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

The current concepts of normal fat absorption and the entero-hepatic circulation of bile acids are being reviewed with emphasis on the steps which are clinically important. Based on an understanding of normal physiology, diseases associated with steatorrhea can be classified according to pathogenetic mechanisms. In some diseases the pathogenesis of the steatorrhea is not understood. Malabsorption of fat and bile salts can have characteristic consequences such as nutritional deficiencies, diarrhea, hyperoxaluria with nephrolithiasis, and cholelithiasis. For quantitative assessment of steatorrhea chemical analysis of fecal fat is necessary.
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PMID:[Absorption and malabsorption of fat and bile acids (author's transl)]. 89 17

Hyperoxaluria was documented in patients with pancreatic insufficiency, adult celiac disease, regional enteritis after ileectomy and partial colectomy, and jejunoileal bypass. The degree of hyperoxaluria correlated directly with the severity of the steatorrhea and inversely with the dietary calcium content. High-calcium diets suppressed oxalate excretion to normal when fecal fat excretion was approximately 30 g/day or less. In patients with more severe steatorrhea, decreasing dietary fat and oxalate content further reduced urinary oxalate excretion. These data suggest that, while steatorrhea is the most important determinant for enhanced absorption of dietary oxalate, variations in dietary calcium content modulate the amount of oxalate absorbed.
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PMID:Hyperoxaluria and intestinal disease. The role of steatorrhea and dietary calcium in regulating intestinal oxalate absorption. 92 Jun 94

Clinical studies suggest that steatorrhoea can be associated with excessive absorption of dietary oxalate. We examined the influence of bile salts, Ca++, and long-chain fatty acid on the absorption of oxalate and water by rat intestine in vivo. Absorption was measured under steady-state conditions during single-pass infusions. Each intestinal segment served as its own control. In jejunum, 10 mM taurocholate, the principal salt in rat bile, depressed absorption of oxalate and water. Absorption was not depressed further by Ca++ or linoleic acid. In ileum, 10 mM taurocholate did not inhibit absorption. Linoleic acid, 2 mM, depressed absorption of both oxalate and water. In colon 10 mM taurocholate decreased absorption. Net water transport was depressed further when linoleic acid was added to the infusion, but oxalate absorption was enhanced. Ca++ negated these effects of linoleic acid. It is concluded that long-chain fatty acids may enhance the absorption of oxalate from the rat colon. This observation may be relevant to understanding hyperoxaluria in patients with steatorrhoea.
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PMID:Regional differences in oxalate absorption by rat intestine: evidence for excessive absorption by the colon in steatorrhoea. 115 92

Hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. Steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.
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PMID:Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case. 136 95

A 58-year-old female patient admitted to hospital for advanced renal failure had a 40 years' history of Crohn's disease and had undergone ileocecal resection. Nevertheless, chronic diarrhea persisted. Subsequently calcium oxalate stones in the urine were repeatedly observed. Progressive renal failure developed. The investigation of the patient showed severe steatorrhea and pronounced hyperoxaluria, and renal biopsy showed severe chronic interstitial nephritis with calcium oxalate crystals. The skin biopsy revealed severe calcium oxalate vasculitis. The pathophysiology and therapy of secondary hyperoxaluria due to small bowel resection are discussed.
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PMID:[Secondary oxalosis following small bowel resection with kidney insufficiency and oxalate vasculopathy]. 160 91

Enteric hyperoxaluria due to malabsorption syndromes has been well documented to cause renal calculi and chronic tubulointerstitial renal damage. Rarely, in the setting of intestinal bypass operations for morbid obesity, enteric hyperoxaluria has produced acute renal failure. We report two patients who suffered acute deterioration of renal function associated with increased intestinal absorption and renal excretion of oxalate associated with steatorrhea. One patient had a large portion of his small bowel resected many years prior to the onset of the renal failure and the second patient had chronic pancreatitis causing steatorrhea. Both patients had renal biopsy documentation of the acute nature of the tubular damage produced by oxalate deposition. The mechanisms of their deterioration of renal function may relate to sudden increases in steatorrhea in association with episodes of volume depletion. Enteric hyperoxaluria may be an easily overlooked and potentially preventable etiology of acute renal dysfunction.
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PMID:Acute deterioration of renal function associated with enteric hyperoxaluria. 222 62

Urinary oxalate concentrations were measured in 45 patients with quiescent Crohn's disease, four patients with chronic pancreatitis and five healthy subjects after a normal oxalate (150 g/day) diet, after a high-fat (150 g/day), normal oxalate diet and after and after a high-oxalate (500 mg/day) diet. Urinary oxalate concentrations were significantly (P less than 0.05) higher in patients with Crohn's disease and steatorrhoea, but not in those with chronic pancreatitis, after administrating a high-oxalate diet compared with healthy subjects. Mean oxalate values were 19.1 mg/24 h in controls compared with 65.8 mg/24 h in Crohn's disease patients. A direct correlation (r = 0.37, P less than 0.01) was established between faecal rats and urinary oxalate after oval oxalate load: this correlation (r = 0.43, P less than 0.01) is closer when only patients with Crohn's disease are considered. The study, therefore, confirmed a correlation between steatorrhoea and hyperoxaluria in patients with Crohn's disease; however, the high percentage of false positive results limits the use of urinary oxalate concentrations as a reliable indicator of lipid malabsorption. It is concluded that, at present, measurement of urinary oxalate cannot be recommended as a valid alternative to the Van de Kamer method for diagnosing lipid malabsorption.
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PMID:Urinary oxalate recovery after oral oxalic load: an alternative method to the quantitative determination of stool fat for the diagnosis of lipid malabsorption. 262 29

Hyperoxaluria and calcium oxalate lithiasis have a multifactorial genesis in bowel diseases. The augmented synthesis of oxalic acid in the liver is of minor importance. A diminished bacterial degradation is to asses up to day only hardly. The increasing absorption is of highest importance by deficient production of calcium oxalate in the intestinal tract and by increasing permeability of colonic mucosa above all in steatorrhoea or in patients with augmented calcium absorption. The crystallization of calcium oxalate in the urine is promoted by shortage of vitamin A, citrate, zinc or magnesium.
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PMID:[Pathogenesis of hyperoxalurias and calcium oxalate calculi in intestinal diseases]. 331 5

Malabsorptive states are frequently associated with increased urinary oxalate excretion. The authors describe a 10-year-old girl with steatorrhea, hyperoxaluria, and a renal calculus in a single functioning kidney. Successful management of steatorrhea corrected both the chronic diarrhea and hyperoxaluria. Enteric hyperoxaluria is a well-known etiology of calcium oxalate urolithiasis in adults. Pediatricians caring for children with malabsorptive conditions should be aware of the risk of urinary calculus formation as a result of increased dietary oxalate absorption.
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PMID:Urolithiasis and enteric hyperoxaluria in a child with steatorrhea. 358 41

Patients with ileal disease have increased absorption of dietary oxalate, hyperoxaluria, and an increased incidence of nephrolithiasis. Patients with steatorrhea of varying etiologies also have hyperoxaluria. To determine whether steatorrhea per se is associated with nephrolithiasis, we reviewed the charts of all adult patients who had a 72-hr fecal fat analysis from 1968 to 1978. The 159 patients with steatorrhea were compared to 162 patients without steatorrhea. The two groups were comparable in age, sex, urine specific gravity, and serum uric acid and phosphorus; serum calcium was slightly less in the steatorrhea group (8.7 +/- 0.1 vs 9.0 +/- 0.1, P less than 0.02). Although 19 patients with steatorrhea had nephrolithiasis compared to 7 control patients (P = 0.01), 15 of these 19 patients had ileal disease and only 4 of the 118 patients with steatorrhea but without ileal disease had stones. Categorical data analysis revealed that steatorrhea, diarrhea (stool weight greater than 225 g/day), male sex, and ileal disease were significantly associated with nephrolithiasis with a relative risk of 3.0, 2.7, 3.1, and 8.0, respectively. When patients without ileal disease were analyzed separately, however, steatorrhea, diarrhea, and sex were no longer risk factors. In contrast, in patients with ileal disease the incidence of nephrolithiasis increased with the severity of steatorrhea. The relative risk of nephrolithiasis in male patients with ileal disease and fecal fat greater than 20 g/day was 26.3 (P less than 0.01). Thus, the presence of both ileal disease and steatorrhea greatly increases the risk of nephrolithiasis; however, neither steatorrhea alone nor ileal disease alone are risk factors for nephrolithiasis.
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PMID:Increased risk of nephrolithiasis in patients with steatorrhea. 707 27


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