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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Almost all segments of the gastrointestinal tract have been used as urinary tract substitutes. The specific nutritional and gastrointestinal complications depend on the particular portion of bowel that is removed from the alimentary tract. The use of stomach theoretically may predispose the patient to hypergastrinemia and peptic ulcer disease, hypocalcemia, and iron deficiency or megaloblastic anemia. Resection of a large amount of jejunum causes malabsorption. Limited use of colon segments usually is well tolerated, but loss of large parts of the colon directly decreases available absorptive area, resulting in diarrhea. Resection of the ileum and ileocecal valve can lead to several disease states. One is mixed secretory-osmotic diarrhea. Decreased ileal reabsorption of bile salts results in fat malabsorption and steatorrhea. The presentation of increased amounts of bile salts and fatty acids to the colon decreases water absorption and stimulates active chloride and water secretion, producing a cholera-like high-volume secretory diarrhea. The loss of the ileocecal valve and ileum segment accelerates intestinal transit time, which does not allow for complete digestion and absorption of food. Water and electrolytes remain associated with undigested food particles and may overwhelm the absorptive capacity of the colon, resulting in an osmotic diarrhea. A second problem is vitamin B12 deficiency. Surgical reduction of sites in the terminal ileum for active and exclusive uptake of vitamin B12 might lead to hypovitaminosis. If this is unrecognized, patients may develop irreversible neurologic injury. A third problem is cholelithiasis. Derangements in bile salt metabolism can occur when as little as 10 cm of ileum is resected, and the propensity to form gallstones is increased. Pigment gallstones appear to be the predominant stone associated with ileal resections. The fourth possible problem is urolithiasis, the etiology of which is multifactorial in patients with ileal resections. With decreased availability of bile salts, fat malabsorption occurs. Fatty acids bind with calcium and magnesium to form soaps, resulting in increased levels of free oxalate available for absorption. Moreover, fatty acids directly increase colonic permeability to oxalate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutritional and gastrointestinal complications of the use of bowel segments in the lower urinary tract. 194 6

In 26 healthy individuals and 114 patients with urolithiasis, total urine protein levels were measured in a single sample by using the stain ponceau S. The findings were statistically analyzed. The levels of the protein were found to be 27-80 mg/l in the healthy individuals, while the distribution of the data was asymmetric as viewed from high values. The patients with urolithiasis exhibited their protein levels according to the type of nephrolithiasis. Proteinuria was demonstrated to be less pronounced in patients with oxalate and urate nephrolithiasis than in patients with coral phosphate calculi. There was a substantial asymmetry in the distribution of total urine protein for all the examined groups of urolithiasis patients, as well as great dispersion values, which fails to regard the parameter alone as a diagnostic criterion for the type of nephrolithiasis. At the same time it was noted that simultaneous examination of the levels of total protein, uric acid, potassium, and sodium enabled the type of a concrement (oxalate or phosphate) to be in vivo estimated with approximately 85% probability.
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PMID:[Total urinary protein in different types of nephrolithiasis]. 194 15

A 46-year-old Japanese man with familial primary hyperoxaluria had been suffering from urolithiasis since the age of 6 years and had been treated by hemodialysis for 8 years before his death. The alpha-ketoglutarate glyoxylate carboligase and serine pyruvate transoxylase activities in the patient's liver had markedly decreased, indicating type I primary hyperoxaluria. Ocular tissues obtained at autopsy were studied immunohistochemically and histochemically. The ocular alterations were characterized by an unusual distribution of oxalate deposits, mainly located in the outer plexiform layer and the nuclear layer but not in the retinal pigment epithelium or in the vascularized layer of the sensory retina. These distributions of the oxalate deposits were determined to be unrelated to the blood vessels.
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PMID:Ocular histopathologic findings in a 46-year-old man with primary hyperoxaluria. 173 9

Hyperoxaluria is an important risk factor in patients who form calcium oxalate stones within the urinary tract. It occurs in patients with primary hyperoxaluria, enteric hyperoxaluria, and the syndrome of idiopathic calcium oxalate urolithiasis. In the latter condition, the specific causes of the hyperoxaluria are not well defined. Diet and the availability of calcium and oxalate from the diet within the intestine are important factors in the hyperoxaluria that is present in some of these patients with idiopathic calcium oxalate urolithiasis. Other abnormalities in endogenous metabolism or transport of oxalate may play a role in the hyperoxaluria in some of these patients.
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PMID:Diet and hyperoxaluria in the syndrome of idiopathic calcium oxalate urolithiasis. 200 1

Evidence suggests that the formation of calcium-oxalate stones in the urine is dependent on the saturation levels of both calcium and oxalate; thus, management of one or both of these ions in individuals susceptible to urolithiasis appears important. Since there are no known naturally occurring enzymes in vertebrates capable of degrading oxalate, we have initiated a study to insert a plant-derived oxalate degrading enzyme gene into human cells as a means of lowering plasma and urinary oxalate concentrations. We present here the cloning of the oxalyl-CoA decarboxylase gene from the bacterium Oxalobacter formigenes and its subsequent expression in a foreign environment. These results provide the basis for eventual transfer of an oxalate decarboxylase gene into mammalian cells.
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PMID:Cloning and expression of the oxalyl-CoA decarboxylase gene from the bacterium, Oxalobacter formigenes: prospects for gene therapy to control Ca-oxalate kidney stone formation. 200 3

The physical chemical approach to the investigation of the calcium oxalate (CaOx) crystallization and urolith formation is the systematic examination of the various aspects of mineral precipitation and growth in pure solution, in the presence of individual urinary components, and in whole urine media. Recent experimental studies have indicated that while small urinary ions such as citrate, magnesium, and phosphocitrate retard the mineralization rate of CaOx, urinary macromolecules may act either as inhibitors of growth or promoters of nucleation. Some CaOx mineralization inhibitors have also been found to influence the growth mechanism of the phase and its flocculation properties. Therefore, urinary macromolecules that are adsorbed on the mineralizing crystals and incorporated into the developing stone may play a significant role in urolithiasis.
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PMID:Physical chemical studies of calcium oxalate crystallization. 200 5

Calcium oxalate (CaOx) urolithiasis in rats is induced by producing hyperoxaluria. Depending on the degree and length of hyperoxaluria, CaOx crystals may either form in the nephron or the bladder and may or may not be retained in the kidneys. Crystals may nucleate in one part of the nephron and be retained in another part. Papillary collecting duct tubular epithelium and its basement membrane appear to be involved in crystal retention in the kidneys.
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PMID:Pathogenesis of oxalate urolithiasis: lessons from experimental studies with rats. 200 7

Glycosaminoglycans (GAG) are polysaccharide chains composed of repeating disaccharides of identical composition. Little is known about the mechanism of their excretion, but there is no doubt that urinary GAGs are degradation products of high molecular weight proteoglycans. Renal excretion takes place chiefly as glomerular filtration, and tubular reabsorption or secretion has not been demonstrated. Differences in the literature comparing GAG excretion in urolithiasis patients and healthy subjects are mainly attributable to methods of analysis and noncomparability of the investigation conditions. We found no differences between the two groups in several series. It is interesting to note that GAG excretion in men is significantly higher than in women, that a circadian rhythm of GAG concentration and excretion occurs in healthy subjects on a standardized diet, and that values are raised postprandially and at night. Seasonal course of GAG excretion curves is almost synchronous for men and women, irrespective of the absolute values, and GAG excretion in the spring and summer significantly exceeds that in winter months by up to 50%. All crystallization models cited demonstrate that GAG reduce the risk of calcium oxalate stone formation. Inhibitors of crystal growth and aggregation act by blocking the growth sites. Inhibition of calcium oxalate crystallization is also attributed to direct binding of calcium to GAG. In the presence of urate ions, and favorable pH, the ability of chondroitin sulfate C to bind calcium may be impaired by as much as 31%. These measurements support the concept that urate ions interact with GAG in urine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of glycosaminoglycans for the formation of calcium oxalate stones. 200 9

Between June 1979 and June 1989, 54 children with urolithiasis were evaluated and treated at the Johns Hopkins Children's Center. The most common symptoms were flank or abdominal pain (58%) and gross hematuria (28%). In 46 children (86%), stones were secondary to a preexisting condition and in only 8 (14%) no apparent cause of stone formation could be found. Thirty-six patients (66%) had a solitary stone, most commonly found in the kidney. Urinary tract infections were present in 25 (47%) of the patients who had stones. Stones composed either of calcium oxalate or struvite were the most frequently recovered in these patients with infections. Twenty-one patients (39%) spontaneously passed their stones whereas 23 (43%) required either surgery or extracorporeal shock-wave lithotripsy to resolve stones. Ten (20%) showed recurrence of their urolithiasis, with follow-up examination periods ranging from 1 month to 10 years. Recent advances in the management of urolithiasis and their applicability to the pediatric population are discussed.
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PMID:Childhood urolithiasis: experiences and advances. 201 20

Previous studies have shown that hypomagnesuria induced by magnesium deficient diet causes calcium oxalate crystal deposition in renal tubules of hyperoxaluric rats and administration of magnesium to these rats results in prevention of calcium oxalate crystallization in their kidneys. Based on these studies magnesium was claimed to be beneficial for calcium oxalate stone patients. However, hypomagnesuria is not a common phenomenon. To better understand the role of magnesium as an inhibitor of calcium oxalate crystallization in urine, we studied the effect of magnesium on calcium oxalate urolithiasis in rats on a regular diet and a hyperoxaluric protocol. Excess magnesium was administered to male rats on regular diet and a lithogenic protocol. Magnesium administration to hyperoxaluric rats did not result in significant changes in urinary excretion of calcium or oxalate or in calcium oxalate relative supersaturation. Urinary excretion of citrate was also not significantly altered. Some animals from both groups, those on magnesium therapy and those not on magnesium therapy had crystals deposited in their renal tubules. We conclude that excess magnesium has no significant effect on calcium oxalate urolithiasis in normomagnesuric conditions.
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PMID:Effect of magnesium on calcium oxalate urolithiasis. 201 99


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