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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In idiopathic recurrent calcium urolithiasis (RCU) in men (n = 37) the metabolic effects of oral tripotassium citrate (PC) were investigated in a longitudinal field study. The patients were either normo- (n = 22) or hypocitraturic (n = 15). Laboratory examinations were performed before, and after 3, 6, and more than 12 months of medication. Acceptance of PC was poor, mainly because of the salty taste of the tablet preparation chosen, and a number of participants dropped out of the study. In the remaining participants, compliance was acceptable when evaluated on the basis of urinary potassium and undesired side effects did not occur. In the short term (up to 3 months), PC evoked compensated metabolic alkalosis (pH and citrate in urine increased; blood gases remained normal), a drop in urinary calcium, together with increasing oxaluria, hydroxyapatite supersaturation, and calcium phosphate crystalluria. In the long term (greater than 12 months) PC urinary pH and citrate "dissociated", in that pH returned to pretreatment baseline values, whereas citrate stayed at high levels. In normocitraturics but not in hypocitraturics, urinary urea and sodium increased with PC. Hypocitraturics appeared to be less sensitive to the effects of PC, as reflected by the relatively small rise in urinary pH and citrate, and they maintained higher mean levels of indicators of bone metabolism (osteocalcin, alkaline phosphatase, hydroxyproline) despite continuous administration of PC. It was concluded that although the PC tablet preparation was effective it may not be an ideal anti-stone drug treatment in the long term and that, especially in hypocitraturics, the intrinsic metabolic defect of RCU may not be sufficiently well controlled.
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PMID:Citrate and recurrent idiopathic calcium urolithiasis. A longitudinal pilot study on the metabolic effects of oral potassium citrate administered over the short-, medium- and long-term medication of male stone patients. 155 90

The main risk factors for calcium urolithiasis that are clinically detectable are low diuresis, hypercalciuria, hyperruricuria, alkaline urinary pH, hyperoxaluria, hypomagnesuria, hypocitraturia. They should be evaluated, all the more precisely that the disease is active, under both the urological and metabolic points of view, using 24 hour urine collection made at home on a free diet with a dietary record. In the majority of the cases the calcic urolithiasis is idiopathic, i.e. not related to a cause of secondary hypercalciuria like primary hyperparathyroidism, or to a hyperroxaluria either primary or of digestive or toxic origin. Its treatment if mainly dietary with high fluid intake (diuresis greater than 2 1/24 h), normoclacic diet (800-1000h mh/24 h) with meat but not dairy product restriction, oxalate salts, carbohydrate and alcohol restriction. These dietary recommendations should be controlled by measuring the above cited parameters in the 24 hour urine samples and by measuring urea excretion which should not exceed 0.33 g/kg of body weight. When diet fails, drugs may be added mainly allopurinol, thiazides and potassium citrate.
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PMID:[Physiopathology, exploration and treatment of calcium lithiasis]. 178 95

Nephrolithiasis is a heterogeneous disorder, with varying chemical composition and pathophysiologic background. Although kidney stones are generally composed of calcium oxalate or calcium phosphate, they may also consist of uric acid, magnesium-ammonium phosphate, or cystine. Stones develop from a wide variety of metabolic or environmental disturbances, including varying forms of hypercalciuria, hypocitraturia, undue urinary acidity, hyperuricosuria, hyperoxaluria, infection with urease-producing organisms, and cystinuria. The cause of stone formation may be ascertained in most patients using the reliable diagnostic protocols that are available for the identification of these disturbances. Effective medical treatments, capable of correcting underlying derangements, have been formulated. They include sodium cellulose phosphate, thiazide, and orthophosphate for hypercalciuric nephrolithiasis; potassium citrate for hypocitraturic calcium nephrolithiasis; acetohydroxamic acid for infection stones; and D-penicillamine and alpha-mercaptopropionylglycine for cystinuria. Using these treatments, new stone formation can now be prevented in most patients.
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PMID:Etiology and treatment of urolithiasis. 196 46

Seventeen hypercalciuria patients (8 control, 9 treatment) with a history of urolithiasis were randomly selected to receive low-calcium, low-oxalate diets with or without the addition of 30 g of dietary fiber as unprocessed wheat bran. Diet alone resulted in a 5.6 percent decrease in calciuria compared with a 23.5 percent decrease with the addition of the fiber. The addition of hydrochlorothiazide and potassium citrate further reduced calciuria by 40.4 percent and 34.5 percent, respectively. Oxaluria was decreased 21.4 percent by diet alone compared with 3.9 percent in the diet and fiber treatment group. Patient compliance to diets was good, and no complications resulted from fiber intake.
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PMID:Effect of unprocessed wheat bran on calciuria and oxaluria in patients with urolithiasis. 215 68

Long-term effects of potassium citrate therapy (usually 60 mEq/day) were examined in 53 patients with renal stones (11 with uric acid lithiasis with complication of calcium stones, 10 with hypocitraturia as the sole abnormality, and 28 with hypocitraturia occurring with other abnormalities such as absorptive hypercalciuria, renal tubular acidosis, hyperuricosuric calcium oxalate nephrolithiasis, and enteric hyperoxaluria). Potassium citrate was given alone in 29 patients, added to thiazide and/or allopurinol treatments in 12 patients who continued to form stones on these treatments, and begun concurrently with thiazide and/or allopurinol in 12 patients with hypocitraturia and other defects (hypercalcuria and/or hyperuricosuria). In all three groups of patients, urinary citrate and pH significantly increased during potassium citrate treatment. Urinary saturation of calcium oxalate significantly declined while that of brushite remained unchanged. The propensity for the spontaneous nucleation of calcium oxalate, determined from the minimum amount of added oxalate required to elicit precipitation, declined. The treatment was effective in preventing new stone formation in all three groups. Stone passage rate declined from 5.14-7.41 stones/patient year before potassium citrate treatment to 0.66-1.33 stones/patient year during treatment, and 75.0-91.7% of patients were in remission. In patients who relapsed on other treatments (with passage of 5.14 stones/patient year), the addition of potassium citrate to the ongoing treatment program reduced stone formation to 1.33 stones/patient year and caused remission in 91.7% of patients. In 14 of 33 patients with preexisting radiopaque stones, there was radiological evidence of a reduced number of stones after 8 months-2 years of potassium citrate treatment. In conclusion, potassium citrate restores normal urinary citrate, decreases saturation and propensity for spontaneous nucleation of calcium oxalate, and inhibits new stone formation.
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PMID:Physiological and physiochemical correction and prevention of calcium stone formation by potassium citrate therapy. 667 57

The circadian (circannual for oxalic acid) variations of 13 urinary variables (volume, creatinine, calcium, oxalic acid, glycolic acid, 17-ketosteroids, 17-hydroxycorticosteroids, phosphates, urea, uric acid, chloride, sodium, and potassium) have been documented in 7 calcium oxalate renal stone formers and 7 healthy men (control group). Urine was collected every 4 h over a period of 24 h. All subjects had the same synchronization: diurnal activity from 07(00) to 23(00) +/- 1 h and nocturnal rest; meals were given at fixed clock hours (08(00), 12(30) and 20(00) +/- 1 h). A statistically-significant rhythm (p less than 0.05) was validated for all variables except urea and calcium in healthy men. In renal stone formers, 6 variables (calcium, oxalic acid, and glycolic acid in particular) had no detectable circadian rhythm. However, a periodicity of c. 8 h (ultradian rhythm) was demonstrated for calcium and oxalic acid with peaks being located around 02(00), 10(00), and 18(00). No circannual variations in oxalic acid output could be observed. The present study shows an alteration of the periodicity of calcium and oxalic metabolisms, i.e. the loss of a circadian (24-h) rhythm and the occurrence of an ultradian rhythm of 8 h. The risk of calcium-oxalate crystallisation appears thus greater at 02(00), 10(00), and 18(00). Furthermore, any study dealing with oxalic acid excretion should state the season of urine collection when comparing renal stone formers and healthy subjects, as significant differences in oxaluria may appear during the summer months and not during the rest of the year.
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PMID:Alterations in circadian rhythmicity in calcium oxalate renal stone formers. 686 98

The serum and urinary biochemical changes observed one month and six months after oral potassium citrate therapy (600 mEq/day) in 119 patients with calcium oxalate calculi were compared with those of 16 untreated cases with lithiasis. The patients that received treatment were previously divided into two groups: group A comprised 61 hypocitraturic patients and group B comprised 58 patients with other urinary disorders who were normo or hypocitraturic. The urinary pH increased by approximately half a point in both treated groups. In group A calciuria increased slightly from 180 +/- 8 to 216 +/- 10 mg/24 h but remained within the normal ranges. Creatinuria, oxaluria, uricosuria and diuresis showed no changes. Citraturia increased very significantly in both groups and more markedly in the hypocitraturic group of patients (from 198 +/- 13 to 476 +/- 35 mg/24 h). The LRC (lithogenic risk coefficient = Ca/Cit x Diu) dropped by 50%. The patients tolerated the treatment regimen well; of the 119 treated patients, only 11 abandoned treatment due to GI intolerance.
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PMID:[Biochemical effects of potassium citrate in the treatment of calcium oxalate lithiasis]. 800 70

In order to better understand the role of diet in etiology of urolithiasis, 84 oxalo-phospho-calcic-lithiasic patients (52 men, 32 women) have been studied by a nutritional week-interview and by urinary and blood testing. Diet data were compared to an ideal standard. Total caloric intake was 2428 +/- 651 calories/d; this intake is high in 7% women and 40% men. 79% out of patients are fat. Protidic intake is 87 +/- 21 g/d higher than 1 g/kg/d in 84.5% of patients. Lipids are high in 38.9 +/- 7%, glucid are low in 45.3 +/- 7%. Calcium intake is 934 +/- 406 mg/d, sodium intake is 12.9 + 3 g/d. Water intake is 2305 +/- 759 ml/d. Different groups of patients are studied: a) 21 patients with mean age of 43 +/- 12 years have recurrent lithiasis (R). This group is compared to 48 patients with 37 +/- 44 years who have a single lithiasis. Half of (R) patients have hypercalciuria, hyperphosphaturia and hyperoxaluria. Diet study is no different between these two groups. b) Other groups are studied: 21 have hyperophosphaturia (HPU) without hypophosphoremia and they have hypercalciuria, hyperuraturia and high urinary urea; diet shows higher glucicid and potassium intake than group with normal phosphaturia; 23 have hypercalciuria (HCU) and high uraturia and phosphaturia: diet study shows no difference with a group with normal calciuria. 21 have hyperoxaluria (HOU): diet study of a normal oxaluric group shows higher lipid intake, lower glucidic and calcium intake; 22 have hyperuraturia (HAU) and higher urinary urea, sodium and potassium than normouraturia group: in this group potassium intake is higher.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Results of dietary evaluation during calcium oxalate and calcium phosphate lithiasis]. 814 88

The effects of clofibrate feeding (5 g/kg diet) on oxalate metabolism were investigated in male and female rats. Following clofibrate feeding, 24-hour urinary excretion of oxalate increased until 4 days and then reached a plateau. Whereas the contribution of dietary oxalate (1.4 g/kg diet, as potassium salt) to urinary oxalate was less than 5% in both control and clofibrate-treated male rats, the contribution of dietary glycolate (1.0 g/kg diet, as sodium salt) to urinary oxalate was six times higher in clofibrate-treated male rats compared with controls, indicating that the clofibrate-induced hyperoxaluria is due to increased endogenous biosynthesis of oxalate. This was supported by the increased lactate dehydrogenase (LDH) activity observed in liver supernatants of clofibrate-treated rats compared with controls, and the increased rate of conversion of glycolate and glyoxylate to oxalate by clofibrate-treated male rat liver supernatants. Female rats had lower excretion of urinary oxalate and lower levels of liver glycolic acid oxidase (GAO) as compared with males. Clofibrate-treated female rat liver supernatants had higher LDH levels and produced more oxalate from glyoxylate. Thus, it can be concluded that the increase in LDH activity may be the cause of the increased endogenous biosynthesis of oxalate leading to increased urinary excretion of oxalate in male and female rats treated with clofibrate.
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PMID:Clofibrate feeding to Sprague-Dawley rats increases endogenous biosynthesis of oxalate and causes hyperoxaluria. 903 Aug 17

Considerable progress has been made regarding pathophysiology, diagnosis, and medical prevention of recurrent renal stone formation. The medical approach is not applied widely because of the availability of extracorporeal shockwave lithotripsy and the complexity of medical diagnostic and treatment modalities. In this review, a simplified program for the medical management of stones is described. From analysis of stone risk factors in 24-hour urine specimens, uncomplicated calcium stone disease is separated from other stone diseases. The uncomplicated calcium stone disease, comprising the illness in the majority of patients with recurrent renal calculi, is characterized by normocalcemia, normouricemia, calcium stones, and the absence of urinary tract infection, bowel disease, or marked hyperoxaluria. Uncomplicated calcium stone disease is separated into a hypercalciuric group and a normocalciuric group. In the simplified treatment program, the hypercalciuric group would be offered thiazide plus potassium citrate, whereas the normocalciuric group would receive potassium citrate alone.
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PMID:Southwestern Internal Medicine Conference: medical management of nephrolithiasis--a new, simplified approach for general practice. 909 51


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