Mild Metabolic Hyperoxaluria and Its Response to Pyridoxine

Abstract

Three cases of mild metabolic hyperoxaluria (with glycollaturia) are described. They showed different types of response to pyridoxine. One responded to low dose, one responded at first to low dose but became resistant, and the third showed temporary response to high dose. One case also had primary hyperparathyroidism and one had medullary sponge kidneys and hypercalciuria. It is important to measure urinary oxalate (and glycoUate) in all cases of calcium oxalate urolithiasis.

Chemical Measurement of Calcium Oxalate Crystalluria: Results in Various Causes of Calcium Urolithiasis

“…Although mild metabolic hyperoxaluria [5] does in our experience cause oxalate crystalluria, this is not seen in figure 3 because urinary oxalate had been reduced vir tually to normal by successful treatment with pyridoxine.…”

“…Figure 2 shows results in primary hyperoxaluria with a very large increase in uri nary calcium oxalate crystal concentration, with urinary calcium concentration below normal and oxalate con centration much higher than normal. Figure 3 shows results in mild metabolic hyperoxaluria [5], Urinary oxa late is virtually normal because these patients had re sponded well to pyridoxine, and calcium oxalate crystal luria is not significantly different from normal. Figure 4 shows that although the calcium oxalate crystalluria is Fig.…”

Treatment of Renal Failure in the Primary Hyperoxalurias

“…The latter method is the more sensitive and detects degrees of pyri doxine sensitivity that are potentially useful but which can only be detected with difficulty, if at all, when only the rate of urinary oxalate excretion is studied. Pharma cological doses of pyridoxine (450-800 mg/24 h in equally divided doses) are usually needed although Gill and Rose [16] and Rose [17] have reported a subgroup of patients whom they termed 'mild metabolic hyperoxalurics' and who responded to much smaller dose of pyri doxine, for example 10-15 mg/24 h. Patients presenting in ESRD may have to be given pyridoxine blindly. The effect of pyridoxine comes on over the course of a few days and wears off with a similar time course when its administration is stopped.…”

Renal calcium phosphate and oxalate deposition in prolonged vitamin B6 deficiency: studies on a rat model of urolithiasis

“…The role of vitamin B 6 in the pathogenesis of kidney stones has been widely investigated, since it was reported to be beneficial in treating patients with type I primary hyperoxaluria [1][2][3][4][5][6][7]. The administration of vitamin B 6 seems to reduce the production of oxalate from glyoxylate by enhancing the activity of alanine-glyoxylate transaminase, as pyridoxal phosphate, one of the biologically active forms of vitamin B 6 , is the cofactor for the enzyme [2][3][4]8,9].…”