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

Fourteen patients underwent small bowel bypass (SBB) takedown for complications such as chronic nausea and vomiting, excessive flatus, intractable diarrhea, liver dysfunction, electrolyte imbalance, hyperoxaluria with renal stones, and arthritis. The average weight loss in these 14 patients after SBB was 93 pounds (34% of initial weight), with a mean follow-up of 23 months. Four of the 14 patients had SBB takedown only and gained an average of 36 pounds over the ensuing 14 months. Similarly, three patients had SBB takedown with delayed (asynchronous) gastric bypass (GB) and gained an average of 55 pounds during the 14 months prior to GB. Following GB these three patients lost only an additional 8 pounds over a 12 month period, leaving them 47 pounds heavier than at the time of SBB takedown. In contrast, seven patients treated with SBB takedown and synchronous GB not only maintained the weight reduction obtained with SBB, but, in addition, had further modest weight reductions (average, 18 pounds), for a mean follow-up of 8 months. There were no serious operative or late complications with any of the above operations. In addition, the complications leading to SBB takedown resolved in each case. It is concluded that synchronous GB is an effective means of maintaining the weight reduction in the morbidly obese patient after SBB takedown.
Surgery 1977 Sep
PMID:Management of the morbidly obese patient after small bowel bypass failure. 88 3

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.
J Formos Med Assoc 1992 Sep
PMID:Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case. 136 95

We report the case of a 31-year-old patient who underwent combined liver and kidney transplantation for primary hyperoxaluria type I. Intensive hemodialysis was performed before the intervention and post-operatively in order to maintain plasma oxalate levels near the normal range. In spite of the correction of the liver enzyme deficiency, oxalate removal from the tissular stores led to prolonged hyperoxaluria, more longer than one year after the transplantation, as already reported. This increased urinary oxalate excretion exposes the renal graft to the risk of recurrence of calcium oxalate deposits and stone formation during a prolonged period. Hemodialysis in the postoperative period and fluid intake allowing a large urine volume might be able to decrease the concentration of urinary oxalate under the critical value of 300 mumol/l, at which supersaturation of urine in respect of calcium oxalate occurs.
Clin Nephrol 1992 Sep
PMID:Combined liver kidney transplantation in primary hyperoxaluria type I. Prevention of the recidive of calcium oxalate deposits in the renal graft. 139 63

To differentiate hyperoxaluria syndromes we measured plasma and urine glycolate by a novel high performance liquid chromatographic procedure. Mean glycolate level was 7.9 +/- 2.4 mumol./l. in plasma and 422 +/- 137 mumol./24 hours in urine from 19 control subjects. Renal clearance was about 50% the glomerular filtration rate irrespective of the underlying disease. There was close correlation between glycolate and oxalate in plasma. Plasma glycolate was normal in all but 8 patients who had primary hyperoxaluria 1. Plasma assay detected the disease more efficiently than urine assay. Pyridoxine decreased oxalate biosynthesis in 2 of the 4 patients treated with it and glycolate assay confirmed this behavior. Glycolate excretion was significantly high in 3 of 8 patients of primary hyperoxaluria 1 patients. Idiopathic stone formers had mild increases in glycolate excretion but this was not related with oxalate excretion. Glycolate levels were normal in 5 patients with enteric hyperoxaluria. We conclude that glycolate assay is essential for identifying patients with primary hyperoxaluria 1 and may represent a valuable tool for differentiating hyperoxaluria.
J Urol 1992 Sep
PMID:Plasma and urine glycolate assays for differentiating the hyperoxaluria syndromes. 150 56

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.
Clin Nephrol 1990 Sep
PMID:Acute deterioration of renal function associated with enteric hyperoxaluria. 222 62

The pharmacokinetics and pathophysiology of oxalic acid in human organism are presented. In the formation of urinary calculi the level of urinary oxalic acid is important, but the knowledge of metabolism and various disturbances is the guide of a successful treatment and metaphylaxis. Therefore, the diagnostics is a prerequisite for successful dietetic and therapeutic measures as shown in absorptive hyperoxaluria.
Z Urol Nephrol 1990 Sep
PMID:[Metabolism and pathophysiology of oxalic acid]. 226 60

Male Sprague-Dawley rats were challenged with various hyperoxaluric agents including ammonium oxalate, hydroxy-L-proline, and ethylene glycol. All treatments resulted in increased urinary oxalate. Associated with hyperoxaluria was an increase in urinary levels of renal enzymes, gamma-glutamyl transpeptidase, N-acetyl-beta-glucosaminidase, and alkaline phosphatase. Most of the rats did not demonstrate any significant change in urinary levels of beta-galactosidase. There was a highly significant positive correlation between urinary oxalate and N-acetyl-beta-glucosaminidase.
J Urol 1989 Sep
PMID:Urinary enzymes and calcium oxalate urolithiasis. 257 Jan 67

An organic marine hydrocolloid (OMH) charged with calcium ('Ox-Absorb') was studied in vitro for oxalate binding and in patients with enteric hyperoxaluria to investigate oxalate excretion and the inhibitory activity on crystal formation of the urine. In-vitro experiments showed complete binding of oxalate to OMH. In clinical studies in nineteen patients with intestinal disorders and stone formation, urinary oxalate excretion was significantly lower during OMH treatment than off treatment. The activity product index of calcium oxalate was reduced on treatment. A pronounced rise in the inhibitory activity of urine was seen in two patients with very low pretreatment values. Most patients experienced virtual normalisation of bowel function, and in those with severe stone formation there was substantial clinical improvement. It is concluded that OMH has the capacity to bind oxalate in vitro and to reduce urinary oxalate excretion. These observations suggest a new promising treatment for enteric hyperoxaluria.
Lancet 1989 Sep 23
PMID:Treatment of enteric hyperoxaluria with calcium-containing organic marine hydrocolloid. 257 Sep 57

Conventional treatment of enteric hyperoxaluria (EHO) consists of dietary restriction of oxalate and fat and correction of its underlying cause whenever possible. Recent work suggests that allopurinol reduces the incidence of urolithiasis and the urinary excretion of both oxalate and uric acid in patients without intestinal disease. We have assessed the effect of allopurinol, 300 mg daily for 2 weeks, on urine biochemistry in patients with EHO due to small bowel Crohn's disease and/or resections. Compliance with treatment was confirmed by a fall in plasma uric acid in every patient. Allopurinol failed to alter 24 h urinary oxalate excretion or oxalate concentration. There were also no significant changes in the urinary excretion of glycollate (like oxalate, a breakdown product of glyoxylate), citrate, magnesium or calcium, each of which was at the lower end of the normal range before and during treatment with allopurinol. It appears unlikely that allopurinol will prove useful in the prevention of urolithiasis in patients with EHO.
Br J Urol 1989 Sep
PMID:Failure of allopurinol to modify urinary composition in enteric hyperoxaluria. 280 58

Two kinds of inborn errors of metabolism, dicarboxylic aciduria and hyperoxaluria, have been studied by means of hydroxyl negative ion chemical ionization [NICI(OH-)], linked with collisionally activated decomposition experiments on the [M-H]- species of the pathognomonic organic acids. This method has led to non-controversial qualitative determinations of C4-C10 dicarboxylic acids and oxalic, glyceric and glyoxylic acids. NICI(OH-) linked with collisionally activated decomposition mass analysed ion kinetic energy spectrometry (CAD MIKES) is proposed herein for diagnostic purposes, as a valid mass spectrometric alternative to standard gas chromatographic/mass spectrometric analysis. The procedure is characterized by simplified sample treatment and by fast execution.
Biomed Mass Spectrom 1985 Sep
PMID:Hydroxyl negative chemical ionization mass spectrometry linked with collisionally activated decomposition. A modern analytical tool in inborn errors of metabolism. 293 87


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