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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Secondary oxalosis is a complication of renal failure. Since oxalate is excreted by the kidney, the severity of oxalate deposition has been directly related to the duration of renal failure. We report a patient with acute renal failure on hemodialysis who received daily ascorbic acid (an oxalate precursor) via parenteral alimentation. He developed widespread secondary oxalosis, which was especially prominent in the kidneys and pancreas. This oxalate burden may have contributed to the complications seen during his hospital course. The provision of ascorbic acid to patients with renal failure should be carefully monitored to avoid accelerated development of secondary oxalosis.
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PMID:Secondary oxalosis as a complication of parenteral alimentation in acute renal failure. 641 68

The daily amount of oxalate in normales is formed by about 90 per cent from endogenous sources. Approximately 10 per cent are due to intestinal absorption of dietary oxalate. The oxalate formed endogenously is derived from aminoacid-, carbohydrate- and ascorbic acid metabolism. Oxalate synthesis is increased in inherited defects of enzymes (primary hyperoxaluria) or as a consequence of exogenous factors (vitamin-B6-deficiency, ethylene glycol intoxication, high dose ascorbic acid application, possibly excessive protein and carbohydrate intake). The intestinal absorption of oxalate is increased in some diseases of the intestinal tract (Morbus Crohn, ulcerative colitis). Oxalate, that is totally excreted in urine, is the principal component for urinary calcium oxalate saturation. Oxalate accumulates in renal failure. The increased plasma oxalate level - as a consequence of impaired renal function and additional metabolic influences - is an important factor for calcium oxalate depositions in uremic patients.
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PMID:[Clinical aspects of oxalate metabolism]. 666 94

Patients on haemodialysis or peritoneal dialysis due to renal failure have an unusually high incidence of kidney stones (from 5 to 51% depending on methodology). However, there is a controversy on the composition of these stones - whether they are calcium oxalate stones or matrix stones. This paper presents ultrastructural evidence that these stones are in fact heterogeneous, ranging from calcium oxalate stones with little organic matrix component, through calcium oxalate and calcium apatite stones with substantial organic matrix component, to matrix stones with little inorganic material component. The correlative analytical methodology developed in this laboratory employing analytical scanning and transmission electron microscopy, electron and x-ray diffraction, as well as biochemistry, was reported previously. For the calcium oxalate stones, scanning electron microscopy showed that numerous small crystals of 1-3 micron in size were exposed to stone surfaces, apparently in an unorganized manner. However, transmission electron microscopy sections showed orderly stacking of crystals held together by organic matrix, just like bricks held together by mortar. For the matrix stones, scanning electron microscopy showed smooth stone surfaces while transmission electron microscopy sections showed focal areas of calcium oxalate or apatite deposits as identified by selected area electron diffraction.
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PMID:Ultrastructural studies of renal stones from patients on continuous ambulatory peritoneal dialysis. 666 57

A fatal case of poisoning by a mixture of methanol and ethylene glycol is described. A 72-year-old man was hospitalized when he was found stuporous to semicomatose, and despite massive bicarbonate therapy, died 36 hr after the admission. While the presence of numerous oxalate crystals in urine strongly suggested ethylene glycol intoxication, the GC analysis of the liquid the patient ingested revealed that he presumably drunk about 150 to 200 ml of a mixture of methanol (80%) and ethylene glycol (20%), the amount well over the lowest lethal dose when the additiveness of toxicity was considered. Retrospective evaluation of the signs suggested that while some of them such as oxalate crystalluria, elevated CPK, hypocalcemia, renal failure are attributable to the toxicity of ethylene glycol, others including elevated serum amylase and cyanosis are indicative of methanol poisoning. Disturbed consciousness was considered to be of metabolic origin; the high anion gap observed (38.2 mEq/liter) may be due not only to lactic acidosis but also to acidogenicity of the two chemicals ingested. The importance of gas chromatographic analysis for identification of the causative chemical(s) is stressed.
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PMID:A case of poisoning by a mixture of methanol and ethylene glycol. 667 Jan 3

Primary hyperoxaluria is a rare metabolic disease characterized by exaggerated production of oxalic acid. Clinically the disease is characterized by recurrent calcium nephrolithiasis, progressive renal failure, and early death in uremia. As the regular dialysis treatment may prolong survival, a new syndrome may develop. This is due to intense and continuous deposition of calcium oxalate crystals in soft and bone tissues. The radiologic aspects of oxalate deposition in four adult patients on chronic renal dialysis with histologic and clinical evidence of massive bone oxalosis are reported.
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PMID:Bone changes in end-stage oxalosis. 678 31

Granulomatous interstitial nephritis occurred in a patient five years after jejunoileal bypass surgery was performed. Calcium oxalate crystals were present in the kidney. This finding was associated with renal failure and to our knowledge has not been previously reported. Hepatic granulomas were also present.
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PMID:Granulomatous interstitial nephritis complicating jejunoileal bypass. 689 48

A 38-year-old woman suffered rapid onset of renal failure between 11 and 15 months after undergoing a jejunoileal bypass for morbid obesity. Microscopic examination of renal biopsy specimens revealed oxalosis and severe tubulointerstitial nephritis. Immunofluorescence microscopy disclosed linear staining of tubular basement membranes with antisera to IgG and C3, which suggests antitubular basement membrane disease, a side effect not previously recognized with jejunoileal bypass. Possible mechanisms leading to the formation of these antibodies include (1) oxalate damage to renal tubules with release of tubular basement membrane antigens, and (2) bacterial overgrowth in the bypass segment, with mucosal damage and release of intestinal mucosal antigens that share antigenetic determinants with renal proximal tubules. Anti-tubular basement membrane disease may be an additional mechanism that produces or enhances renal damage in patients with jejunoileal bypass.
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PMID:Chronic interstitial nephritis. Its occurrence with oxalosis and anti-tubular basement membrane antibodies after jejunoileal bypass. 689 90

In a clinical demonstration, case reports on 3 patients are presented: 1. In a 27-year-old male who developed severe multicentric atypical pneumonia, CNS, liver and renal involvement and signs of rhabdomyolyses suggested infection with Legionella pneumophila. Diagnosis was confirmed by the presence of Dieterle-stain positive organisms and positive culture of lung biopsy tissue. Antibiotic treatment, especially erythromycin, and prolonged mechanical respiration produced complete recovery. 2. The presence of chylomycrons Rin ascitic and pleural fluid in a patient with epimembranous glomerulonephritis and nephrotic syndrome was the first sign of malignant non-Hodgkin lymphoma. Chemotherapy with cyclophosphamid, oncovin and prednisone induced remission of tumor and nephrotic syndrome, which promptly recurred parallel to later reactivation of the malignancy. Paraneoplastically induced nephrotic syndrome, especially due to lymphoma, may precede the malignancy by months. 3. In a 52-year-old male with terminal renal failure due to primary oxalosis a cadaver renal transplant functioned for only 14 months because of oxalate deposits in the transplant. Hemodialysis before and after transplantation modified the clinical course. In place of uremia, the clinical picture was dominated by oxalate-induced gangrenous arteriopathy, arthritis, and heart disease.
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PMID:[Clinical demonstrations. Legionnaires' disease. Tumor-associated nephrotic syndrome. Primary oxalosis]. 703 33

We describe 3 infants with nephrocalcinosis and terminal renal failure. In all 3 there was widespread oxalate deposition: biochemical evidence of primary hyperoxaluria was sought but the presence of severe renal failure and the lack of established normal values for urinary and plasma oxalate and glycollate in infants made this diagnosis difficult to establish.
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PMID:Oxalosis in infancy. 707 2

The daily urinary excretion of oxalate has been found to be lower than normal in patients with renal failure and the decrease to be directly proportional to the impairment of renal function. It has also been found that the gut flora from uremic patients destroys oxalate 'in vitro' more efficiently than the gut flora from normal people. It is postulated that an adaptation occurs in the gut flora of uremics to 'metabolize' oxalate, and this enteric elimination may account for its decreased urinary excretion.
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PMID:Urinary excretion of oxalate in renal failure. 709 40


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