Abstract
In order to evaluate the oxygen release from erythrocyte hemoglobin in diabetics with nephropathy, especially in hemodialyzed cases, P50 and other parameters of oxygen release were investigated in 43 diabetics without nephropathy, 46 diabetics with nephropthy and 20 cases of hemodialysis caused by diabetic nephropathy. Hcparinized blood samples were drawn from the cubital vein before breakfast in nonhemodialyzed cases and from the arterial site of the hemodialyzer before and after hemodialysis in 20 hemodialyzed cases. The results obtained were as follows.
1) In 46 diabetics with nephropathy, P50 in vivo pH (26.0±2.3mmHg) was significantly higher than in diabetics without nephropathy (p<0.01).
2) In 89 diabetics with or without nephropathy, except for hemodialyzed cases, there were significant inverse correlations between P50 in vivo pH and blood pH, and blood hemoglobin concentration (Hb)(p<0.001, p<0.005). 2, 3-diphosphoglycerate (2, 3-DPG) had a similar inverse correlation with Hb (p<0.001), and P50 pH 7.4 had a positive correlation with 2, 3-DPG (p<0.001).
3) In 20 cases of diabetic nephropathy where hemodialysis was carried out, P50 in vivo pH and plasma inorganic phosphate (which were at high levels) and 2, 3-DPG were almost all the in the normal range before dialysis and they all decreased significantly after dialysis (p<0.001, p<0.05, p<0.001). However, blood pH and Hb increased significantly (p<0.001, p<0.005). In the course of hemodialysis, P50 in vivo pH also correlated inversely with blood pH (p<0.001) and positively with Pi (p<0.05). 2, 3-DPG had a significant inverse correlation with Hb (p<0.001).
4) The oxygen release from erythrocyte hemoglobin decreased relatively (0.5-37.3%) after hemodialysis in 18 out of the 20 hemodialyzed patients.
Accordingly, the elevation of P50 in vivo pH in 46 diabetics with nephropathy depended not only on the Bohr effect caused by renal acidosis, but also on the compensatory increase of 2, 3-DPG associated with renal anemia. It was also suggested that the decrease of P50 in vivo pH following hemodialysis was caused mainly by the rapid improvement in renal acidosis, partly by the normalization of hyperphosphatemia, and partly by a decrease of 2, 3-DPG accompanied by water exclusion.
