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

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

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

Enteric hyperoxaluria is due to increased absorption of oxalate, especially in the colon. However, this mechanism is not fully understood. Little is also known about the composition of the intestinal flora in these patients. Eleven patients with hyperoxaluria (greater than 0.45 mmol/24 h) after jejunoileal bypass were therefore studied under surgical ward conditions for 5 days. The patients were maintained on a constant diet. During days 3, 4, and 5 clindamycin (Dalacina), 1.8 g/24 h, was given parenterally in three divided doses. All patients had hyperoxaluria, with a mean oxalate absorption of 0.94 +/- 0.09 mmol/24 h (+/- SEM). No significant disturbances in the colonic microflora were found. The degree of hyperoxaluria did not change during clindamycin administration, in spite of a significant decrease in the number of anaerobic bacteria. Our patients with enteric hyperoxaluria seem to have a normal colonic microflora. The degree of hyperoxaluria did not seem to be related to changes in the intestinal anaerobic flora.
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PMID:The effect of clindamycin on the intestinal flora in patients with enteric hyperoxaluria. 667 47

Enteric hyperoxaluria complicates extensive disease or resection of the small intestine in the presence of an intact colon, and is associated with calcium oxalate nephrolithiasis. In addition to hyperoxaluria these patients have a low urine volume, low urinary ionic strength and hypocitraturia. Many forms of treatment have been recommended, but none has been subjected to a prospective clinical trial. Mild idiopathic hyperoxaluria is reported in 8-50% of idiopathic calcium oxalate stoneformers. Several pathophysiological mechanisms have been proposed, including low dietary calcium and possible oxalate transport defects in the gut and/or the kidney. Mild hyperoxaluria, or a high oxalate:calcium ratio in the urine, may be particularly important risk factors for calcium oxalate stone formation; an approach to the correction of these abnormalities is proposed.
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PMID:Enteric and mild hyperoxaluria. 778 97

Enteric hyperoxaluria and primary hyperparathyroidism have been associated with the development of nephrolithiasis. We report a case involving a patient who had hyperparathyroidism due to a parathyroid adenoma and enteric hyperoxaluria resulting from a small bowel bypass and who had severe stone-related complications. This combination of stone-generating factors has heretofore not been reported. The pathophysiology of these entities is discussed.
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PMID:Nephrolithiasis due to primary hyperparathyroidism and enteric hyperoxaluria: a case report. 865 Aug 79

Primary hyperoxaluria type I is a rare inborn error of metabolism caused by a deficiency of a liver-specific peroxisomal enzyme. It manifests by increased oxalate production that ultimately results in kidney failure, due to urolithiasis and nephrocalcinosis, and finally induces systemic oxalosis and risk of premature death. Primary hyperoxaluria type 2 is mainly responsible of urolithiasis. Enteric hyperoxaluria is a commonly seen adverse event of Crohn disease or after extensive intestinal resection. These affections represent the main etiologies of massive hyperoxaluria. If not recognized very soon and adequately treated, these conditions can progress rapidly to end stage renal failure.
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PMID:[Massive hyperoxaluria]. 1549 71

Enteric hyperoxaluria can lead to renal failure. There have only been a few reports of renal transplantation as treatment of endstage renal disease secondary to enteric hyperoxaluria and results have been mixed. This report describes a patient with Crohn's disease who developed chronic renal failure from enteric hyperoxaluria. He subsequently had a successful renal transplant without any post-operative oxalate related complications and has satisfactory renal function almost three years later. Aggressive pre-transplant hemodialysis was not done. The literature associated with renal transplantation for enteric hyperoxaluria is reviewed.
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PMID:Transplantation for renal failure secondary to enteric hyperoxaluria: a case report. 1759 38

Enteric hyperoxaluria causes tubular deposition calcium oxalate crystals and severe chronic interstitial nephritis. We describe a patient with pre-terminal renal failure due to oxalate nephropathy after ileal resection. Increased oral hydration, low oxalate diet, and oral calcium carbonate and potassium citrate supplements resulted in a significant improvement of renal function. During the three-year follow-up, urinary oxalate concentration was repeatedly reduced below the crystallization threshold and serum creatinine decreased from 4.5 to 1.7 mg/dL. This case illustrates the benefit of combining and optimizing dietary and medical management in enteric hyperoxaluria, even in patients with advanced chronic kidney disease.
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PMID:Pre-terminal renal insufficiency in a patient with enteric hyperoxaluria: effect of medical management on renal function. 2248 38

We report a 29 year old male cystic fibrosis patient with end stage lung disease and normal renal function who underwent a sequential double lung transplant. Medical history included: an ileal resection and pancreatic exocrine dysfunction. The postoperative period was complicated with haemorrhage and repeat surgery, requiring multiple blood transfusions and extensive antibiotic cover. Pancreatic supplements were interrupted. Acute renal failure attributed to haemodynamically-mediated acute tubular necrosis was managed expectantly. He remained dialysis dependent 8 weeks post surgery and was maintained on triple immunosuppression with tacrolimus, mycophenolate and prednisolone. A DTPA study was consistent with ATN. Renal biopsy revealed features consistent with tubular injury due to acute oxalate nephropathy (AON). Further biochemical characterization excluded primary hyperoxaluria but confirmed increased 24 hour urinary oxalate. He was maintained on enhanced frequency HDF and subsequently received an uncomplicated live related renal transplant 10 months post lung transplant with only additional basiliximab. Calcium carbonate was continued to manage post transplant hyperoxaluria and an early renal biopsy excluded recurrent oxalate injury. Enteric hyperoxaluria due to malabsorption in patients with CF especially with ileal resection, in addition to loss of gut Oxalobacter formigenes due to prolonged antimicrobials, increases the risk of AON. Increased awareness of this condition and screening prior to lung transplant is recommended.
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PMID:Acute irreversible oxalate nephropathy in a lung transplant recipient treated successfully with a renal transplant. 2249 48

Kidney transplantation is the treatment of choice for end-stage renal disease whereas indications for intestinal transplantation are currently restricted to patients with irreversible small bowel failure and severe complications of total parenteral nutrition (mostly shortage and infection of venous accesses, major electrolyte disturbances and liver failure). Enteric hyperoxaluria is secondary to certain intestinal diseases like intestinal resections, chronic inflammatory bowel disease and other malabsorption syndromes and can lead to end-stage renal disease requiring kidney transplantation. We report two patients suffering from renal failure due to enteric hyperoxaluria (secondary to extensive intestinal resection) in whom we elected to replace not only the kidney but also the intestine to prevent recurrence of hyperoxaluria in the transplanted kidney.
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PMID:Combined kidney and intestinal transplantation in patients with enteric hyperoxaluria secondary to short bowel syndrome. 2373 Jul 77


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