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

A case of the milk-alkali syndrome is described. The patient presented with a raised serum calcium level without hypercalciuria, nephrocalcinosis and azotaemia. The alkali used was an antacid preparation containing calcium carbonate.
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PMID:The milk-alkali syndrome. A case report. 668 8

Because calcium has been reported to modify gentamicin binding to its proximal tubular brush border membrane receptor, we studied the effects of dietary calcium loading and subsequent hypercalciuria on experimental gentamicin nephrotoxicity. Male Fischer 344 rats were fed one of two diets that were identical except for calcium carbonate content: normal (0.5%) and high (4%). The high-calcium diet made rats hypercalciuric but there were no differences between the two groups in inulin clearance, sodium or osmolar excretion, or serum calcium prior to gentamicin administration. Animals on both diets were treated with gentamicin, 20 mg/kg b.i.d., for periods of 3 to 21 days. Both groups developed acute renal failure, but animals on the high-calcium diet had less severe acute toxic injury, as evidenced by studies of inulin clearance, renal histology, and in vitro cortical uptake of NMN and PAH. Furthermore, calcium-loaded animals tended to have lower peak renal cortical gentamicin levels during the period of acute toxicity. The mechanism by which increased dietary calcium protects against gentamicin nephrotoxicity remains speculative. Calcium and gentamicin may compete for the same brush border receptor or alternatively parathyroid suppression may result in diminution in tubular cell membrane drug binding sites. The possibility that high-calcium diets exert a nonspecific salutory effect on proximal tubular cell integrity has not been excluded.
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PMID:Increasing dietary calcium moderates experimental gentamicin nephrotoxicity. 669 Jun 34

In the years between 1971 and 1979 in the Department of Urological Surgery of the Municipal Weil Emil Hospital in 16 of the 72 coral calculi filling the renal pelvis primary (so-called uric acid) calculi were found to which lytholysis was applied. Fifty-six cases (secondary calculi) were operated, in the majority by conservative surgery (40 cases), 16 patients were nephrectomized. The incidence of coral stones is twice as high in women as in men. Congestion and infections play the major role in their pathogenesis, hypercalciuria is less frequent. Up-to-date possibilities of examination ensure the proper plan of the operation. Complete removal of the stones, abolishment of congestion and infection and postoperative care are very important in the prevention of relapse. In 21 of the 72 cases congenital malformation as was found as a source of congestion. There are various types of conservative operations. Quite often the renal parenchyma is incised, and in this case the peduncle has to be ligated. By cooling the kidney the hypoxic time can be prolonged quite considerably. In the course of the operation the kidney must be made free of stones as the incidence of relapses is high. Analysis of the removed coral stones showed that 68% of them consisted of carbonate-apatite-struvite.
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PMID:[Surgical treatment of coral calculi in the renal pelvis]. 734 66

Reduced citrate in urine and increased fasting excretion of calcium are abnormalities frequently reported in stone forming (SF) patients. Increased dietary acid (or reduced alkali) introduction or absorption may be a potential cause of both these pathological findings. To test this hypothesis, we studied 64 SF patients (32 with fasting hypercalciuria (FH) and 32 without FH (NFH)). After a basal evaluation for nephrolithiasis, while on a 500 mg calcium diet, they were evaluated for: (1) daily intestinal alkali absorption (IAA), by urinary electrolyte excretion; (2) basal concentrations of PTH, calcitonin (CT) and 1,25(OH)2-VitD; (3) oral calcium load for evaluation of changes in calcium and hydroxyproline urinary excretions; (4) intestinal calcium absorption (18 patients), with double curve analysis (stable Sr as tracer); and (5) changes in citrate excretion after an alkali load (50 mEq of a mixture of calcium gluconate, lactate and carbonate) in 10 patients. The results demonstrated: (1) FH stone formers had reduced citrate excretion and lower mean IAA levels than NFH stone formers; (2) FH stone formers also had higher bone resorption levels with lower PTH and higher CT levels; (3) IAA levels were related to both citrate excretion and bone turnover indices; and (4) the increases in citrate excretion after oral alkali load were strictly related to basal IAA values (index of alkali absorption and/or generation after oral load), demonstrating that a different absorptive capacity of alkali rather than a different dietary content may underlie these metabolic abnormalities.
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PMID:Urinary citrate, bone resorption and intestinal alkali absorption in stone formers with fasting hypercalciuria. 774 55

We have shown previously that chronic hyperchloremic metabolic acidosis (CMA) induces severe negative nitrogen balance and renal phosphate depletion and decreases serum insulin-like growth factor-1 (IGF-1) in association with growth hormone (GH) insensitivity in humans. The present study investigated whether acidosis-induced renal nitrogen wasting and renal phosphate depletion are mediated by GH insensitivity/low IGF-1 and thereby responsive to GH treatment. The effects of GH on acidosis-induced changes in divalent cation metabolism and acidosis-induced hypothyroidism were also investigated. CMA (delta[HCO3], -10.5 mmol/L) was induced in six healthy male subjects ingesting 4.2 mmol NH4Cl/kg body weight [BW]/d for 7 days. Recombinant human GH (0.1 U/kg BW/12 h subcutaneously) was administered for 7 days while acid feeding was continued. GH increased serum IGF-1 from 22.1 +/- 1.4 to 87 +/- 8.4 nmol/L (control level, 36.4 +/- 2.2). GH decreased urinary nitrogen excretion, resulting in a cumulative nitrogen retention of 2,404 mmol, thereby correcting the acidosis-induced cumulative increase in nitrogen excretion (2,506 mmol) despite continued acid feeding. GH attenuated the acidosis-induced hyperphosphaturia (cumulative phosphate retention, 91 mmol) and corrected the hypophosphatemia. GH did not affect acidosis-induced ionized hypercalcemia, but further exacerbated acidosis-induced hypercalciuria (cumulative loss, 27.3 mmol). GH significantly further increased serum 1,25-dihydroxyvitamin D (1,25(OH)2D) and further decreased intact PTH (from 10 +/- 1 to 6 +/- 1 pg/mL). Acidosis also induced hypomagnesemia and hypermagnesuria (cumulative loss, 9.4 mmol, ie, renal magnesium wasting), a novel finding, which was significantly attenuated by GH (cumulative retention, 5.0 mmol). In conclusion, GH corrected acidosis-induced renal nitrogen wasting, which may be caused, at least in part, by decreased IGF-1 levels. GH further increased serum 1,25(OH)2D and the systemic calcium load, which account for the suppression of parathyroid hormone (PTH) despite renal PO4 retention and correction of hypophosphatemia. GH attenuated acidosis-induced renal magnesium wasting.
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PMID:Growth hormone corrects acidosis-induced renal nitrogen wasting and renal phosphate depletion and attenuates renal magnesium wasting in humans. 1038 Nov 52

Although calcium supplementation can cause hypercalciuria, the risk of nephrolithiasis has been shown to decrease rather than increase among subjects who had a higher calcium intake. Hypercalciuria is also a well-established side effect of calcitriol administration. However, the risk of nephrolithiasis is not well defined. The present study was undertaken to prospectively determine the effect of calcium with or without calcitriol on physicochemical risk factors associated with calcium oxalate nephrolithiasis in Thai postmenopausal women with osteoporosis. Subjects consisted of 53 Thai women more than 10 years postmenopausal who were randomly allocated to receive 750 mg of calcium carbonate supplement alone (n = 28) or 750 mg of calcium carbonate plus 0.5 microg calcitriol (n = 25) daily. Mean +/- SEM for age was 65.3+/-1.1 years, body weight 53.5+/-1.3 kg. Urine samples for biochemical assays were collected at baseline and 3 months after treatment. Supersaturation for calcium oxalate stone formation was assessed from the 24 h urine constituents by the Tiselius's index, AP(CaOx). Three months of calcium supplement alone resulted in a modest, but not significant, increase in urinary calcium (baseline, 2.90+/-0.43 mmol/day; after treatment 3.58+/-0.54 mmol/day) with no change in urinary oxalate, citrate or magnesium. In contrast, calcium together with calcitriol caused a significant increase in urinary calcium (baseline, 2.87+/-0.41 mmol/day; after treatment, 4.08+/-0.57 mmol/day; p < 0.05). No significant change in other urine constituents after treatment with calcium and calcitriol was detected. Therefore, AP(CaOx) did not significantly increase either after calcium alone (baseline, 1.17+/-0.39; after treatment, 1.36+/-0.28) or after calcium plus calcitriol (baseline, 1.09+/-0.17; after treatment, 1.09+/-0.19). However, after treatments, 12 subjects (23%)--6 receiving calcium supplement alone and 6 receiving calcium plus calcitriol supplement--had high AP(CaOx) values (greater than the upper limit of 95% Cl for AP(CaOx) derived from non-stone-forming Thai women). The post-treatment/baseline ratio was 3.21+/-0.74 for urinary calcium, 1.01+/-0.19 for urinary oxalate, and 2.23+/-0.42 (median 1.15) for AP(CaOx). The post-treatment/baseline ratio of calcium, but not for urinary oxalate, had a significant correlation with the post-treatment/baseline ratio of AP(CaOx). Our findings suggest that the alteration in the risk of calcium oxalate nephrolithiasis based on urinary composition is related to the alteration in urinary calcium. The risk of calcium oxalate nephrolithiasis does not increase significantly after calcium or combined calcium and calcitriol supplement in the majority of postmenopausal women with osteoporosis.
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PMID:Risk of calcium oxalate nephrolithiasis after calcium or combined calcium and calcitriol supplementation in postmenopausal women. 1098 63

The potential risk of recurrence and degradation of renal function justifies the etiological investigation of all lithiasis-associated pathologies. Therefore calculus analysis of the crystalline phases and morphological characteristics is an important factor in the etiological diagnosis of the disease. Microscopic examination and infrared spectroscopy of calculi from 727 children showed that calcium oxalate was the main component in 36.7% of cases, followed by calcium phosphate (31%), struvite (9.9%) and purine groups (7.7%). The most frequently observed crystalline from was carbapatite (26%), then whewellite (21%) and weddellite (15.7%). As regards the etiopathogenic aspect in adults, the relations between hypercalciuria and weddellite, and between hyperoxaluria and whewellite are also found in the child: in subjects with hypercalciuria, 82% of the calculi contained over 20% weddellite; and in subjects with hyperoxaluria, whewellite was the major constituent in 79% of cases (or 95% in the absence of associated hypercalciuria). In 27 calculi mainly composed of whewellite, the morphological analysis indicated primary hyperoxaluria; this diagnosis was confirmed in 25 cases by specific biological investigation. Urinary tract infection is frequently associated with lithiasis, but its lithogenic role cannot be confirmed without calculus analysis. Several criteria can be used as markers to determine the lithogenic etiology of the infection, i.e., the presence of struvite, the carbonate rate of carbapatite, and the whitlockite and/or protein content of the calculus.
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PMID:[Component analysis of urinary calculi in the etiologic diagnosis of urolithiasis in the child]. 1098 88

In autosomal dominant distal renal tubular acidosis type I (dRTA) impaired hydrogen ion secretion is associated with metabolic acidosis, hyperchloremic hypokalemia, hypercalciuria, nephrocalcinosis, and/or nephrolithiasis. A retardation of growth is commonly observed. In this report we present a family with autosomal dominant dRTA with an atypical and discordant clinical picture. The father presented with severe nephrocalcinosis, nephrolithiasis, and isosthenuria but metabolic acidosis was absent. His 6-year-old daughter, however, suffered from metabolic acidosis, hypokalemia, and hypercalciuria. In addition, sonography revealed multiple bilateral renal cysts but no nephrocalcinosis. Mutation analysis of the AE1 gene coding for the renal Cl-/HCO3(-)-exchanger AE1 displayed a heterozygous Arg589Cys exchange in both patients but not in the healthy family members. This point mutation is frequently associated with autosomal dominant dRTA. Diagnosis of autosomal dominant dRTA is supported in this family by results of AE1 mutation analysis.
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PMID:Atypical distal renal tubular acidosis confirmed by mutation analysis. 1114 11

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

We present a case of a 4.5 years old boy suffering from hypercalciuria caused by a not diagnosed distal renal tubular acidosis. In the age of 2.5 years, after a banal infection the routine analysis showed a presence of numerous calcium phosphates in urine. Other diagnostic procedures showed: hypercalciuria, hyperphosphaturia, rather high calcemia and high values of UCa/cr and UPO4/cr ratios. HCO3 in serum 21.2 mmol/l, pH of urine 7.0. Kidneys and urinary tract-usg normal. These results induced the family doctor to make the diagnosis: idiopathic renal hypercalciuria. He advised the therapy with hydrochlorothiazide and limitations of calcium and vitamins D3 oral supply. This decision caused an illusory positive effect: decreased the UCa/cr ratio (to 0.96 mmol/mmol) without any reduction of calcemia. After a period of 12 months the UCa/cr ratio increased up to 1.31 and calcification of renal pyramids appeared. We diagnosed the distal renal tubular acidosis (some medical informations suggested the essential distal renal tubular acidosis) and osteopenia (DXA BMD L1-L4 below -1 s.d.). The therapy with NaHCO3 (about 2.6 mmol/kg) normalized the levels of HCO3a and calcium in serum, decreased the UCa/cr ratio to values 0.09-0.16 mmol/mmol.
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PMID:[Osteopenia and renal calcification in a 4.5 year old child with primary distal renal tubular acidosis treated for idiopathic renal hypercalciuria]. 1143 85


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