Muther R S, McCarron D A, Bennett W M
Nephron. 1982;30(1):36-8. doi: 10.1159/000182429.
We evaluated the effect of endogenous parathyroid hormone (PTH) on serum bicarbonate in 12 patients with postrenal transplant hyperparathyroidism. EDTA-induced hypocalcemia produced a significant rise in serum PTH (p less than 0.001). Associated with the increase in PTH was a significant fall in plasma bicarbonate (p less than 0.001) and increase in the chloride: phosphorus ratio (p less than 0.001). Magnesium remained stable but serum potassium fell in response to EDTA. These observations suggest that endogenous PTH can significantly affect plasma bicarbonate in vivo and may contribute to post renal transplant renal tubular acidosis.
我们评估了内源性甲状旁腺激素(PTH)对12例肾移植后甲状旁腺功能亢进患者血清碳酸氢盐的影响。乙二胺四乙酸(EDTA)诱导的低钙血症使血清PTH显著升高(p<0.001)。与PTH升高相关的是血浆碳酸氢盐显著下降(p<0.001)以及氯磷比值升高(p<0.001)。镁保持稳定,但血清钾因EDTA而下降。这些观察结果表明,内源性PTH可在体内显著影响血浆碳酸氢盐,并可能导致肾移植后肾小管酸中毒。