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Background: The associated factors of peritoneal small solute transport was not fully understood. This research aimed to investigate the connection between dialysate inflammatory markers (e.g. macrophage migration inhibitory factor, MIF) in peritoneal dialysis (PD) effluent and peritoneal solute transport rate (PSTR) properties. Subjects and design: A total of 80 stable PD patients in the First ShaoYang Hospital were enrolled in present study. Overnight PD effluent and serum inflammatory markers including MIF, MCP-1, VEGF, IL-6, TNFα and TGFβ were detected. Pearson correlation analysis and Logistic regression was performed to determine the risk factors for the increased PSTR. Results: A trend toward increased values of MIF, MCP-1 and IL-6 in PD effluent was observed in subjects with high PSTR when compared with those with low PSTR. The Pearson correlation test showed that D/P Cr exhibited positive correlations with dialysis effluent MIF (r = 0.32, p = 0.01), MCP-1 (r = 0.47, p = 0.01), IL-6 (r = 0.48, p = 0.01). Conversely, no significant correlation was found between D/P Cr and TGF-β (r = 0.04, p = 0.70), TNF-ɑ (r = 0.22, p = 0.05), VEGF (r = 0.02, p = 0.86) and serum inflammatory markers. In the unadjusted regression analysis, dialysis effluent MIF (OR 2.41), MCP-1 (OR 1.72), IL-6 (OR 1.55) were associated with high PSTR condition. Multivariate logistic regression analysis showed that the adjusted odds ratios (OR) of dialysis effluent MIF for high PSTR were 2.47 in all subjects (p = 0.03). Conclusion: Elevated MIF, MCP-1 and IL-6 levels in PD effluent were associated with increased PSTR. Elevated dialysis effluent MIF levels was an independent risk factor for high PSTR in subjects with PD treatment. Resumen: Antecedentes: Los factores asociados del transporte peritoneal de pequeños solutos no se conocen completamente. Esta investigación tuvo como objetivo investigar la conexión entre los marcadores inflamatorios del dializado (por ejemplo, el factor inhibidor de la migración de macrófagos [MIF]) en el efluente de diálisis peritoneal (DP) y las propiedades de la tasa de transporte de solutos peritoneal (PSTR). Sujetos y diseño: Se incluyó un total de 80 pacientes con DP estable en el primer Hospital de Shaoyang. Se detectaron efluentes de DP nocturnos y marcadores inflamatorios séricos, incluyendo MIF, MCP-1, VEGF, IL-6, TNF -ɑ, TGF -β. Se realizó un análisis de correlación de Pearson y regresión logística para determinar los factores de riesgo para la PSTR aumentada. Resultados: Se observó una tendencia hacia valores incrementados de MIF, MCP-1 e IL-6 en el efluente de DP en sujetos con PSTR alta, en comparación con aquellos con PSTR baja. La prueba de correlación de Pearson mostró que D/Pcr exhibe correlaciones positivas con el MIF del efluente diálisis (r = 0,32, p = 0,01), MCP-1 (r = 0,47, p = 0,01), IL-6 (r = 0,48, p = 0,01). Por el contrario, no se encontró una correlación significativa entre D/Pcr y TGF-β (r = 0,04, p = 0,70), TNF-ɑ (r = 0,22, p = 0,05), VEGF (r = 0,02, p = 0,86) y marcadores séricos de inflamación. En el análisis de regresión no ajustado, el MIF del efluente diálisis (OR 2,41), la MCP-1 (OR 1,72), la IL-6 (OR 1,55) se asociaron con una PSTR elevada. El análisis de regresión logística multivariante mostró que las odds ratios (OR) ajustadas del MIF del efluente diálisis para PSTR alta fueron de 2,47 en todos los sujetos (p = 0,03). Conclusión: Los niveles elevados de MIF, MCP-1 y IL-6 en el efluente de DP se asociaron con un aumento de la PSTR. Los niveles elevados del MIF del efluente diálisis fueron un factor de riesgo independiente para PSTR elevada en sujetos tratados con DP.

Objective: The objective of this study was to evaluate the influence of ACE I/D gene polymorphisms on diabetic kidney disease (DKD) risk. Methods: All eligible investigations were identified, the number of various genotype in the case and control group were reviewed. The pooled analysis was performed using Stata software. Results: In overall subjects, 24,321 participants with 12,961 cases and 11,360 controls were included. the pooled analysis showed a significant link between D allele, DD or II genotype and DKD risk (D versus I: OR = 1.316, 95% CI: 1.213–1.427, P = 0.000; DD versus ID + II: OR = 1.414, 95% CI: 1.253–1.595, P = 0.000; II versus DD + ID: OR = 0.750, 95% CI: 0.647–0.869, P = 0.000). The subgroup pooled analysis showed that ACE I/D gene polymorphism was correlated with DKD both in Asian and in Chinese population. In addition, ACE I/D gene polymorphism was correlated with type 2 DKD (D versus I: OR = 1.361, 95% CI: 1.243–1.490, P = 0.000; DD versus ID + II: OR = 1.503, 95% CI: 1.310–1.726, P = 0.000; II versus DD + ID: OR = 0.738, 95% CI: 0.626 –0.870, P = 0.000). However, there was no obvious correlation in Caucasian subjects and type 1 diabetic patients. Conclusion: ACE I/D polymorphisms were correlated with DKD in Asian and type 2 diabetic populations. ACE D allele/DD genotype might be a risk factor, while ACE II genotype might be a protective factor for DKD. Resumen: Objetivo: El objetivo de este estudio fue evaluar la influencia de los polimorfismos del gen I/D de la ECA en el riesgo de enfermedad renal diabética (ERD). Métodos: Se identificaron todas las investigaciones elegibles, se revisó el número de varios genotipos en el grupo de casos y controles. El análisis combinado se realizó con el software Stata. Resultados: En el conjunto de los sujetos, se incluyeron 24.321 participantes con 12.961 casos y 11.360 controles. El análisis combinado mostró una relación significativa entre el alelo D, el genotipo DD o II y el riesgo de DKD (D frente a I: OR = 1,316, IC del 95%: 1,213–1,427, P = 0,000; DD frente a ID + II: OR = 1,414, IC del 95%: 1,253-1,595, P = 0,000; II frente a DD + ID: OR = 0,750, 95% CI: 0,647-0,869, P = 0,000). El análisis de subgrupos mostró que el polimorfismo del gen I/D de la ECA se correlacionaba con la DMD tanto en la población asiática como en la china. Además, el polimorfismo del gen I/D de la ECA se correlacionó con la DKD de tipo 2 (D frente a I: OR = 1,361, IC del 95%: 1,243-1,490, P = 0,000; DD frente a ID + II: OR = 1,503, IC del 95%: 1,310-1,726, P = 0,000; II frente a DD + ID: OR = 0,738, 95% CI: 0,626 -0,870, P = 0,000). Sin embargo, no hubo una correlación evidente en los sujetos caucásicos y en los pacientes diabéticos de tipo 1. Conclusión: Los polimorfismos I/D de la ECA se correlacionaron con la DKD en poblaciones asiáticas y diabéticas de tipo 2. El alelo D de la ECA/genotipo DD podría ser un factor de riesgo, mientras que el genotipo II de la ECA podría ser un factor de protección para la DKD.

Objective: The objective of this study was to evaluate the influence of ACE I/D gene polymorphisms on diabetic kidney disease (DKD) risk., Methods: All eligible investigations were identified, the number of various genotype in the case and control group were reviewed. The pooled analysis was performed using Stata software., Results: In overall subjects, 24,321 participants with 12,961 cases and 11,360 controls were included. the pooled analysis showed a significant link between D allele, DD or II genotype and DKD risk (D versus I: OR=1.316, 95% CI: 1.213-1.427, P=0.000; DD versus ID+II: OR=1.414, 95% CI: 1.253-1.595, P=0.000; II versus DD+ID: OR=0.750, 95% CI: 0.647-0.869, P=0.000). The subgroup pooled analysis showed that ACE I/D gene polymorphism was correlated with DKD both in Asian and in Chinese population. In addition, ACE I/D gene polymorphism was correlated with type 2 DKD (D versus I: OR=1.361, 95% CI: 1.243-1.490, P=0.000; DD versus ID+II: OR=1.503, 95% CI: 1.310-1.726, P=0.000; II versus DD+ID: OR=0.738, 95% CI: 0.626 -0.870, P=0.000). However, there was no obvious correlation in Caucasian subjects and type 1 diabetic patients., Conclusion: ACE I/D polymorphisms were correlated with DKD in Asian and type 2 diabetic populations. ACE D allele/DD genotype might be a risk factor, while ACE II genotype might be a protective factor for DKD., (Copyright © 2021 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)