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Updated: Aug 9, 2026

Murine Kidney Transplant Technique
Published on: October 20, 2015
Early acid-base balance disorders during kidney transplantation
K Tejchman1, L Domański, J Sieńko
1Department of General Surgery and Transplantation, Pomeranian Medical University, St. Powstańców Wielkopolskich. 72, 70-111 Szczecin, Poland. karols20@med.pam.szczecin.pl
Introduction:
Reperfusion is a crucial moment in kidney transplantation. Resumption of blood flow is associated with many metabolic changes, which result from the kidney's initial condition and preservation. These biochemical alterations including the acid-base balance are the part of ischemia-reperfusion injury. The study's purpose was to examine acid-base balance during the first 30 minutes after reperfusion of the transplanted kidney.
Materials And Methods:
The 30 recipients (13 men, 17 women) averaged ages of 46 +/- 14 years. Measurements performed nine times (at 0, 1, 3, 5, 10, 15, 20, 25, and 30 minutes after unclamping renal vessels) included: gas analysis, expiratory Pco(2), tidal volume, and respiratory rate. The evaluation of the temporary acid-base balance was performed on the basis of common parameters: pH, Pco(2), [HCO(3)(-)], and base excess (BE). The patients were under general anesthesia with stable external conditions of O(2) saturation, heart rate, blood pressure, and temperature. Blood samples were analyzed using Corning 278 and 248 blood gas analyzer; vital parameters were recorded using Ohmeda 5250 RGM and Dräger Sulla 909V/Julian apparatus.
Results:
The analysis showed increasing metabolic acidosis with coexisting increase in blood Pco(2), changes that were most intense in the first minute of reperfusion. Decreasing mean pH index did not exceed physiologic limits, but the final mean values of [HCO(3)(-)] and BE were in most of cases below the limit. Increased expiratory air Pco(2) was most intense in the first 3 minutes reaching a maximum at about 15 minutes.
Conclusions:
The beginning of reperfusion was the cause of increasing metabolic acidosis, which was partially compensated by blood buffers. Simultaneous increase in expiratory Pco(2), corresponding to the dynamics of acidosis, indicated the existence of respiratory compensation. Sudden increase in acidosis parameters may be the result of lactate accumulation during kidney ischemia. The decreased [HCO(3)(-)] may indicate postreperfusion kidney injury, which must be the subject of further research.
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