Transplanted Kidney Increases Nitric Oxide Formation With Metabolic Acidosis Reduction.

Abstract

As a vasodilator, nitric oxide is considered to play a significant role in the homeostatic regulation of renal hemodynamics. To test the hypothesis that a kidney graft is capable of producing nitric oxide immediately after renal transplant surgery, we examined the possibility that it positively affects local metabolic acidosis. In kidney transplant recipients, we analyzed renal vein and central vein blood samples, which reflect local and systemic metabolic alterations, respectively. Samples were taken immediately after kidney recirculation (that is, the first blood passing through after clamps are released) and at 5, 15, and 30 minutes thereafter. Levels of nitric oxide metabolites (nitrites, nitrates, and their sum), malondialdehyde (an indicator of oxidative damages), and parameters of acid-base balance (pH level, actual excess base, hemoglobin, actual bicarbonate, partial pressure of carbon dioxide, partial pressure of oxygen) were analyzed. Living kidney donors (the recipients' parents) were controls. In renal vein samples, nitrates and the sum of nitrites and nitrates were significantly higher than that shown in control (P < .001) and central vein (P < .05) samples, suggesting an immediate increase in nitric oxide production in the transplanted organ. Metabolic acidosis occurred in both the renal and central vein, indicated by decreased pH and actual bicarbonate level as well as by negative actual base excess level. Only in the renal vein was an increased nitrite and nitrate associated with a reduction of negative actual excess base, thereby suggesting a decrease in anion formation. Transplanted kidneys increase nitric oxide production immediately after organ transplant surgery, which positively affects local metabolic acidosis. The mechanism for this effect is likely local circulation improvement.