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

We examined the medical records of renal transplantation patients at our institution to determine the incidence and etiology of renal calculi after renal transplantation. Of 7 patients identified calculi formed on the basis of congenital hyperoxaluria in 2, secondary to chronic urinary infection in 1 and from iatrogenic causes in 4. We review the various surgical and radiological procedures used to treat these renal transplant patients. We also discuss the role of the new treatment modalities in managing urolithiasis in transplant recipients.
J Urol 1988 Dec
PMID:Current operative management of urinary calculi after renal transplantation. 305 22

The influence of a calcium-rich mineral water on urine crystallisation in patients with recurring kidney stones was investigated. A calcium and magnesium rich water like the one tested increases the calcium and magnesium content of the urine but decreases oxaluria even after a dietary oxalate load.
Minerva Med 1987 Dec 31
PMID:[Prevention of the recurrence of urinary lithiasis: mineral waters with high or low calcium content?]. 343 28

Pyridoxine (vitamin B6), given to patients with primary hyperoxaluria of type I, generally leads to a decrease in urinary excretion of oxalate owing to stimulation of conversion of glyoxylate to glycine instead of oxalate. It is not known, however, whether pyridoxine would equally influence hyperoxalurias of other origins, e.g. idiopathic or enteric. Two groups of patients were therefore given pyridoxine orally for 2 months (300 mg/d). Group 1 consisted of 10 idiopathic stone formers with mild hyperoxaluria of unknown origin. Group 2 consisted of 4 patients with enteric hyperoxaluria after intestinal bypass surgery. As a mean, enteric hyperoxaluria was not influenced by vitamin B6, which suggests that this disorder is the consequence of intestinal hyperabsorption of oxalate rather than of glyoxylate. In contrast, idiopathic hyperoxaluria was influenced by vitamin B6: urinary excretion of oxalate decreased in 8 patients out of 10 and became normal in 7. However, two patients did not respond to pyridoxine; both had concomitant severe hyperuricosuria (greater than 1 g/24 h), an observation suggesting that in these cases hyperoxaluria was of dietary origin. Four of the patients whose urinary excretion of oxalate became normal while on pyridoxine were followed up for 8 to 36 months after treatment: in all of them oxaluria remained normal. One whose oxaluria had returned to the upper normal limit was retreated after 2 years and again displayed a fall in urinary oxalate. It is concluded that pyridoxine given to idiopathic hyperoxalurics may correct the disorder, as in primary hyperoxaluria of type I; this is not the case in enteric hyperoxaluria. The mechanisms governing this sensitivity to vitamin B6 remain to be clarified.
Schweiz Med Wochenschr 1986 Dec 13
PMID:[Pyridoxine can normalize oxaluria in idiopathic renal lithiasis]. 379 70

Oral oxalate loading using sodium oxalate or a vegetable juice was done to evaluate the intestinal absorption of exogenous oxalate in 30 patients with renal stones and 13 healthy controls. Fifteen calcium oxalate stone formers, 7 non-oxalate stone formers and 10 healthy volunteers were given an oral loading of sodium oxalate (500 mg). Urinary oxalate increased promptly, reaching a peak value within 4 to 8 hours after administration of a synthetic oxalate orally in a fasting state. In calcium oxalate stone formers, the mean increment of urinary oxalate and the bioavailability following oral sodium oxalate load were significantly higher than in the healthy controls and non-oxalate stone formers. Furthermore, intestinal hyperabsorption of oxalate in our criterion was defined in six patients with calcium oxalate stones (40%). On the other hand, eight calcium oxalate stone formers and three healthy controls were given vegetable juice. Urinary oxalate was increased only slightly after the ingestion, and there was no difference between calcium oxalate stone formers and normal controls. These results suggest that a certain hyperoxaluria might be induced by intestinal absorption of exogenous oxalate, and that the hyperabsorption might indicate a possible risk factor for calcium oxalate stone formation.
Hinyokika Kiyo 1986 Dec
PMID:[Renal oxalate excretion following oral oxalate load in patients with urinary calculus disease and healthy controls]. 382 24

Urinary excretion rate of oxalate was measured in 79 patients with idiopathic calcium (Ca) nephrolithiasis and the results were compared with those obtained in 28 healthy volunteers. The group of stone formers consisted of 20 patients with idiopathic hypercalciuria (IHC) of the absorptive type, 23 patients with IHC of the renal type, 11 patients with hypercalciuria secondary to dietary factors, 1 patient with hyperuricosuria (as an isolated finding) and 24 patients without hypercalciuria nor hyperuricosuria. Classification was based upon the urinary excretion rate of uric acid, as well as that of calcium measured under 3 different dietary conditions (i.e. free diet, free diet supplemented with 3 g Ca/day for 3 days, and diet free of dairy products for 5 days). On a free diet, normal values of oxaluria ranged from 125 to 435 mumol/24 h; an elevated value was observed in 11 (14%) patients, 5 of whom belonged to the subgroup without hypercalciuria nor hyperuricosuria. On a low Ca diet, mild hyperoxaluria occurred in 3 controls and in 19 patients, the tendency to develop hyperoxaluria being particularly marked in the subgroup with absorptive-IHC. Moreover, there was a positive correlation between oxaluria on a low Ca diet and the estimated degree of intestinal absorption of Ca. This study confirms the finding that on a free diet, the incidence of mild hyperoxaluria amongst idiopathic stone formers is rather low. It shows, however, that a significant percentage of patients classically referred to as "without metabolic disorder" have in fact slight hyperoxaluria, an observation with a potential therapeutic impact. Finally, it shows that on a low Ca diet, patients with absorptive-IHC are particularly prone to develop hyperoxaluria: the latter observation renders questionable the relevance of a low Ca diet for patients with absorptive IHC, unless their intake of oxalate is simultaneously reduced.
Schweiz Med Wochenschr 1982 Dec 04
PMID:[Incidence of hyperoxaluria in idiopathic calcium nephrolithiasis]. 717 77

Of 150 patients in whom jejunoileal bypass was performed for the treatment of morbid obesity, the intestinal bypass was converted to a gastric bypass in nine individuals. The indications for conversion have been weight regain, inadequate weight loss or pathologic hyperoxaluria with recurrent kidney stone formation. In all of our patients, dismantling of the jejunoileostomy and the gastric procedure was done simultaneously.
Surg Gynecol Obstet 1980 Dec
PMID:Conversion of malfunctioning intestinal bypass to gastric bypass. 744 33

A shortened small intestine may end at a stoma or be anastomosed to the colon. Patients with a jejunostomy, but not those with a colon, lose large amounts of sodium. The intake and absorption of sodium can be increased by sipping a sodium-glucose solution; stomal loss can be reduced by restricting water or low-sodium drinks. If a stoma is situated less than 100 cm along the jejunum, a constant negative sodium balance may necessitate parenteral saline supplements. Gastric anti-secretory drugs or a somatostatin analogue reduce jejunostomy losses in such patients but do not restore a positive sodium balance. Loperamide or codeine phosphate benefit some patients. Magnesium deficiency can usually be corrected by oral magnesium oxide supplements. An elemental or hydrolysed diet is not beneficial. Patients with a jejunostomy can maintain a normal diet without fat reduction. When the colon is present, unabsorbed carbohydrate is fermented to absorbable short chain fatty acids. Unabsorbed long chain fatty acids and bile salts cause watery diarrhoea and increased colonic oxalate absorption with hyperoxaluria. Such patients benefit from a high carbohydrate, low-fat and low-oxalate diet. Parenteral nutrition is needed only by the few patients unable to maintain health or avoid socially disabling diarrhoea despite these measures.
Aliment Pharmacol Ther 1994 Dec
PMID:Review article: practical management of the short bowel. 769 44

To evaluate the clinical utility of in vitro calcium oxalate monohydrate (COM) crystallization kinetics measurements and to determine the effect of quantitative removal of urinary Tamm-Horsfall glycoprotein on such measurements, we examined 24-hour, room temperature urine collections of patients from our Stone Clinic and of normal subjects from our research laboratories at Ochsner Medical Institutions in New Orleans, LA, and compared their COM kinetic parameters in vitro before and after urine ultrafiltration (30 kd). Data from 53 calcium oxalate stone-forming patients (26% women; mean age, 47 years) who demonstrated radiographic or other evidence of forming at least one stone were compared with data from 22 healthy volunteers (25% women; mean age, 40 years). Hypercalciuria (> 7.5 mm/24 hr), hyperoxaluria (> 0.5 mm/24 hr), and hypocitraturia (< 2.0 mm/24 hr) were present in 38%, 26%, and 26% of the patient population, respectively. Urinary creatinine, urate, calcium, citrate, phosphate, oxalate, pH, volume, total immunoreactive-disaggregated Tamm-Horsfall glycoprotein, and the urine's effects on COM solubility, percent crystal growth inhibition, and crystal agglomeration inhibition [tm] were determined. Calcium oxalate monohydrate agglomeration inhibition, [tm], was reduced in stone-forming patients. It decreased with increasing stone frequency, making [tm] a useful tool for measuring the risk of stone recurrence. Urinary Tamm-Horsfall glycoprotein and citrate concentrations were linearly related to COM agglomeration inhibition. Their effects were synergistic. Tamm-Horsfall glycoprotein removal from urine reduced COM agglomeration inhibition dramatically. Alkali therapy increased urinary citrate concentration and increased [tm].(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Kidney Dis 1994 Dec
PMID:Calcium oxalate stone agglomeration reflects stone-forming activity: citrate inhibition depends on macromolecules larger than 30 kilodalton. 798 66

About 80% of all renal stones contain calcium oxalate and/or calcium phosphate as their main crystalline components. The most important risk factors for increases in calcium oxalate crystallization are low urine volume, hyperoxaluria and hypocitraturia. Hypercalciuria, however, is of secondary importance as a cause of increased crystallization: whereas calcium and oxalate crystallize in a 1:1 ratio, the molar concentration ratio in urine amounts to about 10:1 in favor of calcium. Therefore, increases in urinary calcium will not be followed by a rise in crystallization as long as oxalate remains constant, whereas even the slightest increases in urinary oxalate immediately cause more crystals to precipitate. Thus, low calcium diet is not only unnecessary but is contraindicated since it may cause secondary hyperoxaluria (increased intestinal oxalate absorption) and osteopenia (negative calcium balance). On the other hand, overconsumption of animal protein (meat, poultry, fish) induces more pronounced hyperoxaluria and hypocitraturia and contributes to an overall negative calcium balance. It is, however, only by the interplay of "bad" dietary habits with underlying abnormalities such as up-regulation of calcitriol production, incomplete renal tubular acidosis or defective macromolecular crystallization inhibitors, that people become recurrent calcium renal stone formers.
Schweiz Med Wochenschr 1995 Dec 26
PMID:[Diagnostic markers in calcium nephrolithiasis--current and traditional ideas with a new look]. 857 Oct 96

The introduction of renal ultrasound technology has shown renal calcification to be more common in infancy than was previously believed. Understanding the role of inhibitors and promoters in crystal formation helps elucidate the pathophysiology of nephrocalcinosis. Identification of the presence or absence of hypercalcemia and hypercalciuria is an effective way to direct the diagnostic work-up of infants with nephrocalcinosis. The sonographic image of renal calcification resolves spontaneously in many infants. Whether microscopic nephrocalcinosis persists below the threshold of ultrasonographic detection is unknown. Renal calcification can be associated with persistent renal function abnormalities if hypercalciuria continues, such as in VLBW infants who receive long-term furosemide therapy after discharge from the hospital. Renal calcification may also progress to renal failure, such as in infants with primary hyperoxaluria, owing to the persistence of hyperoxaluria, a potent promoter of calcium crystal formation.
Pediatr Clin North Am 1995 Dec
PMID:Renal calcification in the first year of life. 861 92


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