Reduction of Nicotinamide-Adenine Dinucleotide by Glyoxylate in Animal Organs

Sawaki, Shunji; Hattori, Norifumi; Yamada, Kozo

doi:10.5925/jnsv1954.12.303

Cited by 6 publications

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References 3 publications

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“…Pyridoxine deficiency will thus lead to decreased conversion of glyoxylate to glycine and increased conversion of glyoxylate to oxalate. Glyoxylate is oxidized to oxalate in the cytosol by lactate dehydrogenase and nicotinamide adenine dinucleotide (4). The ingestion of precursors of glyoxylate, such as ethylene glycol, will also result in increased oxalate biosynthesis (5).…”

Section: Metabolism Of Oxalate and Oxalosismentioning

confidence: 99%

Vascular Occlusion and Cardiac Conduction Disturbances in a Patient Undergoing Peritoneal Dialysis

Kay

1993

Seminars in Dialysis

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A 46-year-old woman, who had previously been well, developed nausea, vomiting, and anorexia in May 199 1. Her medical history was remarkable only for arthritis involving the knees and the proximal interphalangeal joints of the hands, which was treated for 2 years with ibuprofen and hydroxychloroquine sulfate while she was in her twenties. Her family history was remarkable for a sister who died at age 5 of "nephritis." Twin brothers both had chronic renal failure caused by primary oxalosis. One had died at age 29 of myocardial infarction and the other at age 34 of complications of gangrene. Neither parent had been diagnosed with renal disease, and both died in their sixties of myocardial infarction. The patient had no children. Laboratory studies revealed a hematocrit of 26.6%, a BUN of 124 mg/dl, a serum creatinine of 11.2 mg/dl, a serum calcium of 9.2 mg/dl, and a serum phosphate of 7.9 mg/dl. Liver function studies were normal. Urinalysis revealed proteinuria and pyuria without crystals or casts. A 24-hour urine collection revealed normal urinary oxalate excretion. Both kidneys were small and hyperechoic on ultrasonographic examination. Extensive evaluation revealed no clear cause for renal failure. A Tenckhoff catheter was placed, and maintenance peritoneal dialysis was initiated in July 199 1 for uremic symptoms. A regimen of calcium carbonate, erythropoietin, and Nephrocaps was begun.Shortly after beginning peritoneal dialysis, the patient noticed transient episodes in which her fingertips became cyanotic, painful, and cool to the touch for periods of about 10 minutes. Subsequently, transient mottling of the skin on her legs developed. She also noted the onset of calf pain when walking. The frequency of these episodes increased over the course of 1 month, and she was referred for rheumatological evaluation.On examination, livedo reticularis was present on both lower legs. The fingers were cool to the touch, and the toes were cyanotic. Joint deformities and signs of inflammation were absent. The arterial pulses were normal in both upper extremities and in both femoral arteries: however, the popliteal, posterior tibial, and dorsalis pedis arterial pulses were very weak bilaterally. No bruits were audible. Laboratory studies revealed an erythrocyte sedimentation rate of 75 mm/hr, cholesterol of 240 mg/dl, and triglycerides of 176 mg/dl. Antinuclear antibodies, rheumatoid factor, and cryoglobulins were absent. The CH50 was slightly elevated to 276, and levels of Clq, C3, and C4 were normal. Serum oxalate was 99 mmol/L (normal, <6 mmol/L). Biopsies of the skin on both lower legs demonstrated deposition of calcium oxalate crystals within the lumina and muscular walls of the subcutaneous arteries (Fig. 1). No evidence of vasculitis or cholesterol emboli was found.Aortography demonstrated narrowing of the left anterior tibial and right distal popliteal arteries and occlusion of both posterior tibial arteries at or near their origins. There was collateral blood flow to both ankles.Treatment with 10 mg oral nifedipine...

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Section: Metabolism Of Oxalate and Oxalosismentioning

confidence: 99%