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

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

For the first time neonatal variant of Bartter syndrome to 14.5-year old girl is presented in Lithuania. It is a rare genetical disease with autosomal recessive inheritance. The patient was born prematurely, had polyhydramnion, polyuria and polydypsia, a craving for salt, specific outlook and was mentally retarded, had muscle weakness and nephrocalcinosis. Hypokalemia, hyperreninemia and metabolic alkalosis were found. Urine analysis revealed impaired renal concentration capacity, hypercalciuria and hypernatriuria. She had the symptom of systemic disease - osteopenia. Literature review on Bartter's syndrome is done.
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PMID:[Bartter syndrome and it's neonatal type]. 1276 27

Dent's disease and familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) are inherited diseases in which hypercalciuria, nephrocalcinosis, and renal failure are prominent features. Dent's disease resembles a Fanconi syndrome, with impaired reabsorption in the proximal tubule; FHHNC, with urinary loss of magnesium and calcium, is associated with impaired cation transport in the thick ascending limb of Henle's loop. Gene mapping in families and positional cloning led in both cases to identification of the responsible gene. Dent's disease is associated with mutations that disrupt function of a voltage-gated chloride channel, CLC-5, expressed in subapical endosomes of the proximal tubule and in other nephron segments. Impaired function of this channel disturbs reabsorption of filtered proteins, as well as other transport functions of the proximal tubule, and leads, apparently indirectly, to hypercalciuria and renal failure. FHHNC results from mutations in paracellin-1, a tight-junction protein that appears to be important in conducting or regulating paracellular cation transport. Impaired function of paracellin-1 leads specifically to urinary losses of magnesium and calcium, but because transcellular transport is intact these patients do not have hypokalemia or salt wasting. Identification of both genes represent triumphs of a genetic approach to solving problems of pathophysiology.
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PMID:Inherited hypercalciuric syndromes: Dent's disease (CLC-5) and familial hypomagnesemia with hypercalciuria (paracellin-1). 1473 May 10

Over 70 years ago, potassium was found to have a natriuretic effect and was used in patients with heart failure. However, it took many years for its role in the control of blood pressure to be recognized. Recently, epidemiological and clinical studies in man and experimental studies in animals have shown that increasing potassium intake towers blood pressure and that communities with a high potassium intake tend to have lower population blood pressures. Several studies have shown an interaction between salt intake and potassium intake. However, the recent DASH-Sodium (Dietary Approaches to Stop Hypertension) study demonstrates an additive effect of a low salt and high potassium diet on blood pressure. Increasing potassium intake may have other beneficial effects, for example, reducing the risk of stroke and preventing the development of renal disease independent of its effect on blood pressure. A high potassium intake reduces calcium excretion and could play an important role in the management of hypercalciuria and kidney stone formation, as well as bone demineralization. Potassium intake may also play an important role in carbohydrate intolerance. A reduced serum potassium increases the risk of lethal ventricular arrhythmias in those at risk, i.e. patients with ischemic heart disease, heart failure or left ventricular hypertrophy, and increasing potassium intake may prevent this. In this article, we address the evidence for the important role of potassium intake in regulating blood pressure and other beneficial effects of potassium which may be independent of and additional to its effect on blood pressure.
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PMID:Potassium: more beneficial effects. 1501 47

Nutrition plays a major role in the pathogenesis of the most widespread forms of nephrolithiasis, i.e. calcium (calcium oxalate and phosphate) and uric acid stone disease. For this reason, dietary measures are the first level of intervention in primary prevention, as well as in secondary prevention of recurrences. An unbalanced diet or particular sensitivity to various foods in stone formers can lead to urinary alterations such as hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia and an excessively acid urinary pH. Over the course of time, these conditions contribute to the formation or recurrence of kidney stones, due to the effect they exert on the lithogenous salt profile. The fundamental aspects of the nutritional approach to the treatment of idiopathic nephrolithiasis are body weight, diet and water intake. This paper will present data resulting from our own investigations and the most significant evidence in literature.
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PMID:Body weight, diet and water intake in preventing stone disease. 1513 30

Typical manifestations of hyperaldosteronism include salt retention, hypokalemia, and metabolic alkalosis. However, a consequence infrequently recognized and described is hypocitraturia. In combination with hypercalciuria, aldosterone-induced hypocitraturia can trigger calcium nephrolithiasis. The authors report a case of an individual with primary hyperaldosteronism from an adrenal adenoma that resulted in hypocitraturia. The patient had severe recurrent renal calcium calculi that corrected with adrenalectomy. The clinical physiology of renal calcium and citrate handling in hyperaldosteronism is reviewed.
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PMID:Recurrent calcium nephrolithiasis associated with primary aldosteronism. 1521 56

Congestive heart failure (CHF) is a clinical syndrome with origins rooted in a salt-avid state largely mediated by effector hormones of the circulating renin-angiotensin-aldosterone system. Other participating neurohormones include catecholamines, endothelin-1, and arginine vasopressin. CHF is accompanied by a systemic illness of uncertain causality. Features include the appearance of oxidative/nitrosative stress and a wasting of tissues including bone. Herein we hypothesized that inappropriate (relative to dietary Na+) elevations in plasma aldosterone (Aldo) contribute to an altered redox state, augmented excretion of divalent cations, and in turn, a loss of bone minerals and strength. In uninephrectomized rats that received chronic Aldo and 1% NaCl treatment for 4-6 wk, we monitored plasma alpha1-antiproteinase activity, which is an inverse correlate of oxidative/nitrosative stress; plasma concentrations of ionized Mg2+ and Ca2+; urinary Mg2+ and Ca2+ excretion; and bone mineral composition and strength to flexure stress. Compared with controls, we found reductions in plasma alpha1-antiproteinase activity and ionized Mg2+ and Ca2+ together with persistently elevated urinary Mg2+ and Ca2+ excretion, a progressive loss of bone mineral density and content with reduced Mg2+ and Ca2+ concentrations, and a reduction in cortical bone strength. Thus the hypermagnesuria and hypercalciuria that accompany chronic Aldo-1% NaCl treatment contribute to the systemic appearance of oxidative/nitrosative stress and a wasting of bone minerals and strength.
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PMID:Loss of bone minerals and strength in rats with aldosteronism. 1547 29

Urinary stone disease is frequent, and characterized by a high recurrence rate. Prevention of recurrent urolithiasis is possible using an appropriate diet with or without medications. Patients should be encouraged to have a high fluid intake. For an adult, urine volume should exceed 2000 ml/day. Diet modification should be done according to the various metabolic factors contributing to the formation of the stone (ie, hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricuria, and so forth). Calcium intake should be around 1000 mg/day, protein intake limited to 1.2 g/kg/day, and salt intake kept to less than 100-150 mEq/jour. For uric acid urolithiasis, patient should limit uric acid intake to less than 500 mg/day. If these dietary manoeuvers fail, one can use thiazide diuretics to treat hypercalciuria, potassium citrate to correct hypocitraturia or sodium bicarbonate to alkalanize urine and prevent uric acid stone formation.
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PMID:[Medical treatment of urinary lithiasis]. 1549 68

Knockout mouse models and human inherited diseases have provided important new insights into the physiologic role of chloride transport by CLC Cl(-) channels and KCC K-Cl co-transporters. ClC-K/barrtin Cl(-) channels are important for renal salt reabsorption and possibly for acid secretion by intercalated cells. The endosomal ClC-5 protein is crucial for proximal tubular endocytosis. Its disruption in mice and patients with Dent's disease leads to hypercalciuria and kidney stones through a pathologic cascade that may be entirely explained by an impairment of endocytosis. KCC4 is important for recycling Cl(-) for the basolateral anion exchanger in intercalated cells, as is evident from the renal tubular acidosis resulting from its knockout. Finally, both KCC3 and KCC4 are crucial for proximal tubular cell volume regulation.
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PMID:Chloride transport in the kidney: lessons from human disease and knockout mice. 1582 7

This paper discusses the physiology of sodium effects on calcium metabolism and possible implications of increased salt intake on bone remodelling and bone mass. Osteoporosis is an increasing public health problem affecting more than 200 million of women around the world. The major complications of osteoporosis are fractures, which are frequently associated with high morbidity and mortality. A number of clinical, epidemiological and experimental studies aim at identifying lifestyle factors that may improve bone mass and prevent bone loss. Different nutrients are proposed to play a role in bone development during growth and in the maintenance of bone mass thereafter. However, the importance of sodium intake for bone health has not been elucidated. It is well known that high dietary sodium intake decreases renal calcium reabsorption, which in turn leads to a greater urinary calcium excretion. This effect has been demonstrated in studies in humans of all ages as well as in experimental animals. It is not clear to what extent sodium-induced calcium loss is compensated for by increased intestinal calcium absorption. It is suspected that, if not fully compensated, sustained hypercalciuria due to increased sodium intake may diminish bone mass. Postmenopausal women showed that increased dietary salt may indeed augment bone resorption. Sodium effects on bone mass in various studies are inconsistent and there is still no evidence that increased salt intake is a risk factor in the aetiology of osteoporosis A randomized longitudinal study of different sodium intake in two groups of subject could clarify the role of sodium in bone mass.
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PMID:[Effects of sodium chloride on bone health]. 1596 7


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