hyperoxaluria/diaree

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Urolithiasis and enteric hyperoxaluria in a child with steatorrhea.

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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

Severe renal oxalosis in five young Beefmaster calves.

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Severe renal oxalosis was diagnosed in 4 male and 1 female purebred Beefmaster calves from herds in southeastern and northwestern United States. Clinical signs included weakness, anorexia, lethargy, alopecia, dehydration, and diarrhea. Results of serum biochemical analysis for 2 calves were

Secondary oxalosis induced acute kidney injury in allograft kidneys.

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Secondary oxalosis causing acute kidney injury (AKI) has been widely reported in native kidneys but its occurrence in allograft kidneys is relatively uncommon. We present three patients with acute kidney allograft dysfunction secondary to tubular oxalate microcrystal deposits confirmed on allograft

[Secondary oxalosis following small bowel resection with kidney insufficiency and oxalate vasculopathy].

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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

Vitamin C-induced hyperoxaluria causing reversible tubulointerstitial nephritis and chronic renal failure: a case report.

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Vitamin C is a precursor of oxalate and promoter of its absorption, potentially causing hyperoxaluria. Malabsorption causes Calcium (Ca) chelation with fatty acids, producing enteric hyperoxaluria. METHODS A 73-year-old man with both risk factors was hospitalized with serum creatinine of 8.4 mg/dL

Primary hyperoxaluria.

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A 5-month-old female infant who had chronic diarrhea and acute renal failure was referred to Chulalongkorn Hospital for further investigation and management. Laboratory investigation revealed elevated blood urea nitrogen and creatinine level, hypocalcemia, hyperphosphatemia, and hyponatremia.

Acute oxalate nephropathy causing late renal transplant dysfunction due to enteric hyperoxaluria.

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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

Encapsulating peritoneal sclerosis in a patient with primary hyperoxaluria type 1: a case report.

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Primary hyperoxaluria type 1 (PH1) is a rare metabolic disorder caused by a defect in glyoxylate metabolism attributable to low or absent activity of the liver-specific peroxisomal enzyme alanine/glyoxylate aminotransferase. This defect leads to enhanced conversion of glyoxylate to poorly soluble

Steatorrhea and Hyperoxaluria in Severely Obese Patients Before and After Roux-en-Y Gastric Bypass.

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Hyperoxaluria after Roux-en-Y gastric bypass (RYGB) is generally attributed to fat malabsorption. If hyperoxaluria is indeed caused by fat malabsorption, magnitudes of hyperoxaluria and steatorrhea should correlate. Severely obese patients, prior to bypass, ingest excess dietary fat that can produce

Increased risk of nephrolithiasis in patients with steatorrhea.

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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

Metabolic risk factors in pediatric stone formers: a report from an emerging economy.

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The goal of this study was to investigate metabolic risk factors in pediatric stone formers in an emerging economy. A prospective, data collection enrolled 250 children age <1-15 years at our center. Risk factors were evaluated by gender and in age groups <1-5, 6-10 and 11-15 years. Patients were

[Nephrolithiasis in patients with intestinal diseases].

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Intestinal diseases may cause the formation of urinary stones through changes in the metabolism of oxalate, calcium, and uric acid. The oxalate that is excreted into urine comes from the catabolism of ascorbic acid and some amino acids or from intestinal absorption of food oxalate. Calcium is

[Absorption and malabsorption of fat and bile acids (author's transl)].

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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

Calcium oxalate crystal related kidney injury in a patient receiving Roux-en Y hepaticojejunostomy due to gall bladder cancer.

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BACKGROUND Calcium oxalate nephropathy is rare in current practice. It was a common complication during jejunoileal bypass, but much less seen in modern gastric bypass surgery for morbid obesity. The major cause of it is enteric hyperoxaluria. METHODS We report on a patient here with acute kidney

Acute oxalate nephropathy associated with Clostridiumdifficile infection.

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Acute oxalate nephropathy has been associated with chronic diarrheal illness and only one case has been reported due to acute diarrhea secondary to Clostridium difficile colitis. To the best of our knowledge, this is the second case report of acute oxalate nephropathy due to

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