The effect of different serum potassium levels on progression of chronic kidney disease

Introduction The kidney plays a major role in potassium homeostasis by renal mechanisms that transport and regulate potassium secretion, reabsorption and excretion. Hyperkalemia is a common electrolyte disturbance in patients with chronic kidney disease (CKD). In CKD individuals, a few studies suggested weak links between hyperkalemia, hypokalemia or different serum potassium levels (sK) and progression of CKD. The aim of this study was to demonstrate the effect of different sK levels on disease progression in CKD patients. Material and Methods The study was performed with 1171 stage I-IV CKD patients followed for at least one year. GFR (glomeruler filtration rate) values were calculated at the beginning and end of the follow-up period. Besides, average GFR values were analyzed during follow-up. GFR was calculated with CKD-EPI formula. Patients with reduced GFR were identified by detecting differences in GFR levels. sK was evaluated categorically: Group 1; < 3.5 mmol/l, Group 2; 3.5 to 4.0 mmol/l, Group 3; 4.0 to 4.5 mmol/l, Group 4; 4.5 to 5.0 mmol/l, Group 5; 5.0 to 5.5 mmol/l, Group 6; >5.5 mmol/l. Hyperkalaemia was defined as sK intervals of ≥5.0 mmol/l. sK < 3.5 mmol/L was classified as hypokalaemia. Binary logistic regression models predicting the reduction in GFR were used. Results The median age of the patients was 66 years. 45.9% (n = 537) of the patients were male and 54.1% (n = 634) were female. The mean sK level was 4.6 ± 0.4 mmol/l. 26.1% of the patients had hyperkalemia. Only 0.6% of the patients had hypokalemia. GFR levels were significantly decreased during follow-up (p <0.001). sK level was negatively correlated with the final GFR of patients (r = 0.016, p = 0.016). In patients with reduced GFR, sK (p=0.002), phosphor (p<0.001), urea (p<0.001), magnesium (p=0.018) and uric acid (p=0.021) level higher, but calcium (p<0.001) and albumin (p=0.002) level lower than in patients without reduced GFR. Moreover, the frequency of using beta-blockers (p=0.012), calcium canal blockers (p=0.018) and ACEi/ARB (p=0.020) in patients with reduced GFR was higher. The frequency of diabetes and anemia was higher in patients with decreased GFR (p=0.002, p=0.037, respectively). The frequency of sK=3.5 to 4.0 mmol/l was lower in patients with decreased GFR, whereas the frequency of sK=5.0 to 5.5 mmol/l was higher. All the univariate significant and relevant covariates were tested in binary logistic regression for serum potassium. In regression model, hyperkalaemia or sK=3.5 to 4.0 mmol/l, sK=5.0 to 5.5, calcium and urea levels, using ACE/ARB were associated with declining in GFR. sK=5.0 to 5.5 (OR 1.49; CI 95% 1.03–1.97; p = 0.030) and hyperkalaemia (OR 1.44; CI 95% 1.06–1.95; p = 0.017) were significantly associated with declining in GFR while sK=3.5 to 4.0 mmol/l were protective against GFR reduction (OR 0.51; CI 95% 0.28–0.92; p = 0.025). In the multivariate model adjusting for albumin, calcium, urea level, ACEi/ARB, beta blocker and calcium canal blocker use, sK=5.0 to 5.5 (OR 1.21; CI 95% 1.04–1.45; p = 0.036) and hyperkalaemia (OR 1.31; CI 95% 1.10–1.81; p = 0.022) were independent predictor for decreased GFR while sK=3.5 to 4.0 mmol/l were independent predictor against for decreased GFR (OR 0.62; CI 95% 0.53–0.73; p = 0.035). Conclusion In conclusion, hyperkalemia and sK=5.0 to 5.5 are associated with decreased GFR in CKD population. On the contrary sK=3.5 to 4.0 mmol/l are protective against GFR reduction. Therefore, serum potassium levels should be monitored in the management of patients with CKD.