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1.
Arch Med Res ; 49(1): 36-43, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29665969

RESUMO

BACKGROUND: Chronic kidney disease (CKD) is a leading complication of type 2 diabetes mellitus (T2DM) and is considered as a public health problem. Copeptin is a surrogate marker of arginine vasopressin (AVP) system and is proposed as a biomarker of decline renal function. OBJECTIVE: Evaluate whether plasma copeptin levels may be used as a biomarker of decline renal function in patients with T2DM. RESEARCH DESIGN AND METHODS: A total of 480 patients with T2DM and different stages of CKD were included. Plasma levels of copeptin, cystatin-C, and other biochemical parameters were measured. The correlation between copeptin and glomerular filtration rate (GFR), estimated based on plasma cystatin-C levels, was investigated. RESULTS: Plasma copeptin levels were gradually increased from the stage 1-5 of CKD in the patients with T2DM. In univariate linear regression analysis, high plasma levels of copeptin were associated with lower GFR (Standardized ß = -0.535, R2 = 0.287, p <0.0001). This association remained significant even after being adjusted for glucose levels and years of T2DM diagnosis, mean blood pressure, pharmacological treatment, gender, and age. CONCLUSIONS: The results show that high plasma copeptin levels are associated with the decline of renal function in patients with T2DM and, therefore, copeptin may be considered as a biomarker of renal function. Further evaluation of plasma copeptin levels to predict morbidity and mortality of T2DM patients, with or without CKD, has been taken into our consideration.


Assuntos
Arginina Vasopressina/fisiologia , Cistatina C/sangue , Diabetes Mellitus Tipo 2/sangue , Taxa de Filtração Glomerular/fisiologia , Glicopeptídeos/sangue , Biomarcadores/sangue , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neurofisinas , Precursores de Proteínas , Insuficiência Renal Crônica/sangue , Vasopressinas
2.
Rev Med Inst Mex Seguro Soc ; 55(Suppl 2): S158-66, 2017.
Artigo em Espanhol | MEDLINE | ID: mdl-29697237

RESUMO

BACKGROUND: Mortality for cardiovascular disease (CVD) in patients with chronic kidney disease (CKD) is higher. In the end-stage renal disease (ESRD) the mortality is 20 times greater in comparison with general population. Natriuretic peptides, particularly type-B natriuretic peptide (BNP) have been studied as potential markers of risk of cardiovascular (CV) mortality. The aim of this paper is to determine whether BNP acts as a prognostic marker for CV mortality in patients with ESRD. METHODS: We studied 53 patients with ESRD prevalent in peritoneal dialysis without clinical evidence of heart failure at baseline was studied. The impact of variables was performed with linear regression model. The probability of survival was estimated by Kaplan-Meir analysis and the difference between survivals between groups with log-rank test according the levels of BNP. Adjusted hazard ratios were calculated with Cox proportional hazards analysis. RESULTS: BNP strongly predicts CVD mortality. The Cox regression model showed that BNP is a predictor of death from CVD. Patients with high levels of BNP were at increased risk of death. Several pathophysiological mechanisms not well defined are involved. CONCLUSIONS: BNP predicts CVD mortality in patients with ESRD. Serum measurement of this peptide can be useful for risk stratification in these patients and adjust treatment.


INTRODUCCIÓN: la mortalidad por enfermedad cardiovascular (ECV) en pacientes con enfermedad renal crónica (ERC) es alta. En la población con ERC terminal (ERCT) la mortalidad es hasta 20 veces mayor en comparación a la población general. Los péptidos natriuréticos, especialmente el péptido natriurético tipo-B (BNP), han sido estudiados como posibles marcadores de riesgo de mortalidad por ECV. El objetivo de este trabajo es determinar si el BNP actúa como un marcador pronóstico para mortalidad por ECV en pacientes con ERCT. MÉTODOS: se estudiaron 53 pacientes con ERCT prevalentes en diálisis peritoneal sin evidencia clínica de insuficiencia cardiaca al inicio del estudio. El impacto de las variables se realizó con el modelo de regresión lineal. La probabilidad de sobrevida fue estimada con el análisis de Kaplan-Meier y la diferencia entre grupos con el test de Log-Rank, acorde a los niveles de BNP dividido en tertiles. La asociación de riesgo fue calculada con el análisis proporcional de Cox ajustado. RESULTADOS: el BNP fuertemente predice la mortalidad por ECV. El modelo de regresión de Cox mostró que el BNP es un predictor de muerte por ECV. Pacientes con niveles altos de BNP tuvieron mayor riesgo de muerte. Varios mecanismos fisiopatológicos no bien definidos están involucrados. CONCLUSIONES: el BNP predice la mortalidad por ECV en pacientes con ERCT. La medición sérica de este péptido puede ser útil para la estratificación de riesgo en estos pacientes y ajustar el plan terapéutico

3.
Int J Nephrol Renovasc Dis ; 6: 259-68, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24348062

RESUMO

BACKGROUND: A reduction of dopaminergic (DAergic) activity with increased prolactin levels has been found in obese and hypertensive patients, suggesting its involvement as a pathophysiological mechanism promoting hypertension. Similarly, leptin action increasing sympathetic activity has been proposed to be involved in mechanisms of hypertension. The aim of this study was to analyze the effects of DA, norepinephrine (NE), and prolactin on leptin release and leptin gene (OB) expression in adipocytes from obese and hypertensive patients. METHODS: Leptin release and OB gene expression were analyzed in cultured adipocytes from 16 obese and hypertensive patients treated with DA (0.001, 0.01, 0.1, and 1.0 µmol/L), NE (1.0 µmol/L), insulin (0.1 µmol/L), and prolactin (1.0 µmol/L), and from five nonobese and normotensive controls treated with DA (1 µmol/L), NE (1 µmol/L), insulin (0.1 µmol/L), and prolactin (1.0 µmol/L). RESULTS: A dose-related reduction of leptin release and OB gene messenger ribonucleic acid expression under different doses of DA was observed in adipocytes from obese hypertensive patients. Whereas prolactin treatment elicited a significant increase of both leptin release and OB gene expression, NE reduced these parameters. Although similar effects of DA and NE were observed in adipocytes from controls, baseline values in controls were reduced to 20% of the value in adipocytes from obese hypertensive patients. CONCLUSION: These results suggest that DAergic deficiency contributes to metabolic disorders linked to hyperleptinemia in obese and hypertensive patients.

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