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

Hyperoxaluria is rarely considered as a cause of rapidly progressive renal failure. A case is reported of a patient in whom rapidly renal failure developed after subtotal small bowel resection. A diagnosis of calcium oxalate deposits nephropathy was confirmed by renal biopsy. This cause of renal failure may be underestimated and should be systematically searched for in all patients with malabsorption.
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PMID:Hyperoxaluria: an underestimated cause of rapidly progressive renal failure. 1188 21

Secondary hyperoxaluria is due either to increased intestinal oxalate absorption or to excessive dietary oxalate intake. Certain intestinal diseases like short bowel syndrome, chronic inflammatory bowel disease or cystic fibrosis and other malabsorption syndromes are known to increase the risk of secondary hyperoxaluria. Although the urinary oxalate excretion is usually lower than in primary hyperoxaluria, it may still lead to significant morbidity by recurrent urolithiasis or progressive nephrocalcinosis. A clear distinction between primary and secondary hyperoxalurias is important. As correct classification may be difficult, appropriate diagnostic tools are needed to delineate the metabolic background as a basis for optimal treatment. We developed an individual approach for the evaluation of patients with suspected secondary hyperoxaluria. First, 24 h urines are examined repeatedly for lithogenic (e.g. calcium, oxalate, uric acid) and stone-inhibitory (e.g. citrate, magnesium) substances, and the patients are asked to fill in a dietary survey form. Urinary saturation is calculated using the computer based program EQUIL2, and the BONN-Risk-index is determined. The measurement of plasma oxalate and of urinary glycolate helps to distinguish between primary and secondary hyperoxalurias. If secondary hyperoxaluria is suspected, the stool is examined for Oxalobacter formigenes, an intestinal oxalate degrading bacterium, as lack or absence may lead to increased intestinal oxalate absorption. The last diagnostic step is to study the intestinal oxalate absorption using [13C2]oxalate. Depending on the results, various therapeutic options are available: 1) a diet low in oxalate, but normal or high in calcium, 2) a high fluid intake (>1.5 L/m2/d), 3) medications to increase the urinary solubility, 4) specific therapeutic measures in patients with malabsorption syndromes, depending on the underlying pathology, and 5) intestinal recolonization of Oxalobacter formigenes or the treatment with other oxalate degrading bacteria.
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PMID:Diagnostic and therapeutic approaches in patients with secondary hyperoxaluria. 1295 11

Orlistat, an anti-obesity drug, is a potent and specific inhibitor of intestinal lipases. In light of the recent US FDA approval of the over-the-counter sale of orlistat (60 mg three times daily), clinicians need to be aware that its use may be associated with less well known, but sometimes clinically relevant, adverse effects. More specifically, the use of orlistat has been associated with several mild-to-moderate gastrointestinal adverse effects, such as oily stools, diarrhoea, abdominal pain and faecal spotting. A few cases of serious hepatic adverse effects (cholelithiasis, cholostatic hepatitis and subacute liver failure) have been reported. However, the effects of orlistat on non-alcoholic fatty liver disease are beneficial. Orlistat-induced weight loss seems to have beneficial effects on blood pressure. No effect has been observed on calcium, phosphorus, magnesium, iron, copper or zinc balance or on bone biomarkers. Interestingly, the use of orlistat has been associated with rare cases of acute kidney injury, possibly due to the increased fat malabsorption resulting from the inhibition of pancreatic and gastric lipase by orlistat, leading to the formation of soaps with calcium and resulting in increased free oxalate absorption and enteric hyperoxaluria. Orlistat has a beneficial effect on carbohydrate metabolism. No significant effect on cancer risk has been reported with orlistat.Orlistat interferes with the absorption of many drugs (such as warfarin, amiodarone, ciclosporin and thyroxine as well as fat-soluble vitamins), affecting their bioavailability and effectiveness. This review considers orlistat-related adverse effects and drug interactions. The clinical relevance and pathogenesis of these effects is also discussed.
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PMID:Orlistat-associated adverse effects and drug interactions: a critical review. 1809 46

Surgical intervention has become an accepted therapeutic alternative for the patient with medically complicated obesity. Multiple investigators have reported significant and sustained weight loss after bariatric surgery that is associated with improvement of many weight-related medical comorbidities, and statistically significant decreased overall mortality for surgically treated as compared with medically treated subjects. Although the Roux-en-Y gastric bypass (RYGB) is considered an acceptably safe treatment, an increasing number of patients are being recognized with nephrolithiasis after this, the most common bariatric surgery currently performed. The main risk factor appears to be hyperoxaluria, although low urine volume and citrate concentrations may contribute. The incidence of these urinary risk factors among the total post-RYGB population is unknown, but may be more than previously suspected based on small pilot studies. The etiology of the hyperoxaluria is unknown, but may be related to subtle and seemingly subclinical fat malabsorption. Clearly, further study is needed, especially to define better treatment options than the standard advice for a low-fat, low-oxalate diet, and use of calcium as an oxalate binder.
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PMID:Nephrolithiasis after bariatric surgery for obesity. 1835 97

Calcium oxalate (CaOx) deposition in the renal allograft is an under recognized and important cause of acute tubular injury and early allograft dysfunction. We present a case of late transplant dysfunction due to acute oxalate nephropathy. The patient presented with diarrhea and deteriorating graft function, and a diagnosis of enteric hyperoxaluria secondary to pancreatic insufficiency was made. This had occurred, as the patient had been noncompliant with his pancreatic enzyme replacement therapy. Treatment to reduce his circulating oxalate load was initiated, including twice-daily hemodialysis, low fat and oxalate diet and appropriate administration of pancreatic enzyme supplements. Graft function subsequently recovered. The possibility of fat malabsorption leading to enteric hyperoxaluria should be considered in renal graft recipients presenting with loose stools and graft dysfunction.
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PMID:Acute oxalate nephropathy causing late renal transplant dysfunction due to enteric hyperoxaluria. 1855 38

Bariatric surgery is now recognized as a sure and effective way for weight reduction in morbid obesity. However some procedures induce intestinal malabsorption leading to enteric hyperoxaluria. So bariatric surgery could place these patients not only at risk for nephrolithiasis but also for oxalate induced nephropathy and chronic renal failure. Because of the growing incidence of obesity worldwide, physicians and patients should be aware of such potential complications. There is no mean to discuss this treatment because of its spectacular efficiency on obesity and its comorbidities. But it is necessary to choose the surgical technique according to the risk factors of the patients. Following surgery, preventive treatment strategies are indicated, such as modified dietary lifestyle and specific drugs as we suggested to limit or even avoid these complications. However observance could fail in the long term. In case of oxalate nephropathy, surgery may be proposed to restore the intestinal tract but with the risk of overweight relapse. To illustrate this matter, we report here significant observations of three patients, which, having successfully benefited from the same bariatric surgery, have presented lithiasic complications for two of them and oxalate nephropathy leading to chronic renal failure and hemodialysis for the third.
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PMID:[Bariatric surgery, calcium oxalate urinary stones and oxalate nephropathy]. 2113 57

We report a case of 48-year-old woman with history of diabetes and hypertension, who presented with acute to chronic kidney injury. Sixteen months before presentation, she had undergone Roux-en-Y gastric by-pass (RYGB) for morbid obesity. Kidney biopsy showed lesions consistent with oxalate nephropathy and deposition of calcium oxalate crystals. An extensive workshop excluded other causes of kidney injury. The patient subsequently required dialysis with no improvement of renal function on follow-up. The mechanism by which patients develop hyperoxaluria after RYGB remains obscure; it is suggested that RYGB provokes fat malabsorption, which results in increased load of free fatty acid in the intestine. Thus, calcium binds to free fatty acids provoking reduced synthesis of calcium oxalate. Consequently, increased quantity of oxalate remains free and is absorbed in the intestine causing hyperoxaluria. Similar to our case, oxalate nephropathy after RYGB is seen in patients with diabetes, hypertension and chronic kidney injury. Treatment includes low-fat, low-oxalate diet along with administration of calcium supplements. Unfortunately, prognosis is rather poor with the majority of patients eventually requiring permanent dialysis. Therefore, patients with history of chronic kidney disease undergoing RYGB should be closely monitored, particularly those with long standing history of diabetes and hypertension.
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PMID:Oxalate nephropathy in a diabetic patient after gastric by-pass. 2126 87

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

Decreased kidney function from kidney deposition of calcium oxalate has been described previously in inflammatory bowel disease and after jejuno-ileal and Roux-en-Y gastric bypass surgeries. Although celiac disease is the most prevalent bowel abnormality associated with intestinal malabsorption, its relationship to high kidney oxalate burden and decreased kidney function has not been established. We report a case of subclinical celiac disease and hyperoxaluria that presented with loss of kidney function as a result of high oxalate load in the absence of overt diarrhea, documented intestinal fat malabsorption, and nephrolithiasis. Subclinical celiac disease is commonly overlooked and hyperoxaluria is not usually investigated in kidney patients. We propose that this entity should be suspected in patients with chronic kidney disease in which the cause of kidney damage has not been clearly established.
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PMID:Subclinical celiac disease and crystal-induced kidney disease following kidney transplant. 2273 30

Oxalate arthropathy is a rare cause of arthritis characterized by deposition of calcium oxalate crystals within synovial fluid. This condition typically occurs in patients with underlying primary or secondary hyperoxaluria. Primary hyperoxaluria constitutes a group of genetic disorders resulting in endogenous overproduction of oxalate, whereas secondary hyperoxaluria results from gastrointestinal disorders associated with fat malabsorption and increased absorption of dietary oxalate. In both conditions, oxalate crystals can deposit in the kidney leading to renal failure. Since oxalate is primarily renally eliminated, it accumulates throughout the body in renal failure, a state termed oxalosis. Affected organs can include bones, joints, heart, eyes, and skin. Since patients can present with renal failure and oxalosis before the underlying diagnosis of hyperoxaluria has been made, it is important to consider hyperoxaluria in patients who present with unexplained soft tissue crystal deposition. The best treatment of oxalosis is prevention. If patients present with advanced disease, treatment of oxalate arthritis consists of symptom management and control of the underlying disease process.
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PMID:Update on oxalate crystal disease. 2366 69


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