium stone ones. Our data suggest that the prevalence of HT in kidney stone patients and particularly in calcium stone formers is similar to that of a general population. The role of hypercalciuria as the link for HT-urolithiasis association seems quite uncertain. Struvite and uric acid stone formers have higher risk for HT than calcium stone formers, probably due to the old age or to the associated metabolic abnormalities.
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PMID:Hypertension in kidney stone patients. 885 53

Thiazidic diuretics are first line drugs for treatment of hypertension, due to their proven capacity to reduce cardiovascular morbidity and mortality in hypertensive subjects, including the elderly. In addition, they are very useful in the treatment of heart failure and volumen overload in liver and renal diseases. On the other hand, diuretics are efficacious to prevent calcium-related renal stone formation with or without accompanying hypercalciuria. Finally, related to their capacity to reduce urinary calcium excretion they prevent postmenopausal and senile bone mass loose, and reduce the incidence of hip fracture with relevant socioeconomic consequences.
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PMID:[Thiazide diuretics and calcium metabolism: role in renal lithiasis and osteoporosis]. 898 70

Treatment for X-linked hypophosphatemia (XLH; vitamin D metabolites and phosphate salts) may result in hypercalcemia, hypercalciuria, nephrocalcinosis, and hyperparathyroidism. Cardiovascular abnormalities occur in association with these complications, but have not been reported in XLH. We hypothesized that such abnormalities may occur in XLH and evaluated cardiovascular status in 13 patients with this disease. All patients were asymptomatic and had normal cardiovascular physical examinations and Holter studies. Serum calcium and creatinine clearance were normal in all. However, all patients had mild to moderate nephrocalcinosis. Left ventricular hypertrophy was diagnosed by electrocardiogram in three and by ultrasonography in seven children. Baseline blood pressure (BP) was normal (mean +/- SD, 116 +/- 15/74 +/- 6 mm Hg). During exercise stress testing, systolic BP increased in all patients, but the maximal systolic pressure was less than that in healthy age- and sex-matched controls (156 +/- 20 vs. 175 +/- 23; P = 0.002, by t test). An abnormal increase in diastolic BP occurred at all levels of work load in XLH patients; their peak exercise diastolic BP was 91 +/- 12 vs. 72 +/- 6 mm Hg in controls (P < 0.0001, by t test). Whether these abnormal findings are primary defects in XLH or represent complications of treatment is unclear. Patients with XLH should be monitored closely for the development of hypertension and left ventricular hypertrophy. Investigation of the mechanisms involved and establishment of therapeutic guidelines are indicated.
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PMID:Cardiovascular abnormalities in patients with X-linked hypophosphatemia. 925 16

Advances in the molecular genetics of inherited renal tubulopathies have allowed some insight into the normal mechanisms of tubular cation and anion reabsorption. It is now possible to view Bartter's syndrome, Gitelman's syndrome and pseudohypoaldosteronism type 1 as having genetic abnormalities which produce tubular defects that are similar to those induced by the pharmacological actions of loop diuretics, thiazide diuretics or potassium-sparing diuretics, respectively. Although these rare monogenic disorders with dramatic phenotypes seem to have little relevance to everyday clinical practice, it is possible that subtle abnormalities of the regulation of the ENaCs may play a role in low-renin forms of 'essential' hypertension. Similarly, subtle abnormalities in the function of the electroneutral sodium-(potassium)-chloride cotransporters (NKCC2 and NCCT) and the renal CLC-type chloride channels (CLC5) may be major determinants of urinary calcium excretion with roles in the pathogenesis of 'idiopathic' hypercalciuria and osteoporosis. Because of the intricate and diverse molecular mechanisms by which tubular reabsorption of water and solutes takes place in each different nephron segment, it is likely that other renal channels and transporters will be implicated in the pathogenesis of further monogenic disorders, and that these will allow additional insights into tubular functioning. Recent studies have demonstrated that in addition to abnormalities in the NKCC2 and ROMK1 genes, mutations at a third genetic locus can also cause Bartter's syndrome. Linkage studies, followed by mutational analyses have found deletions and point mutations in the gene encoding one of the TAL-specific chloride channels, CLCKB, in 17 Bartter's families. This chloride channel is similar in structure to CLC5, and is located on the long arm of chromosome 1. Importantly, there appears to be a phenotypic difference between subjects with Bartter's syndrome due to CLCKB abnormalities and those with NKCC2 or ROMK1 mutations. Despite the fact that all of these Bartter's patients had significant hypercalciuria, nephrocalcinosis was not found in any of the 17 subjects with CLCKB mutations, compared to 19 of 20 patients with NKCC2 or ROMK1 mutations. These findings have also demonstrated a key role for CLCKB as a major basolateral chloride channel involved in mTAL sodium and chloride reabsorption (Figure 2).
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PMID:Straightening out the renal tubule: advances in the molecular basis of the inherited tubulopathies. 951 7

This study tested the hypothesis that the increased renal perfusion pressure in DOC-salt hypertension is essential for the maintenance of sodium balance and is responsible for the hypercalciuria associated with this model. Twelve chronically instrumented dogs were placed on a high salt intake and mean arterial pressure (MAP) was measured 24 h/day. After a control period, a 17-day DOC infusion period was begun. In six dogs, however, renal perfusion pressure (RPP) to both kidneys was maintained at control levels for the first 12 days of the DOC infusion by the continuous, servo-controlled adjustment of a suprarenal silastic occluder on the abdominal aorta. The servo-controlled dogs had significantly more sodium retention and a greater increase in blood pressure than the six control DOC hypertensive dogs. Urinary calcium excretion in the control dogs began to increase from 24 +/- 6 mg/day on day 1 of DOC, and increased progressively to 100 +/- 14 and 175 +/- 30 mg/day by days 7 and 12, respectively. Plasma ionized calcium decreased, and parathyroid hormone (PTH) (1-84) increased, significantly by day 4. The hypercalciuria was not different in the servo-controlled dogs for the first 7 days of DOC, but was attenuated thereafter. Thus, increased RPP is important in restoring sodium balance and in maintaining the calciuresis in DOC-salt hypertension; however, other mechanisms also are important, particularly during the onset of hypertension.
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PMID:Renal perfusion pressure is an important determinant of sodium and calcium excretion in DOC-salt hypertension. 979 36

The differential diagnosis of hematuria with or without proteinuria is extensive, and isolated hematuria is a common problem in children and adolescents. Extensive evaluation is often necessary for the child presenting with macroscopic plus microscopic hematuria including nonglomerular and glomerular etiologies, while children with only isolated microscopic hematuria can generally be followed after baseline evaluation to rule out infection, hypercalciuria, familial hematuria, sickle cell disease, post-streptococcal glomerulonephritis (GN), and structural abnormalities (cysts, stones, obstruction, Wilms tumor). Children with the combination of hematuria and proteinuria require rapid systematic evaluation, generally including renal biopsy, except in cases where post-streptococcal GN can be clearly documented. Post-streptococcal GN occurs 7-21 days after a streptococcal infection, is associated with an acute fall in C3 levels with return to normal by approximately 8 weeks, rarely causes acute renal failure, and in children has a pattern of gradual resolution of hypertension, hematuria, and proteinuria over a course of 6-12 months.
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PMID:Asymptomatic hematuria in childhood: a practical approach to evaluation. 1079 63

Therapeutic indications of potassium citrate include: 1. Oxaluric renal stone disease and some cases of uric acid stone disease. Prevention of stone formation in patients with renal polycystic disease. Prevention of stone relapse after ESWL or lithotomy; 2. Distal renal tubular acidosis complicated by hypercalciuria, mainly in children. 3. Renal hypercalciuria and hyperoxaluria. 4. Prevention of renal complications at the time of glaucoma treatment with acetazolamide. 5. Potassium supplementation during treatment of hypertension. Potassium citrate is usually contraindicated in the case of: 1. Urinary tract infection. 2. Struvite renal stone disease. 3. Hyperpotassemia and advanced chronic renal failure. 4. Peptic ulcer or gastritis. 5. Gastrointestinal bleeding. 6. Disorders of coagulation, crural varices. 7. Metabolic alkalosis. Potassium citrate, when used at therapeutic doses, is to be considered as quite safe. The average daily dose even if admitted as a single dose day engages 60-75% of free renal capacity for potassium excretion. Physiologic and therapeutic citrate concentration in urine exceeds much those available for other inhibitors. The therapeutic dose does not induce any significant changes in any biochemical or endocrine parameter of blood except mild transient metabolic alkalosis. The decrease of urine calcium and increase in oxalate calcium phosphate excretion is observed. In hypo-cytriaturic patients the response to therapeutic dose of citrate is smaller. One-year remission of stone disease is observed in 70-75% cases.
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PMID:[Therapeutic use of potassium citrate]. 1147 49


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