CKD is an increasing public health problem that can lead to coronary events [12] and reduce glomerular filtration rate (GFR), which is an independent risk factor of cardiovascular mortality caused by acute myocardial infarction, heart failure, thromboembolic disease, and sudden cardiac death (SCD). These events account for 26.5% of all-cause mortality and 64% of cardiac mortality in ESRD patients [13, 14].

QT interval represents the total time course of ventricular depolarization and repolarization. It varies with heart rate. The extended QTc interval is a hallmark of ventricular arrhythmias, SCD, and all-cause mortality [15]. Previous studies [9,10,11] have proved that with the declination of renal function, the QT interval and QTc are prolonged, especially in maintenance hemodialysis patients. Yet, changes in QT interval and QTc change in patients undergoing maintenance PD have not been explored.

In this study, we examined changes in QT interval and QTc in 66 ESRD patients who underwent peritoneal dialysis. Firstly, we observed the therapeutic effect on the patients. During the whole follow-up period, and especially after 6 and 12 months post dialysis, the dialysis adequacy was up to standard with a total Kt/v > 1.7, and a total Ccr > 50 L.Furthermore, the blood pressure control, anemia correction, malnutrition, calcium, phosphorus metabolism disorders, and acid-base balance disorders of patients showed significant improvement during PD compared to those before dialysis. At the same time, after 6 and 12 months, all clinical indexes were similar, and the differences were not statistically significant. Secondly, the changes of QT interval and QTc were observed in PD patients during dialysis. Liu et al [9] reported that the prolongation of QTc interval worsened with the decreased in renal function. Among patients with CKD stages 3, 4, 5 and patients who underwent hemodialysis, the proportion of patients with prolonged QTc and severely prolonged QTc were 32.43 and 1.4%, 40.23 and 6.9%, 59.06 and 10.1%, 64.31 and 12.6%, respectively [9]. Covic et al [10] and Malhis et al [11] observed an increase in QT interval and QTc in the pre- and post-hemodialysis period. In this study, however, QT interval and QTc were not prolonged when patients underwent PD treatment. Due to different gender, the definition of QT interval and QTc prolongation remained different. Therefore, the changes of QT interval and QTc before and after PD in male and female patients were compared, respectively. The obtained data showed that the QT interval and QTc were not prolonged before and after PD in both males and females and were similar after PD for 6 months and 12 months.

It remains unclear why the QT interval and QTc were significantly longer after hemodialysis but not after PD. The prolongation of QT interval was caused by increased inward current (i.e., the sodium or calcium channels) or a K+ decreased outward current (i.e., potassium channel). The currents (Ikr and Iks) have a key role in myocardial repolarization. A prolonged action potential duration (APD) could lead to early changes after depolarization that is caused by inward depolarizing currents (L-type Ca2+ channels and Na+-Ca2+ exchange currents), inducing ventricular arrhythmias like torsade de pointes (TdP). ESRD patients are often accompanied by serious electrolyte acid-base balance disorder, such as hyperkalemia, hypocalcemia, metabolic acidosis, while potassium, calcium, magnesium and metabolic acidosis are important factors for electrical stability of the myocardium [16, 17]. It is well known that hemodialysis can quickly stabilize electrolyte acid-base balance disorder in ESRD patients. The low concentrations of potassium and calcium in the dialysate can be quickly removed potassium in serum. However, a large number of studies have shown a negative correlation between QTc interval change and calcium concentrations and potassium reduction during hemodialysis. Sherif et al [6] found that each mmol/L increase of serum K+ concentration might result in a 16 ms reduction of the QTc interval. Moreover, Alabd et al [18] have reported a negative correlation between decreased serum potassium and the change of QTc duration before and after dialysis. The higher decrease in the serum potassium has been associated with the longer QTc after dialysis. Also, Genovesi and colleagues [19] discovered that compared to patients who used dialysate with higher concentrations of potassium and calcium, patients who used dialysate with lower concentrations of potassium and calcium more had QTc intervals greater than 440 ms.

The non-prolongation of QT interval and QTc in PD patients might be related to the following: firstly, compared with hemodialysis, PD has a lower ability to remove toxins per unit time, so most PD patients usually undergo continuous ambulatory peritoneal dialysis (CAPD). However, this method avoids drastic changes in the concentrations of various ions in the serum in a short time, and the concentration of various ions is in a relatively stable state. Secondly, peritoneal dialysate has two different calcium concentrations: physiological calcium and high calcium. Therefore, the appropriate calcium concentration dialysate is chosen for patients according to the patients’ serum calcium concentrations. Although peritoneal dialysate is potassium-free dialysate, the patients have complete pre-dialysis education. They can be supplemented with potassium tablets and eat foods that are rich in potassium during PD to maintain the serum potassium in a stable state and avoid hypokalemia.

The heart’s blood supply depends on diastolic perfusion, and the impact on myocardial blood supply is more direct if the diastolic blood pressure remains low. This effect is particularly prominent in patients with coronary artery stenosis and left ventricular hypertrophy. Low diastolic blood pressure can cause subendocardial myocardial ischemia that can significantly affect the ventricular repolarization process, resulting in QT and QTc prolongation. Renal anemia is a frequent complication in CKD patients. The prevalence of QT prolongation in patients with anemia is common [20, 21]. The pathophysiological links between anemia and prolonged QT intervals are most probably hypoxia, autonomic dysfunction, and decreased myocardial oxygen supply. In addition, the impairment of delayed rectifier potassium channels and calcium channels might explain the changes in repolarization [22]. In our study, multiple linear regression analysis and Pearson correlation coefficient showed that diastolic blood pressure, calcium concentration and hemoglobin levels were influential factors for QTc prolongation before peritoneal dialysis that were negatively correlated with QTc ESRD patients, which is similar to the previous research results [19,20,21]. However, with the progression of PD, the symptoms and clinical indexes showed significant improvement, and our results showed that the clinical and biochemical indexes did not affect the QT interval and QTc anymore.

This study has a few limitations. This was a single-center retrospective study with a small sample. A multi-center study with a larger sample size with a longer follow-up is required to study the effects of PD on QT interval.