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

Hematuria of unknown origin occurs in 30% of patients with diabetic nephropathy. In nondiabetic persons, hematuria may be caused by hypercalciuria with or without nephrolithiasis. Eight children with type I diabetes mellitus, hematuria, and hypercalciuria were observed in our clinic during a 1-year period. Two of these also had evidence of renal papillary necrosis. To assess the importance of hypercalciuria in the pathogenesis of hematuria in children with diabetes mellitus, we measured urinary calcium excretion in a large population of such patients. The calcium to creatinine ratio in the urine of diabetic children (0.21 +/- 0.01) was greater than that of nondiabetic children (0.12 +/- 0.01). A calcium to creatinine ratio of 0.28 was established as the upper limit of normal in our nondiabetic population, and 27% of the diabetic children were hypercalciuric on this basis. The diabetic children with hypercalciuria also had hyperphosphaturia and a urinary CaHPO4 X 2H2O molar ion product three times that found in the nondiabetic control population. These data suggest that many children with diabetes are at risk for renal damage due to hypercalciuria. Because hypercalciuria is more common in diabetic than nondiabetic children, it may play a previously unrecognized role in the renal disease associated with diabetes mellitus.
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PMID:Hematuria and hypercalciuria in children with diabetes mellitus. 357 34

To define the degree of renal tubular involvement in idiopathic calcium nephrolithiasis, 18 patients (aged 23-60 years, 15 men and 3 women, with 1-30 years of renal stone history) with normal glomerular filtration rate (GFR) and effective renal plasma flow with no history of urinary tract infection and on no dietary or drug therapy underwent the following studies: measurement of proximal tubular maximum reabsorption of glucose (Tmglucose) and secretion of para-aminohippurate (TmPAH), urinary concentrating ability after 14 h of fluid deprivation, and urinary net acid excretion following an oral dose of ammonium chloride, 0.1 g/kg of body weight. Seventeen healthy subjects in the same age range served as control. Patients with calcium nephrolithiasis, with normal renal hemodynamic functions, have significantly lower proximal tubular maximum reabsorptive and secretory functions, diminished urinary concentrating mechanism, and reduced urinary net acid excretion following an oral acid load. These tubular functional abnormalities were observed in patients with or without hypercalciuria.
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PMID:Renal tubular dysfunctions in patients with idiopathic calcium nephrolithiasis. 369 99

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

The case of a 11 year old boy with medullary sponge Kidney and nephrolithiasis discovered because of abdominal pain is described. Functional tubular impairment (concentrating defect, distal tubular acidosis) was present. No hypercalciuria nor hyperparathyroidism was detected. The diagnosis of medullary sponge Kidney was confirmed histopathologically. The pediatric cases described in the literature are characterized by a higher incidence of concentrating defect and acidosis, while the adults subjects often show hypercalciuria and or hyperparathyroidism. The careful study of tubular functions in the pediatric cases appears to be very useful to understand which are primary tubular disturbances and which are only secondary.
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PMID:[Medullary sponge kidney. Description of a pediatric case]. 378 97

The long-term effects of potassium citrate therapy (usually 20 mEq. 3 times daily during 1 to 4.33 years) were examined in 89 patients with hypocitraturic calcium nephrolithiasis or uric acid lithiasis, with or without calcium nephrolithiasis. Hypocitraturia caused by renal tubular acidosis or chronic diarrheal syndrome was associated with other metabolic abnormalities, such as hypercalciuria or hyperuricosuria, or occurred alone. Potassium citrate therapy caused a sustained increase in urinary pH and potassium, and restored urinary citrate to normal levels. No substantial or significant changes occurred in urinary uric acid, oxalate, sodium or phosphorus levels, or total volume. Owing to these physiological changes, uric acid solubility increased, urinary saturation of calcium oxalate decreased and the propensity for spontaneous nucleation of calcium oxalate was reduced to normal. Therefore, the physicochemical environment of urine following treatment became less conducive to the crystallization of calcium oxalate or uric acid, since it stimulated that of normal subjects without stones. Commensurate with the aforementioned physiological and physicochemical changes the treatment produced clinical improvement, since individual stone formation decreased in 97.8 per cent of the patients, remission was obtained in 79.8 per cent and the need for surgical treatment of newly formed stones was eliminated. In patients with relapse after other treatment, such as thiazide, the addition of potassium citrate induced clinical improvement. Thus, our study provides physiological, physicochemical and clinical validation for the use of potassium citrate in the treatment of hypocitraturic calcium nephrolithiasis and uric acid lithiasis with or without calcium nephrolithiasis.
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PMID:Long-term treatment of calcium nephrolithiasis with potassium citrate. 389 44

Thiazides are considered to be effective in preventing recurrence of various types of nephrolithiasis, but the optimum dosage has not been established. To address this issue, 5 idiopathic stone formers with hypercalciuria on low Ca diet received chlorthalidone (CT) in 3 different oral doses and were randomly assigned either to the sequence 25-50-100 mg/day or the reverse (2 months per dose, monthly blood and urine measurements). The anticalciuric effect of CT was significant only at 50 and 100 mg/day, at the expense of a dose-dependent decrease in U-citrate excretion. We also observed a dose-dependent decrease in blood levels of K, increases in those of HCO3 and urate, as well as in U-pH, a tendency for blood levels of Mg and U-oxalate excretion to fall, and no change in U-urate excretion. Therefore, to derive the optimal CT dose the Tiselius' risk index was applied, which is based on the values of urinary [Ca], [oxalate], [Mg], [citrate] and volume. CT produced a decrement in risk index which was similar at each of the doses tested. Thus, raising CT doses beyond 25 mg/day does not hold out the prospect of improved prophylaxis. This agrees with Ettinger's preliminary data (Urol. Res., 1984) showing a similar protective effect of CT at 25 and 50 mg/day despite the absence of a significant anticalciuric effect at 25 mg/day.
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PMID:[Optimal dosage of chlorthalidone in the prevention of the recurrence of nephrolithiasis is 25 mg per day]. 396 48

The clinical records of ten premature infants with nephrolithiasis were reviewed. The probable mechanism of stone formation was hypercalciuria due to furosemide therapy (nine patients) and congenital hyperparathyroidism (one patient). The relatively high rates of urinary excretion of calcium from immature kidneys predisposed these neonates to the development of calcium stones. Renal calculi in neonates are complications of distinct, treatable conditions, and premature babies receiving furosemide treatment should be screened by ultrasonography for renal calcifications.
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PMID:Nephrolithiasis in premature infants. 396 25

12 adult patients with medullary sponge kidney (MSK), followed up for 1 to 14 years (mean 7 years) are presented. MSK was initially diagnosed in 4 cases. In 8 cases the initial diagnosis included pyelonephritis, nephrocalcinosis, and nephrolithiasis. Renal calculi (4 patients), urinary tract infection (8) and hematuria (5) were the most frequent symptoms. Renal tubular acidosis was documented in 2 patients and hypercalciuria without hyperparathyroidism in 2. Over the years renal calculi increased in size in 4 patients. Renal function was stable in 11. In one patient with associated, well controlled hypertension, serum creatinin rose from 141 to 298 mumol/l over 14 years.
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PMID:[Medullary sponge kidney. Diagnosis and course in 12 cases]. 397 81

Recent data have shown that administration of indomethacin to patients with hypercalciuric nephrolithiasis decreased urinary calcium excretion, implying a possible pathogenic role for renal prostaglandins in hypercalciuria. To explore this hypothesis we administered indomethacin, ketoprofen and aspirin to normal volunteers for 6 days and assessed daily creatinine clearance and urinary excretion of sodium and calcium. In contrast to previous studies, subjects were maintained on a constant metabolic diet. These nonsteroidal anti-inflammatory drugs decreased urinary sodium excretion but had no effect on creatinine clearance or urinary calcium excretion. In summary, our data do not support an important physiologic role of renal prostaglandins in renal calcium excretion in normal subjects.
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PMID:Lack of effect of prostaglandin inhibition on calcium excretion in normal volunteers. 399 16

We report two patients with systemic lupus erythematosus (SLE) who were found to have complete (acidotic) distal renal tubular acidosis (DRTA). One patient had nephrocalcinosis and renal magnesium wasting with tetany; the other patient had nephrolithiasis and nephrotic syndrome secondary to membranous glomerulopathy. Both patients had decreased urinary citrate excretion but neither had hypercalciuria. We discuss the association of DRTA with immunologic disorders and the possible role of hypocitraturia in promoting renal calcification in these patients. We suggest that patients with renal calcification be evaluated for DRTA, and that patients found to have DRTA be further evaluated for signs, symptoms, and laboratory evidence of immunologic disorders.
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PMID:Complete distal renal tubular acidosis in systemic lupus: clinical and laboratory findings. 402 29


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