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      Progresión de la enfermedad renal crónica en pacientes con enfermedad poliquística autosómica dominante Translated title: Chronic kidney disease progression in patients with autosomal dominant polycystic kidney disease

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          Abstract

          Objetivos: El objetivo del presente estudio es analizar los factores que influyen en la progresión de la insuficiencia renal crónica en pacientes con enfermedad poliquística autosómica dominante (PQRAD). Material y métodos: Estudiamos a 101 pacientes (edad media: 43,6 ± 17,3, 43,6% varones). La mediana (rango intercuartílico) de seguimiento es de 69 (128-35) meses desde 1997 hasta 2010. Analizamos la progresión de dos formas: 1) tiempo hasta evento renal definido como la reducción del filtrado glomerular estimado (FGe) en un 50% desde la primera visita y/o entrada en diálisis, y 2) cambio medio en el FGe/año. Se recogieron en cada visita datos clínicos y demográficos, presión arterial sistólica (PAS) y diastólica (PAD), medicación concomitante y parámetros analíticos. También se recogió el tamaño renal basal medido por ecografía. Resultados: Treinta y un pacientes tuvieron un evento renal. La mediana de tiempo hasta la aparición del evento es de 102 (131-53) meses. Los pacientes que tuvieron un evento renal tenían basalmente mayor PAS y PAD (p = 0,017 y p = 0,001, respectivamente), mayores niveles de acido úrico (p = 0,041), mayor colesterol LDL (p = 0,001), mayor proteinuria (p = 0,033) y mayor tamaño renal (p = 0,05). El cambio medio de FGe/anual fue de -3,52 ± 7,3 ml/min/1,73 m², 49 pacientes presentaron un descenso rápido de función renal: Grupo A (> -3,52 ml/min/1,73 m²) y 52 pacientes tuvieron una progresión lenta de la insuficiencia renal: Grupo B (< -3,2 ml/min/1,73 m²). Por regresión de Cox, en un modelo ajustado, la PAS y la menor edad al diagnóstico son las variables que mantienen su poder predictivo de mal pronóstico renal (p = 0,026). Conclusiones: La función renal inicial, proteinuria, tamaño renal, hipercolesterolemia, hiperuricemia y PAS basal son factores que influyen en la progresión de la insuficiencia renal en la PQRAD, siendo la PAS y la menor edad los factores que mantienen su poder predictivo independiente en el análisis multivariante.

          Translated abstract

          Objectives: The aim of this study was to analyse the factors influencing chronic kidney disease (CKD) progression in patients with autosomal dominant polycystic kidney disease (ADPKD). Material and Method: We studied 101 patients (mean age: 43±17.3 years, 43.56% male) followed during a median (interquartile range) follow-up time of 69 (35-128) months from 1997 to 2010. The primary end point was: time to a 50% decrease of estimated glomerular filtration rate (eGFR) (CKD-EPI) since the first-time visit and/or time to initiation of renal replacement therapy, and the annual mean change of eGFR was also analysed. Clinical and demographic data, blood pressure, concomitant medications, and analytical parameters were collected at each visit. Baseline kidney size was also recorded by ultrasound. Results: Thirty-one patients achieved the primary end point after a median (IQR) time of 102 (53-131) months. Those patients who achieved the primary end point had higher SBP and DBP (P=0.017 and P=0.001), higher LDL-cholesterol (P=0.011), higher creatinine (P=0.006), higher uricemia (P=0.041), more severe proteinuria (P=0.033) and greater kidney size (P=0.05). The mean annual eGFR change was of -3.52±7.3ml/min/1.73m². Forty-nine patients had a rapid decline in renal function: Group A (higher than -3.52ml/min/1.73m²) and 52 patients had a lower renal disease progression: Group B (<-3.2 ml/min/1.73 m²). Adjusted Cox regression analysis showed that higher SBP and younger age at the first visit were independent variables for poorer renal outcome (P=0.026). Conclusions: Initial kidney function, proteinuria, renal size, hypercholesterolemia, hyperuricemia, and SBP are the factors that influence CKD progression in ADPKD. SBP and younger age at diagnosis are the only factors that maintain their independent predictive value in a multivariant analysis.

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          A new equation to estimate glomerular filtration rate.

          Equations to estimate glomerular filtration rate (GFR) are routinely used to assess kidney function. Current equations have limited precision and systematically underestimate measured GFR at higher values. To develop a new estimating equation for GFR: the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. Cross-sectional analysis with separate pooled data sets for equation development and validation and a representative sample of the U.S. population for prevalence estimates. Research studies and clinical populations ("studies") with measured GFR and NHANES (National Health and Nutrition Examination Survey), 1999 to 2006. 8254 participants in 10 studies (equation development data set) and 3896 participants in 16 studies (validation data set). Prevalence estimates were based on 16,032 participants in NHANES. GFR, measured as the clearance of exogenous filtration markers (iothalamate in the development data set; iothalamate and other markers in the validation data set), and linear regression to estimate the logarithm of measured GFR from standardized creatinine levels, sex, race, and age. In the validation data set, the CKD-EPI equation performed better than the Modification of Diet in Renal Disease Study equation, especially at higher GFR (P < 0.001 for all subsequent comparisons), with less bias (median difference between measured and estimated GFR, 2.5 vs. 5.5 mL/min per 1.73 m(2)), improved precision (interquartile range [IQR] of the differences, 16.6 vs. 18.3 mL/min per 1.73 m(2)), and greater accuracy (percentage of estimated GFR within 30% of measured GFR, 84.1% vs. 80.6%). In NHANES, the median estimated GFR was 94.5 mL/min per 1.73 m(2) (IQR, 79.7 to 108.1) vs. 85.0 (IQR, 72.9 to 98.5) mL/min per 1.73 m(2), and the prevalence of chronic kidney disease was 11.5% (95% CI, 10.6% to 12.4%) versus 13.1% (CI, 12.1% to 14.0%). The sample contained a limited number of elderly people and racial and ethnic minorities with measured GFR. The CKD-EPI creatinine equation is more accurate than the Modification of Diet in Renal Disease Study equation and could replace it for routine clinical use. National Institute of Diabetes and Digestive and Kidney Diseases.
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            Effect of allopurinol in chronic kidney disease progression and cardiovascular risk.

            Hyperuricemia is associated with hypertension, inflammation, renal disease progression, and cardiovascular disease. However, no data are available regarding the effect of allopurinol in patients with chronic kidney disease. We conducted a prospective, randomized trial of 113 patients with estimated GFR (eGFR) <60 ml/min. Patients were randomly assigned to treatment with allopurinol 100 mg/d (n = 57) or to continue the usual therapy (n = 56). Clinical, biochemical, and inflammatory parameters were measured at baseline and at 6, 12, and 24 months of treatment. The objectives of study were: (1) renal disease progression; (2) cardiovascular events; and (3) hospitalizations of any causes. Serum uric acid and C-reactive protein levels were significantly decreased in subjects treated with allopurinol. In the control group, eGFR decreased 3.3 +/- 1.2 ml/min per 1.73 m(2), and in the allopurinol group, eGFR increased 1.3 +/- 1.3 ml/min per 1.73 m(2) after 24 months. Allopurinol treatment slowed down renal disease progression independently of age, gender, diabetes, C-reactive protein, albuminuria, and renin-angiotensin system blockers use. After a mean follow-up time of 23.4 +/- 7.8 months, 22 patients suffered a cardiovascular event. Diabetes mellitus, previous coronary heart disease, and C-reactive protein levels increased cardiovascular risk. Allopurinol treatment reduces risk of cardiovascular events in 71% compared with standard therapy. Allopurinol decreases C-reactive protein and slows down the progression of renal disease in patients with chronic kidney disease. In addition, allopurinol reduces cardiovascular and hospitalization risk in these subjects.
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              Clinical practice. Autosomal dominant polycystic kidney disease.

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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                nefrologia
                Nefrología (Madrid)
                Nefrología (Madr.)
                Sociedad Española de Nefrología (Cantabria, Santander, Spain )
                0211-6995
                1989-2284
                2012
                : 32
                : 2
                : 197-205
                Affiliations
                [01] Madrid orgnameHospital General Universitario Gregorio Marañón orgdiv1Servicio de Nefrología
                [02] Madrid orgnameClínica Dialcentro
                Article
                S0211-69952012000200011
                1577af56-31ec-430b-a166-9e039cb4c141

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 01 October 2011
                : 06 December 2011
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 51, Pages: 9
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                SciELO Spain


                Enfermedades renales poliquísticas,Polycystic kidney diseases

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