Calcium Carbimide in the Treatment of Primary Hyperoxaluria

Solomons, Clive C.; Goodman, S. I.; Riley, Conrad M.

doi:10.1056/nejm196701262760404

Cited by 53 publications

(9 citation statements)

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“…1). Several inhibitors of either aldehyde dehydrogenase or glycolate oxidase have been tested in animals and in humans with mixed results [26,27]. Newer inhibitors of aldehyde dehydrogenase such as fomepizole were recently proposed for treatment of ethylene glycol poisoning [28] and may potentially be used for kidney stone therapy.…”

Section: Discussionmentioning

confidence: 99%

Pyridoxamine lowers kidney crystals in experimental hyperoxaluria: A potential therapy for primary hyperoxaluria

Chetyrkin

Kim

Belmont

et al. 2005

Kidney International

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Section: Discussionmentioning

confidence: 99%

Pyridoxamine lowers kidney crystals in experimental hyperoxaluria: A potential therapy for primary hyperoxaluria

Chetyrkin

Kim

Belmont

et al. 2005

Kidney International

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“…The same patient also received L-histidine on an empirical basis without effect. The aldehyde dehydrogenase inhibitor calcium carbimide was found by Solomons and his coworkers (Solomons, Goodman, and Riley, 1967) to lower oxalate excretion in one patient who received a kidney transplant, local irradiation, and corticosteroid therapy. However, no consistent effect was found during another study in three patients (Zarembski, Hodgkinson, and Cochran, 1967).…”

Section: Discussionmentioning

confidence: 92%

Treatment of Primary Hyperoxaluria

Dent¹,

Stamp²

1970

Archives of Disease in Childhood

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735. Treatment of primary hyperoxaluria. Nine patients with primary hyperoxaluria have been followed regularly for 1 to 11 years, and their treatment and progress are discussed in relation to the known natural history of the disease. 6 of them probably have the usual form of primary hyperoxaluria associated with increased glycollic acid excretion, while 3 who are sibs have the recently described variant associated with L-glyceric aciduria and normal glycollic acid excretion.All 9 patients have been on regimens designed to increase the urinary solubility of calcium oxalate, with or without the simultaneous lowering of urinary calcium and raising of urinary phosphate excretions. 8 patients have been treated for 1 -7j years (average duration 4 years) with oral magnesium hydroxide, and 2 patients have been treated with sodium phosphate. One of the latter was changed after 31 years to magnesium hydroxide and the other has been on sodium phosphate combined with a low calcium diet and cellulose phosphate continuously for 5j years. 2, not at first diagnosed as hyperoxalurics, were first given sodium bicarbonate for their presumably secondary renal tubular acidosis.The over-all progress of the whole group is felt to have been better than could be expected from the known natural history of primary hyperoxaluria.

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“…Of the first 8 transplants in 5 patients in Table 2, no pyridoxine therapy was given in 7 (Zarembski et al, 1969;Deodhar et al, 1969;Mahony et al, 1972;Koch et al, 1972) and, in one case, an inadequate dose of 100 mg daily was given (Solomons, Goodman and Riley, 1967 The authors say that it is unclear whether these deposits resulted from the basic disease or occurred as the terminal effect in the rejected fibrotic kidney (Halverstadt and Wenzl, 1974). Jacobsen and Mosbaek's patient was maintained on peritoneal dialysis for several months before transplantation, the graft never functioned satisfactorily and after 2 weeks of oliguria, during which only two haemodialyses were given, a creatinine clearance of 7 ml/min with a urinary excretion of 1875 ml/24 hr, was achieved.…”

Section: Discussionmentioning

confidence: 99%