Higher baseline blood potassium levels, measured from samples taken 10 min (T-10) or just before reperfusion (T0), are independent risk factors for post-reperfusion hyperkalemia [1, 3]. Xia et al. found a strong association between pre-reperfusion potassium levels and PRHK incidence (OR = 35.84, 95% CI: 11 to 116.75, p < 0.001) [2]. Liang Zhang et al. reported similar findings (OR = 4.45, 95% CI: 1.54 to 12.84, p < 0.006) [6], as did Chen et al. (OR = 2.95, 95% CI: 1.91 to 4.54, p < 0.001) [7]. A baseline potassium level of 4.45 mmol/L [8] and 4-4.5 mmol/L [2] were good predictors of reperfusion hyperkalemia.

The volume of blood transfused before reperfusion is another risk factor for PRHK. Some studies reported an odds ratio of 1.125 (95% CI: 1.091 to 1.160, p < 0.001) [7], and (OR = 1, 95% CI: 1.000 to 1.00, p-value < 0.002) [4], while others found no association between transfusion volume and PRHK occurrence [1, 6].

During the past decade, LT from donation after circulatory death (DCD) grafts has increased dramatically worldwide due to the severe shortage of deceased liver grafts [6, 9]. More studies recently, have focused on the association between DCD grafts and PRHK incidence. Patients receiving DCD grafts had three-fold greater odds of developing early postreperfusion hyperkalemia, compared to those with brain-dead donors (OR = 3.87, 95% CI: 1.43 to 10.46, p-value < 0.008) [2]. Another propensity score-matched cohort study confirmed this, showing higher rates of hyperkalemia in DCD graft recipients compared to DBD grafts (33.8% versus 18.9%, P < 0.05) [10]. Liang Zhang et al. found that patients with PRHK were more likely to have ECD grafts and higher effluent potassium (eK+) levels than those without PRHK (7.65 [5.68–12.20] vs. 5.90 [4.40–6.88] mmol/L, P = 0.003). They identified elevated eK + concentrations after a standard portal vein flush (PVF) as a significant predictor of potassium level increases after reperfusion [6]. Wen-Jin Zhang et al. showed that recipients of macrosteatotic DCD grafts had significantly higher hyperkalemia rates (78.6%, P < 0.001) than those with non-macrosteatotic grafts or diffuse swelling [11]. However, other studies found no significant differences in the incidence of PRHK between DCD and DBD groups [12].

After procurement, the liver grafts are usually preserved in a cold solution until implantation. The two most common preservation solutions are the University of Wisconsin (UW) solution, the “gold standard” [9] since 1987’, and histidine-tryptophan-ketoglutarate (HTK) solutions. HTK has lower osmolarity, viscosity, and potassium content (9 mEq/L vs. 125 mEq/L) compared to UW. This may reduce the risk of hyperkalemia during reperfusion and help flush the microvasculature better due to its lower viscosity [9]. However, a study by Juang, S-E et al. looked at the effects of UW and HTK on blood potassium levels in living-donor liver transplantation. They found that despite its higher potassium content, the UW solution did not negatively affect serum potassium levels. Both solutions kept patients’ potassium levels within the normal range [13].

Normal potassium (K+) levels in extra and intracellular fluids depend on a balance between active cellular uptake with the help of sodium-potassium adenosine triphosphatase and passive potassium efflux from the cell. Prolonged cold ischemia time (PCIT) can lead to membrane dysfunction and lower sodium-potassium ATPase activity, allowing more potassium to exit the cell. This raises questions about the links between CIT duration, reperfusion injury severity, and post-reperfusion hyperkalemia. Surprisingly, studies on liver transplantation patients found no link between serum potassium changes after revascularization and ischemia time [1, 3, 6].

Recipients with high MELD scores often have more pretransplant health issues and intraoperative complications. Studies on patients undergoing LT with living-donor [3, 4] and orthotopic liver transplantation [6, 8] found no significant association between MELD score and the incidence of PRHK. The average intraoperative potassium levels and the rates of hypokalemia or hyperkalemia did not differ between patients with low and high MELD scores [3, 14].

Various studies showed no significant reported no significant associations between anhepatic time and PRHK incidence [3, 6, 11].

The storage time of transfused RBCs (more than 14 days) [7], and higher graft weight [6] are independent risk factors for PRHK. Administering certain medications before reperfusion, like angiotensin receptor blockers, sodium bicarbonate, or bolus catecholamines, along with metabolic acidosis [1], low cardiac output [2], elevated effluent K levels [6], and anesthesia time [11], and serum Albumin level [4], are also potential risk factors for PRHK. In the late reperfusion period, using venovenous bypass, having intraoperative urine output under 500 ml [2], transplanting from an elderly donor, and a donor with a prolonged hospital stay (> 5 days) significantly raise the risk of hyperkalemia [2].