calcium oxalate/diarrhea

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

UNASSIGNED Oxalate nephropathy is a rare disease. Especially chronic oxalate nephropathy still has many unknown aspects as compared to acute oxalate nephropathy with relatively well-known causality. UNASSIGNED The patient was a 70-year-old woman who had a history of small bowel resection 25 years

The effects of long-term treatment with potassium citrate, 30 to 80 meq/d over 2.13 +/- 0.76 (SD) years, were examined in 37 patients with "idiopathic" hypocitraturic calcium-oxalate nephrolithiasis, in whom the main causes of hypocitraturia (renal tubular acidosis, chronic diarrhea, urinary tract

Urolithiasis is a problem that is generally increasing in the tropics as it is in most Western countries. There are 2 main types of the disorder-bladder stones in children, a form of the disorder that disappeared from Europe in the late 19th and early 20th centuries, and upper urinary tract stones

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

BACKGROUND According to Thai traditional medicine, Pentace burmanica Kurz. stem bark has been used as crude drug for treating diarrhea. However, the crude drug is also found susceptible to adulteration. OBJECTIVE To develop specific standardization parameters of P. burmanica stem bark in Thailand

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 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

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

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

We report the case of a white woman with insulin-dependent diabetes for 12 years who had rapid deterioration in renal function over a 7-month period. A renal biopsy showed widespread deposition of a polarizing crystalline material consistent with calcium oxalate. Fat malabsorption due to diabetic

Hyperoxaluria can result in oxalate nephropathy with intratubular calcium oxalate crystallization and acute tubular injury. Primary inherited enzymatic deficiency or secondary causes such as excessive dietary intake, enteric increased absorption, or high doses of vitamin C, which is metabolized to

Uric acid stones occur in 10% of all kidney stones and are the second most-common cause of urinary stones after calcium oxalate and calcium phosphate calculi. The most important risk factor for uric acid crystallization and stone formation is a low urine pH (below 5.5) rather than an increased

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

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