Altered diurnal rhythm should not be considered as a usual complication of renal disease. Inadequate antihypertensive pharmacotherapy could be related to the abnormalities of nighttime BP fall when it is detected.

Diabetic kidney disease (DKD) has been pointed out as a prominent cause of chronic and end-stage renal disease (ESRD). There is a genetic predisposition to DKD, although clinically relevant loci are yet to be identified. We utilized a custom target next-generation sequencing 70-gene panel to screen a discovery cohort of 150 controls, DKD and DKD-ESRD patients. Relevant SNPs for the susceptibility and clinical evolution of DKD were replicated in an independent validation cohort of 824 controls and patients. A network analysis aiming to assess the impact of variability along specific pathways was also conducted. Forty-eight SNPs displayed significantly different frequencies in the study groups. Of these, 28 with p-values lower than 0.01 were selected for replication. MYH9 rs710181 was inversely associated with the risk of DKD (OR = 0.52 (0.28–0.97), p = 0.033), whilst SOWAHB rs13140552 and CNDP1 rs4891564 were not carried by cases or controls, respectively (p = 0.044 and 0.023). In addition, the RGMA rs1969589 CC genotype was significantly correlated with lower albumin-to-creatinine ratios in the DKD patients (711.8 ± 113.0 vs. 1375.9 ± 474.1 mg/g for TC/TT; mean difference = 823.5 (84.46–1563.0); p = 0.030). No biological pathway stood out as more significantly affected by genetic variability. Our findings reveal new variants that could be useful as biomarkers of DKD onset and/or evolution.

Dual blockade of the renin-angiotensin system (RAS) has increased antiproteinuric effects and so a higher incidence of secondary effects can be expected when this kind of treatment is administered. The aim of this study was to assess the safety of dual blockade of RAS. Seventy-five (54 men and 21 women) patients has been treated in our unit with dual RAS blockade due to proteinuria higher than 1 g/24 h. Mean age was 57.1 +/- 14.0 years. Fifty-three patients had chronic renal failure (CRF) at baseline. Analytical data of 6 months visit and last follow-up visit were recorded. A small reduction of systolic blood pressure and diastolic blood pressure was observed in both treatment groups throughout the study. Neither the CRF patients nor those with normal renal function showed any reduction in mean plasma haemoglobin levels, but differences between groups were significant at the second and third visits (anova). No change was detected in haematocrit. Mean K+ significantly increase at the second visit in the CRF group (from 4.80 +/- 0.64 to 5.23 +/- 0.81 mmol/l, p < 0.001, Student's t-test). There were no changes in normal kidney function group (4.58 +/- 0.37 vs. 4.63 +/- 0.44). At baseline plasmatic creatinine was higher in the CRF group (2.09 +/- 0.60 0.20 mg/dl vs. 0.99 +/- 0.20 mg/dl, p < 0.001, Student's t-test) and creatinine clearance was lower (48.6 +/- 20.7 ml/min vs. 107.0 +/- 0.30 ml/min, p < 0.001, Student's t-test). There was a small increase in creatinine along the follow-up when compared with the normal renal function group (p < 0.001, anova). Conversely, creatinine clearance remain unchanged in the normal renal function group, and there was a decrease in creatinine in CRF patients (p < 0.001). Dual RAS blockade seems to be safe in renal patients even when mild to moderate renal failure is present. Severe hyperkalaemia is uncommon. Small increments in plasmatic creatinine can be seen but they are hardly dangerous. Combined treatment does not significantly influence erythropoiesis.

INTRODUCCIÓNLa MAPA es un elemento diagnóstico de extraordinario interés para la enfermedad más común que podemos encontrar en nuestra sociedad. Su uso se ha generalizado progresivamente en la práctica clínica tanto general como especializada. Además de sus utilidades desde el punto de vista experimental y para la investigación clínica (1,2), se han definido dos usos esenciales para la técnica. El primero de ellos es la confirmación del diagnóstico de HTA (o dicho al revés, la negación del diagnóstico 23 [0212-7199(2001) 18: 6; pp 305-308] ANALES DE MEDICINA INTERNA

Objetivo Determinar el valor pronóstico de tener un índice tobillo-brazo (ITB) bajo para padecer distintas enfermedades cardiovasculares y si mejora la capacidad predictiva de las principales funciones de riesgo cardiovascular. Diseño Estudio de cohorte poblacional. Emplazamiento Área sanitaria Don Benito-Villanueva de la Serena (Badajoz). España. Participantes Se seleccionaron 2.833 sujetos representativos de los residentes, entre 25 y 79 años. Mediciones Se midió el ITB en la inclusión y se registró el primer episodio de cardiopatía isquémica o ictus, la mortalidad cardiovascular y total en siete años de seguimiento. Se calcularon los hazard ratio (HR), ajustados por factores de riesgo cardiovascular, para el ITB bajo (< 0,9). Se determinaron los índices de reclasificación neta por categorías, clínica y continua para las funciones REGICOR, FRESCO cardiopatía isquémica, FRESCO enfermedad cardiovascular y SCORE. Resultados Se analizaron 2.665 sujetos tras excluir las personas con antecedentes cardiovasculares y las pérdidas. El ITB bajo se asoció con un mayor riesgo, alcanzando una HR (IC 95%) de 6,45 (3,00 – 13,86), 2,60 (1,15 – 5,91), 3,43 (1,39 – 8,44), 2,21 (1,27 – 3,86) para ictus, cardiopatía isquémica, mortalidad cardiovascular y total, respectivamente. La inclusión del ITB mejoró el índice de reclasificación (IC 95%) en el riesgo intermedio según FRESCO cardiovascular en un 24,1% (10,1 – 38,2). Conclusiones El ITB bajo está asociado con un incremento importante del riesgo de ictus, cardiopatía isquémica, mortalidad cardiovascular y total en nuestro medio. La inclusión del ITB mejoró la reclasificación de las personas con riesgo intermedio, según FRESCO cardiovascular, por lo que estaría justificada su utilización en esa categoría de riesgo.