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

Prostanoids belong to the growing family of eicosanoids, which are all derived from arachidonic acid. Prostanoids act as modulators and mediators in a large spectrum of physiological and pathophysiological processes within the kidney. On the one hand, the potent vasoconstrictor and platelet-aggregating thromboxane (TX) A2 is involved in the pathophysiology of a variety of glomerular diseases, such as haemolytic-uraemic syndrome and immune-mediated glomerulopathies. Prostaglandin (PG) E2, on the other hand, interferes with tubular electrolyte and water handling. Clinical data support the hypothesis that this member of the prostanoid family contributes to the pathophysiology of Bartter's syndrome, hyperprostaglandin E syndrome, idiopathic hypercalciuria and renal diabetes insipidus. Both prostanoids, TXA2 and PGE2, are involved in the pathophysiology of obstructive uropathies. The physiological and protective role of renal vasodilator prostanoids (PGI2 and PGE2) has been studied during treatment with non-steroidal anti-inflammatory drugs. Part of the pharmacological effects of frusemide and converting enzyme inhibitors is mediated by PGI2 and PGE2. The role of renal prostanoids in cyclosporine toxicity is still equivocal. Future investigations on the physiological and pathophysiological role of renal prostanoids will have to consider the multiple interactions between prostanoids on the one hand, and classical hormones and other mediators (e.g. cytokines) on the other hand.
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PMID:Prostanoids in paediatric kidney diseases. 191 Nov 54

The effects of salt (sodium chloride) supplementation of rat diets (80 g/kg diet), with or without lactose (150 g/kg), were studied in weanling rats over 14 d. Dietary salt increased water intake and reduced weight gain and food conversion efficiency, but these variables were unaffected by lactose. Salt-supplemented rats exhibited a three- to fivefold increase in urinary calcium excretion and a small increase in urinary magnesium and phosphorus excretion, irrespective of dietary lactose content. In addition, salt supplementation reduced plasma alkaline phosphatase (EC 3.1.3.1) activity. Lactose increased urinary Ca and Mg excretion and plasma Ca and P concentrations. Salt reduced tibia mass but not tibia mass expressed relative to body-weight, but neither variable was affected by lactose. Both tibia Mg content and concentration were reduced by salt but unaffected by lactose, and neither tibia P content nor concentration was affected by salt or lactose. Tibia Ca content was reduced by salt but this was prevented by lactose. Tibia Ca concentration was unaffected by salt or lactose, although there was a reduction (not significant) in tibia Ca concentration in animals fed on the lactose-free diet. These results show that lactose had no independent effect on bone and that reduced accretion of bone mass and mineral content in rats fed on the high-salt diets was due, at least in part, to reduced growth. Failure to offset sodium-induced hypercalciuria by a compensatory increase in net Ca absorption may have contributed to reduced bone Ca accretion. The protective effect of lactose against reduced bone Ca accretion may be due to increased Ca absorption.
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PMID:Effect of dietary lactose on salt-mediated changes in mineral metabolism and bone composition in the rat. 193 8

Furosemide, a potent natriuretic agent, is well known to increase urinary calcium excretion. We study the effects of long term administration of furosemide on the calcium balance, renal function and histopathological changes of the kidneys and the parathyroid glands in the rat. Furosemide (20 mg/kg) was administered 3-4 times per week for 62 weeks intraperitoneally in 10 male rats. The same volume of normal saline was administered intraperitoneally in 9 male rats as control. All were given with standard diet (CE-2) and deionized water. While urinary calcium and creatinine were measured every 1-4 weeks, serum calcium and creatinine were measured in the first week and at the end of examination. 24 hours urinary excretion of calcium was elevated to two to three folds (a significant increase over the control: p less than 0.01) after the furosemide loading, though serum calcium and creatinine levels remained as in control. Despite a marked hypercalciuria in the furosemide loaded rats, there was no evidence of stone formation in the kidney or in the urinary tract. On histopathological examination renal parenchyma showed some pyelonephritic changes but without evidence of crystal formation, while no significant change was noted in the parathyroid glands. Based on these data we concluded that in our model, 1) there was a significant calcium loss in the absence of any change in the serum calcium, but 2) this hypercalciuria alone was not lithogenic, and 3) parathyroid glands showed no discernible secondary morphological changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of long-term administration of furosemide on calcium balance, kidney and parathyroid gland]. 230 11

With 2 groups of 10 patients the influence of an additional therapy with 1 g magnesium sulfate/h during i.v. tocolysis with the betamimetic fenoterol (2 micrograms/min) upon parameters of water and electrolyte balance has been investigated. The whole of the magnesium administered during the 24 hours investigational period has been eliminated via the kidneys. Most probably due to a competition within the distal tubulus hypermagnesemia was associated with hypocalcemia and hypercalciuria, followed by a rise in parathyroid hormone. As PTH is able to compensate hypocalcemia not only by means of bone mobilisation but also by an increase in enteral Ca absorption, estimated losses of calcium are minimal. These may be neglected, as additional therapy with magnesium sulfate--besides the advantages yet known (cardioprotection, saving of betamimetic dosage, reduction of drug tolerance development)--reduces betamimetic induced water retention, thus significantly diminishing lung edema hazard during tocolytic therapy.
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PMID:[Effect of co-medication with magnesium sulfate in beta-mimetic tocolysis on parameters of water-electrolyte balance]. 231 70

Previous studies revealed that administration of 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3] to calcium (Ca)-deficient rats causes a dose-dependent reduction in markedly elevated serum 1,25-(OH)2D3 level. Although the results suggested that the metabolism of 1,25-(OH)2D3 was accelerated by 24,25-(OH)2D3, those experiments could not define whether the enhanced metabolism of 1,25-(OH)2D3 played a role in the reduction in the serum 1,25-(OH)2D3 level. In the present study, in order to address this issue more specifically, serum 1,25-(OH)2D3 was maintained solely by exogenous administration through miniosmotic pumps of 1,25-(OH)2D3 into vitamin D-deficient rats. Thus, by measuring the serum 1,25-(OH)2D3 concentration, the effect of 24,25-(OH)2D3 on the MCR of 1,25-(OH)2D3 could be examined. Administration of 24,25-(OH)2D3 caused a dose-dependent enhancement in the MCR of 1,25-(OH)2D3, and 1 microgram/100 g rat.day 24,25-(OH)2D3, which elevated serum 24,25-(OH)2D3 to 8.6 +/- 1.3 ng/ml, significantly increased MCR and suppressed serum levels of 1,25-(OH)2D3. The effect of 24,25-(OH)2D3 on 1,25-(OH)2D3 metabolism developed with a rapid time course, and the recovery of iv injected [1 beta-3H]1,25-(OH)2D3 in blood was significantly reduced within 1 h. In addition, there was an increase in radioactivity in the water-soluble fraction of serum as well as in urine, suggesting that 1,25-(OH)2D3 is rapidly degraded to a water-soluble metabolite(s). Furthermore, the reduction in serum 1,25-(OH)2D3 was associated with a reduction in both serum and urinary Ca levels. Because the conversion of [3H]24,25-(OH)2D3 to [3H]1,24,25-(OH)2D3 or other metabolites was minimal in these rats, 24,25-(OH)2D3 appears to act without being converted into other metabolites. These results demonstrate that 24,25-(OH)2D3 rapidly stimulates the metabolism of 1,25-(OH)2D3 and reduces its serum level. It is suggested that 24,25-(OH)2D3 plays a role in modifying serum 1,25-(OH)2D3 concentrations by affecting the metabolism of 1,25-(OH)2D3 and may have a therapeutic values in the treatment of hypercalcemia or hypercalciuria caused by 1,25-(OH)2D3 excess.
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PMID:Effect of 24,25-dihydroxyvitamin D3 on 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] metabolism in vitamin D-deficient rats infused with 1,25-(OH)2D3. 278 9

Abnormalities in renal tubular function have been reported in adult patients with idiopathic renal hypercalciuria. To determine if such abnormalities are present early in the natural history of renal hypercalciuria, we evaluated renal tubular function in ten children with idiopathic renal hypercalciuria, aged 5-17 years. Seven of the children presented with urolithiasis and three with hematuria. Urinary calcium excretion ranged from 4 to 9 mg/kg per day, (5.2 +/- 0.5, mean +/- SEM) with a mean fasting urinary calcium to creatinine ration of 0.31 +/- 0.03. Studies described in this report were performed after 1 week of ingesting a diet containing 1,000 mg calcium, 3,000 mg sodium, and 100 mg purine. Clearance of creatinine ranged from 84 to 159 ml/min per 1.73 m2. Tm phosphate (mg/100 ml GFR) was normal in each child (mean 4.66 +/- 0.06 mg/100 ml GFR). Fractional excretion of uric acid, sodium and beta-2-microglobulin were also normal in each child. Serum bicarbonate concentrations ranged from 21.5 to 27 mEq/l with a mean of 24.4 +/- 0.5 mEq/l and all patients lowered urinary pH to less than 5.5. Hypotonic diuresis demonstrated normal free water clearance with a mean of 12.8 ml/min per 100 ml Cin. Distal sodium delivery and fractional distal sodium reabsorption were normal with a mean of 13.6 +/- 1.2% and 92.7 +/- 0.5%, respectively. Water deprivation studies demonstrated a range of maximum urinary osmolality from 711 to 1,020 mosmol/kg H2O with a mean of 864 +/- 34 mosmol/kg H2O. Seven healthy children, ingesting an identical study diet, concentrated their urine to a mean of 1,059 +/- 31 mosmol/kg h2O.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function in children with idiopathic hypercalciuria. 315 15

Renal and systemic prostanoid activity was assessed in various renal tubular disorders, using mass spectrometric determination of urinary excretion rates of primary prostaglandins (PGE2, PGF2 alpha, PGI2, and TXA2) and their systemically produced index metabolites. Only PGE2 levels (normal range: 2.0-16.4 ng/h per 1.73 m2) are elevated in Bartter syndrome (median: 43.4, range: 6.7-166.3), nephrogenic diabetes insipidus (46.2, 12.1-1290), Fanconi syndrome (96.6, 19.3-135.5), and in a complex tubular disorder in premature infants (40.7, 22.3-132.1), for which the term hyperprostaglandin E syndrome has been introduced. In this disorder with a Bartter-syndrome-like tubulopathy, the systemic features of the disease such as fever, diarrhoea and osteopenia with hypercalciuria were associated with increased systemic PGE2 activity. In most patients the urinary excretion rate of the systemic index metabolite of PGE2 (PGE-M) was markedly elevated (1028, 285-4709; normal range: 104-664 ng/h per 1.73 m2). Hypercalciuria per se was associated neither with increased renal nor with systemic PGE2 hyperactivity. Most problems in infants with hyperprostaglandin E syndrome could be controlled by long-term indomethacin treatment in contrast to the moderate and partial effect of this treatment in patients with Fanconi syndrome. Thus increased PGE2 synthesis plays a major role in the pathogenesis of hyperprostaglandin E syndrome, while in Fanconi syndrome PGE2 hyperactivity in the kidney is a secondary event and only aggravates the water and electrolyte wastage.
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PMID:Role of prostaglandins in hyperprostaglandin E syndrome and in selected renal tubular disorders. 315 22

1. Because urinary prostaglandin excretion could play a role in idiopathic hypercalciuria (IH), we studied the excretion of prostaglandin E (PGE), calcium and sodium at various urine flows in 21 patients (14 males) with urolithiasis and IH, seven stone formers (five males) with normal calciuria and 20 controls (11 males). Dietary composition was comparable and sodium intake was restricted to 100-120 mmol/day. 2. Analyses were performed on 30 min urine collections obtained after overnight water deprivation and during water diuresis. Male IH patients had increased levels of urinary PGE at all ranges of urine flow. PGE excretion correlated directly with urine flow in patients and controls, but the slope of this relationship in individual IH male patients was steeper than in controls (P less than 0.01). Calciuria correlated directly with urine output in patients with IH but not in controls. Calcium and sodium excretion were directly correlated (P less than 0.0001) in patients and controls. There were no significant differences between absorptive IH (seven patients) and renal IH (eight patients). There were no significant differences between stone formers with normocalciuria and control subjects. 3. The findings suggest that increased urinary PGE could play a role in the hypercalciuria syndrome, possibly by promoting natriuresis.
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PMID:Increased urinary excretion of prostaglandin E in patients with idiopathic hypercalciuria. 320 91

This study is presented as a debate on nephrolithiasis by a urologist and an internist. The reason is that in 1986 the urologist has become successful at desintegrating almost any stone without open surgery, whereas the internist's approach to the same problem is entirely based upon an understanding of pathophysiological mechanisms. After having reviewed the major risk factors for renal stone disease, i.e. small urine volume, hypercalciuria, hyperoxaluria, hyperuricosuria, very high or very low urine pH and hypocitraturia, the author shows that now it is not only possible to selectively correct each of these disorders, but that in doing so the internist does change the natural history of the disease. For instance, definite remissions have been obtained by advising patients to increase water intake, by administering thiazides to hypercalciurics, pyridoxine to some hyperoxalurics, allopurinol to hyperuricosurics, urease inhibitors to struvite stone formers and citrate to hypocitraturics. Therefore, the author concludes that the role of the urologist and that of the internist are complementary: although the former now desintegrates the stone without open surgery, the latter, who takes care of the same patient next, is now largely able to prevent relapse of nephrolithiasis after determining the cause of the disease.
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PMID:[Renal lithiasis: the internist's viewpoint 1986]. 373 61

Chronic mineralocorticoid excess results in the predicted retention of salt and water followed by a period of escape from sodium retention and hypercalciuria. We studied a rat model during mineralocorticoid escape (ME) with clearance and micropuncture studies to ascertain the nephron site and possible role of parathyroid hormone. Rats during ME were hypercalciuric compared with a matched saline group. Clearance studies revealed a marked difference in the calcium-to-sodium fractional excretion ratio (FECa/FENa) between saline-expanded and mineralocorticoid (desoxycorticosterone acetate, DOCA)-escaped animals (saline-expanded, 0.40 +/- 0.09 vs. DOCA, 1.02 +/- 0.14; P less than 0.01). The addition of either hydrochlorothiazide (HCTZ) or amiloride (AMIL) to the ME animals significantly lowered this ratio from that seen in the intact ME group (DOCA-HCTZ, 0.47 +/- 0.07; DOCA-AMIL, 0.83 +/- 0.14). Neither parathyroidectomy (PTX) nor parathyroid hormone infusions (PTH) in ME animals altered the FECa/FENa from that seen in the intact ME group (DOCA-PTX, 1.15 +/- 0.20; DOCA-PTH, 1.25 +/- 0.18). Segmental micropuncture along the length of superficial nephrons demonstrated no differences in calcium delivery to late proximal, early distal, and late distal sites. However, FECa was markedly increased in ME animals compared with saline controls (saline, 0.48 +/- 0.13% vs. DOCA, 1.62 +/- 0.24%; P less than 0.05). We conclude that the hypercalciuria of ME is independent of PTH and can be significantly reduced by HCTZ or AMIL. Micropuncture and clearance data suggest that the hypercalciuria of ME is mediated in the terminal nephron. The differences in the results when superimposing various factors that influence distal nephron calcium reabsorption on ME may be related to differences in their site(s) of activity on calcium transport.
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PMID:Hypercalciuria of mineralocorticoid escape: clearance and micropuncture studies in the rat. 377 84


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