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

A 61 year old man had chronic renal failure because of oxaluria and renal calculi. Two years before death, while on hemodialysis, he developed severe progressive peripheral neuropathy. At autopsy calcium oxalate crystals were found in the peripheral nerves and other tissues. Nerve lesions included segmental demyelination, axonal degeneration and crystalline deposits within the myelin sheath. Ultrastructurally there were foci of osmiophilic granular material within myelin lamellae and endoneurium, and pleomorphic lamellar bodies in the perinuclear Schwann cell cytoplasm. It is probable that chronic hemodialysis favors the deposition of oxalate in the Schwann cells and the development of neuropathy in patients with primary hyperoxaluria and renal failure.
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PMID:Peripheral neuropathy in oxalosis. A case report with electron microscopic observations. 17 8

An 18-year-old female with primary oxalosis, seen first when she was in advanced renal failure, developed a severe necrotizing angiopathy which began after a rapid decrease in renal function requiring chronic dialysis. Because of the severe angiopathy the preliminary diagnosis of an acute autoimmune vasculitis had been made. The correct diagnosis was revealed by renal biopsy and a renal transplantation performed. Soon after severe oxalosis led to failure of the renal transplant and death. The patient had also had familial spherocytosis, inherited from her father, while the oxalosis had been inherited from her mother. It is suggested that early transplantation at the onset of renal failure, as long as the blood oxalate level is still tolerably low, may give better results than have so far been reported.
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PMID:[Angiopathy in a case of primary oxalosis combined with familial spherocytosis (author's transl)]. 36 90

Primary hyperoxaluria is a rare congenital disorder characterized by large quantities of urinary oxalate with resultant nephrocalcinosis and nephrolithiasis and by deposits of calcium oxalate in other organs. Renal failure occurs early in life. Reports of unsuccessful renal transplantation attempts in this disorder underscore the need for antemortem diagnosis. Percutaneous bone biopsy is a relatively new procedure that is easily done at bedside, safe, and of potentially high yield in the demonstration of tissue oxalate. Three cases presented here show the characteristic histologic picture seen in this disease. In one case, the diagnosis was established by bone biopsy.
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PMID:Bone biopsy to diagnose hyperoxaluria in patients with renal failure. 43 79

Oxalate nephrosis resulted in progressive renal failure in 4 patients after jejunoileal bypass for morbid obesity. In general, increased levels of oxalates in the blood and urine of such patients result from enhanced absorption of exogenous oxalates. Urinary calculous formation is determined further by concomitant deficiency of inhibitor substances, whereas oxalate nephrosis probably occurs as a result of oxalate deposition in renal interstitium via the blood stream. Clinical manifestations of oxalate nephrosis include pain, infection, hematuria and renal failure. Routine postoperative renal function studies and early renal biopsy in suspicious cases are urged to establish early diagnosis. Continued deterioration of renal function, despite therapy with oxalate restruction and oxalate binding agents, indicates a reversal of the bypass to preserve unaffected renal substance.
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PMID:Renal failure owing to oxalate nephrosis after jejunoileal bypass. 43 32

Although pyridoxine hydrochloride (vitamin B6) is known to reduce the endogenous production of oxalate in some individuals with primary oxalosis, the dose for a satisfactory trial of treatment is not established. We report two cases of primary oxalosis on a daily regimen of 1 g pyridoxine hydrochloride, in which 24-hr urinary oxalate excretion decreased by 60% and 70%, respectively, with corresponding clinical benefit. The responses have been sustained up to 2.5 yr in one case, and 20 mo in the other. In the patient with renal failure, serum creatinine decreased from 243 to 146 mumole/liter after 15 mo of treatment. The decrease in glycollic acid excretion in both patients was consistent with an increase of glyoxalate transaminase activity by the vitamin. Supranormal levels of erythrocyte glutamic oxaloacetate transaminase (egot) activity were observed during therapy, and these may be useful as a measure of the effective dose of pyridoxine.
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PMID:Primary oxalosis: clinical and biochemical response to high-dose pyridoxine therapy. 44 95

A 45-year-old man underwent a jejunoileal shunt procedure for obesity. Twenty months later he developed severe oxalosis and chronic renal failure, which required maintenance hemodialysis. The sequential observation of two biopsy specimens and the necropsy (over a span of 39 months) suggests that oxalate deposition caused tubular obstruction and destruction with subsequent atrophy of nephrons. This indicates that patients undergoing intestinal bypass are at risk for developing irreversible renal failure due to enteric hyperoxaluria.
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PMID:Oxalosis and chronic renal failure after intestinal bypass. 83 9

A patient who underwent jejunoileal bypass for morbid obesity developed servere renal failure associated with hyperoxaluria and renal oxalosis. Renal function improved and oxalate excretion decreased following hemodialysis and restoration of gastrointestinal continuity.
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PMID:Acute reversible renal failure following jejunoileal bypass for morbid obesity: a clinical and pathological (EM) study of a case. 91 50

In a child with renal failure and oliguria due to hyperoxaluria myelophthisis developed as a result of extensive bone-marrow replacement with calcium oxalate crystals and an accompanying fibrous proliferations. The histopathology associated with this metabolic disorder was demonstrated in posterior iliac crest bone-marrow trephine biopsies, renal biopsies, and nephrectomy specimens. Crystals were demonstrated in biopsy specimens of transplanted kidneys within six weeks following renal transplantation.
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PMID:Oxalosis. An unusual cause of myelophthisis in childhood. 99 70

Calcium oxalate crystals were demonstrated in the retinal pigment epithelium (RPE) of a 66-year old white man with changes in the fundus oculi consistent with the flecked retina ayndrome. The patient had a history of rheumatoid arthritis, mild hypertension, and mild renal insufficiency presumed due to his hypertension. He underwent prolonged abdominal surgery under methoxyflurane anesthesia, following which he developed acute irreversible renal failure. Calcium oxalate crystals were demonstrated postoperatively in a kidney biopsy specimen. He subsequently was maintained on renal dialysis with decreasing renal function. Several weeks before his death fundus examination revealed a picture suggestive of a flecked retina syndrome. At autopsy, widespread oxalosis was found including crystals in the RPE and in some areas in the neural retina and cillary epithelium.
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PMID:Flecked retina. Appearance secondary to oxalate crystals from methoxyflurane anesthesia. 111 83

All general anesthetics employed clinically have significant and reversible effects on renal hemodynamics, water, and electrolyte excretion at concentrations in which they are usually employed for surgical anesthesia. Some of the mechanisms by which these effects are produced are discussed. The minmal depressant effect on renal function of epidural anesthesia is possibly related to local anesthetic effects on the central system and/or the kidney. Methoxyflurane has been demonstrated to produce renal dysfunction when administered in high concentrations for prolonged periods of time to obese patients. Metabolites of methosyflurane including fluoride and/or oxalate appear to be the cause of this problem. Problems of anesthetic management in patients with renal failure have been briefly summarized with specific attention to the undersirable effects of some neuromuscular blocking drugs.
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PMID:Effects of anesthetics on the kidney. 116 70


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