The prognosis and risk factors of baseline high peritoneal transporters on patients with peritoneal dialysis

Abstract

The relationship between baseline high peritoneal solute transport rate (PSTR) and the prognosis of peritoneal dialysis (PD) patients remains unclear. The present study combined clinical data and basic experiments to investigate the impact of baseline PSTR and the underlying molecular mechanisms. A total of 204 incident CAPD patients from four PD centres in Shanghai between 1 January 2014 and 30 September 2020 were grouped based on a peritoneal equilibration test after the first month of dialysis. Analysed with multivariate Cox and logistic regression models, baseline high PSTR was a significant risk factor for technique failure (AHR 5.70; 95% CI 1.581 to 20.548 p = 0.008). Baseline hyperuricemia was an independent predictor of mortality (AHR 1.006 95%CI 1.003 to 1.008, p < 0.001) and baseline high PSTR (AOR 1.007; 95%CI 1.003 to 1.012; p = 0.020). Since uric acid was closely related to high PSTR and adverse prognosis, the in vitro experiments were performed to explore the underlying mechanisms of which uric acid affected peritoneum. We found hyperuricemia induced epithelial‐to‐mesenchymal transition (EMT) of cultured human peritoneal mesothelial cells by activating TGF‐β1/Smad3 signalling pathway and nuclear transcription factors. Conclusively, high baseline PSTR induced by hyperuricaemia through EMT was an important reason of poor outcomes in CAPD patients.

The centre-calculated cutoff value is better for identifying fast peritoneal solute transfer of patients on peritoneal dialysis than the traditional value: a retrospective cohort study

“…The increased mortality risk associated with fast PSTR has been well documented [ 3 , 4 , 11 ]. However, some studies also claimed that fast PSTR was not an independent risk factor for mortality [ 23 , 24 ]. As our results showed, the fast PSTR group in our centre classification had a higher mortality risk than the non-fast PSTR group, but this was not presented under the traditional classification.…”

Peritoneal dialysis and peritoneal fibrosis: molecular mechanisms, risk factors and prospects for prevention

“…Окрім загальновизнаних уремічних токсинів, обговорюється й участь інших метаболітів у профіброгенних процесах. Так, продемонстровано, що гіперурикемія, індукує EMT культивованих перитонеальних мезотеліальних клітин шляхом активації сигнального шляху TGF-β1/Smad3 і факторів транскрипції [32,39]. Клінічно, висока концентрація сечової кислоти крові статистично значущо асоціювалась зі зниженням резидуальної функції нирок, високою транспортною характеристикою та загальною смертністю ПД пацієнтів [39][40][41].…”