Influencia de la concentración de calcio en el líquido de hemodiálisis sobre el control de la tensión arterial / Influence of calcium concentration in haemodialysis fluid on blood pressure control

Introducción: La hipertensión arterial es altamente prevalente en los pacientes en hemodiálisis. Implica un mayor riesgo cardiovascular y es fundamental su control. A pesar de medidas dietéticas, optimización de la pauta de hemodiálisis y tratamiento farmacológico, existe un porcentaje de pacientes en nuestras unidades que continúan hipertensos. Es por ello que nos planteamos que la reducción de calcio en el líquido de diálisis puede ayudar al manejo de los pacientes hipertensos en hemodiálisis. Material y métodos: Se seleccionaron todos los pacientes hipertensos de nuestra unidad de hemodiálisis. Se comprobó estado de normovolemia mediante bioimpedancia espectroscópica y se disminuyó la concentración de calcio del líquido de hemodiálisis a 2,5 mEq/l, con un seguimiento de 12 meses. Resultados: Cumplieron criterios de hipertensión arterial no volumen-dependiente 24 pacientes (edad 61±15 años, varones el 48%, diabetes el 43%). Se observó una disminución significativa en la tensión arterial sistólica y diastólica a los 6 y 12 meses de la reducción de la concentración del calcio de diálisis, sin acompañarse de mayor inestabilidad hemodinámica (tensión arterial sistólica basal 162 ± 14; a los 6 meses 146 ± 18; a los 12 meses 141 ± 21 mmHg; p = 0,001) (tensión arterial diastólica basal 76 ± 14; a los 6 meses 70 ± 12; a los 12 meses 65 ± 11mmHg; p = 0,005) Existió un aumento de los niveles plasmáticos de PTH de forma no significativa. No se evidenciaron efectos secundarios. Conclusiones: La hemodiálisis con calcio en el líquido de 2,5mEq/l es una alternativa terapéutica eficaz y segura para el control de hipertensión arterial de difícil manejo en los pacientes de hemodiálisis

Background: Hypertension is a highly prevalent disorder among patients undergoing haemodialysis. It contributes to greater cardiovascular risk and must be controlled. However, despite dietary measures, haemodialysis regimen optimisation and pharmacological treatment, some patients in our units continue to maintain high blood pressure levels. The objective of the study is to demonstrate that reducing calcium in dialysis fluid can help treat hypertension patients undergoing haemodialysis. Material and methods: We selected all of the hypertensive patients from our haemodialysis unit. We checked their normovolemic status by means of bioimpedance spectroscopy, decreasing the haemodialysis fluid's calcium concentration to 2.5 mEq/l, with a follow-up period of 12 months. Results: A total of 24 patients met the non-volume dependent hypertension criteria (age 61±15 years, males 48%, diabetes 43%). A significant systolic and diastolic blood pressure decrease was observed at 6 and 12 months as a result of reducing the dialysis calcium concentration; this was not accompanied by greater haemodynamic instability (baseline systolic blood pressure: 162 ± 14 mmHg; at 6 months: 146 ± 18 mmHg; at 12 months: 141 ± 21 mmHg; P = .001) (baseline diastolic blood pressure: 76 ± 14 mmHg; at 6 months: 70 ± 12 mmHg; at 12 months: 65 ± 11 mmHg; P = .005). A non-significant increase in plasma parathyroid hormone levels was also found. No side effects were observed. Conclusions: Adding 2.5 mEq/l of calcium to dialysis fluid is a safe and effective therapeutic alternative to control hard-to-manage hypertension among haemodialysis patients

Influence of calcium concentration in haemodialysis fluid on blood pressure control. / Influencia de la concentración de calcio en el líquido de hemodiálisis sobre el control de la tensión arterial.

BACKGROUND: Hypertension is a highly prevalent disorder among patients undergoing haemodialysis. It contributes to greater cardiovascular risk and must be controlled. However, despite dietary measures, haemodialysis regimen optimisation and pharmacological treatment, some patients in our units continue to maintain high blood pressure levels. The objective of the study is to demonstrate that reducing calcium in dialysis fluid can help treat hypertension patients undergoing haemodialysis. MATERIAL AND METHODS: We selected all of the hypertensive patients from our haemodialysis unit. We checked their normovolemic status by means of bioimpedance spectroscopy, decreasing the haemodialysis fluid's calcium concentration to 2.5mEq/l, with a follow-up period of 12 months. RESULTS: A total of 24 patients met the non-volume dependent hypertension criteria (age 61±15 years, males 48%, diabetes 43%). A significant systolic and diastolic blood pressure decrease was observed at 6 and 12 months as a result of reducing the dialysis calcium concentration; this was not accompanied by greater haemodynamic instability (baseline systolic blood pressure: 162±14 mmHg; at 6 months: 146±18 mmHg; at 12 months: 141±21 mmHg; P=.001) (baseline diastolic blood pressure: 76±14 mmHg; at 6 months: 70±12 mmHg; at 12 months: 65±11 mmHg; P=.005). A non-significant increase in plasma parathyroid hormone levels was also found. No side effects were observed. CONCLUSIONS: Adding 2.5mEq/l of calcium to dialysis fluid is a safe and effective therapeutic alternative to control hard-to-manage hypertension among haemodialysis patients.

Receta para prescribir fósforo durante hemodiálisis / Follow a recipe to prescribe phosphate during hemodialysis

La adición de fósforo (P) en el líquido de hemodiálisis (LD) mediante enema con fosfato de sodio (enema Casen®) se utiliza habitualmente en pacientes con hipofosforemia. El cálculo de la cantidad y los problemas que puede presentar no se describen en la literatura. Nuestro trabajo hace un abordaje práctico de cómo poner fósforo en LD con una fórmula razonada para calcular cuánto volumen de enema añadir en función del concentrado de diálisis utilizado y los problemas que pueden aparecer (AU)

The addition of phosphorus (P) to the dialysate (LD) in the form of enema Casen® is common practice in patients with hypophosphatemia. The estimation of the amount to be used and the identification of the problems that may can occur are not well defined. As a result of our work we propose a practical approach of how to proceed to increase phosphate concentration in the hemodialysate. We present a reasoned formula to calculate how much enema has to be added and the problems that may arise (AU)

Follow a recipe to prescribe phosphate during hemodialysis. / Receta para prescribir fósforo durante hemodiálisis.

The addition of phosphorus (P) to the dialysate (LD) in the form of enema Casen® is common practice in patients with hypophosphatemia. The estimation of the amount to be used and the identification of the problems that may can occur are not well defined. As a result of our work we propose a practical approach of how to proceed to increase phosphate concentration in the hemodialysate. We present a reasoned formula to calculate how much enema has to be added and the problems that may arise.

Factors related with the progression of chronic kidney disease.

BACKGROUND: Our aims were to determine the rate of progression of chronic kidney disease (CKD) and to identify predictors, with particular emphasis on bone and mineral metabolism. METHODS: Retrospective and observational study including 300 patients with advanced CKD (61.2% males, 33.1% diabetics; age 65.6±14 years). Mean follow-up time was 19.4±10.1 months. Baseline estimated glomerular filtration rate (eGFR) (MDRD-4) was 22.5±7.18 mL/min. To calculate the rate of decline in eGFR, we used the slope of the regression line between all determinations of eGFR and follow-up time. We calculated the mean values for proteinuria and serum phosphate, calcium, uric acid, and PTH, as well as 24-hour urinary excretion of urea nitrogen over time for each patient. Follow-up was at least 6 months and included at least 4 measurements of eGFR. RESULTS: The mean rate of decline eGFR (-1.64 mL/min/1.73 m²/year) was inversely correlated with serum phosphate levels (4.3±2.1 mg/dL, P<.001), PTH (256.3±193.7 ng/L, p<.001) and proteinuria (0.84±1.31 g/day, P=.004) and directly correlated with mean serum calcium (P<.001) and the presence of hypertension (P<.02). However, only serum phosphate, serum PTH, and proteinuria persisted as predictors in the multivariate analysis. Stable-GFR patients (positive slope) were older (P=.041) and had lower serum phosphate and PTH levels (P<.01 and P<.01 respectively) and lower proteinuria (P<.01). CONCLUSIONS: The rate of decrease in eGFR was correlated with serum phosphate and PTH levels and proteinuria. All of these factors can be modified with an adequate treatment.

Factors related with the progression of chronic kidney disease

Background: Our aims were to determine the rate of progression of chronic kidney disease (CKD) and to identify predictors, with particular emphasis on bone and mineral metabolism. Methods: Retrospective and observational study including 300 patients with advanced CKD (61.2% males, 33.1% diabetics; age 65.6±14 years). Mean follow-up time was19.4±10.1 months. Baseline estimated glomerular filtration rate (eGFR) (MDRD-4) was 22.5±7.18mL/min. To calculate the rate of decline in eGFR, we used the slope of the regression line between all determinations of eGFR and follow-up time. We calculated the mean values for proteinuria and serum phosphate, calcium, uric acid, and PTH, as well as 24-hour urinary excretion of urea nitrogen over time for each patient. Follow-up was at least 6 months and included at least 4 measurements of eGFR. Results: The mean rate of decline eGFR (-1.64 mL/min/1.73m2/year) was inversely correlated with serum phosphate levels (4.3±2.1 mg/dL, p<.001), PTH (256.3±193.7ng/L, p<.001) and proteinuria (0.84±1.31g/day, p=.004) and directly correlated with mean serum calcium (p<.001) and the presence of hypertension (p<.02). However, only serum phosphate, serum PTH, and proteinuria persisted as predictors in the multivariate analysis. Stable-GFR patients (positive slope) were older (p=.041) and had lower serum phosphate and PTH levels (p<.01 and p<.01 respectively) and lower proteinuria (p<.01). Conclusions: The rate of decrease in eGFR was correlated with serum phosphate and PTH levels and proteinuria. All of these factors can be modified with an adequate treatment (AU)

Antecedentes: Nuestro propósito era determinar el índice de progresión de la enfermedad renal crónica (ERC) e identificar predictores, con especial énfasis en el metabolismo mineral y óseo. Métodos: Estudio retrospectivo y de observación que incluye a 300 pacientes con ERC avanzada (61,2 % varones, 33,1 % diabéticos; edad 65,6 ± 14 años). El tiempo medio de seguimiento fue de 19,4 ± 10,1 meses. El índice de filtración glomerular estimado (FGe) de referencia (MDRD-4) fue de 22,5 ± 7,18 ml/min. Para calcular la tasa de reducción en el IFGe, utilizamos la pendiente de la línea de regresión entre todas las determinaciones de IFGe y el tiempo de seguimiento. Calculamos los valores medios de proteinuria y fosfato sérico, calcio, ácido úrico y hormona paratiroidea (PTH), así como la excreción urinaria de 24 horas de nitrógeno ureico de cada paciente. El seguimiento fue, como mínimo, de 6 meses e incluyó al menos 4 mediciones de FGe. Resultados: La tasa media de reducción de FGe (-1,64 ml/min/1,73 m2/año) estaba inversamente correlacionada con los niveles de fosfato sérico (4,3 ± 2,1 mg/dl, p < 0,001), PTH (256,3 ± 193,7 mg/l, p < 0,001) y proteinuria (0,84 ± 1,31 g/día, p = 0,004) y directamente correlacionada con el calcio sérico medio (p < 0,001) y la presencia de hipertensión (p < 0,02). Sin embargo, únicamente el fosfato sérico, la PTH sérica y la proteinuria persistieron como predictores en el análisis multivariable. Los pacientes con IFG estable (pendiente positiva) eran mayores (p = 0,041) y presentaban niveles más bajos de fosfato sérico y PTH (p < 0,01 y p < 0,01, respectivamente), y proteinuria más baja (p < 0,01). Conclusiones: La tasa de reducción en el FGe estaba correlacionada con los niveles de fosfato sérico y PTH y la proteinuria. Todos estos factores pueden modificarse con el tratamiento adecuado (AU)

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

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 (AU)

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 (AU)

Chronic kidney disease progression in patients with autosomal dominant polycystic kidney disease.

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.

Factors related to the absence of anemia in hemodialysis patients.

BACKGROUND: A small number of hemodialysis (HD) patients have normal hemoglobin (Hb) levels without the need for erythropoiesis-stimulating agents (ESAs). The factors associated with this condition have been little studied. The objective of this prospective study was to determine these factors in a prevalent population of HD patients. MATERIALS AND METHODS: All patients who had normal Hb levels and who had not received ESAs in the last 6 months (non-ESA group) were included. Epidemiological and laboratory data were collected and we performed an abdominal ultrasound to assess hepatic and renal cysts. This group was compared to a control group of 205 prevalent HD patients on ESA therapy (control group). RESULTS: We included 45 patients (16% from the whole group) in the non-ESA group. In this group, there was a higher proportion of men (76.5 vs. 61%), patients were younger (61.1 ± 14.7 vs. 67.5 ± 15.2 years), had a longer duration of renal replacement therapy (RRT) (9.4 ± 8.3 vs. 5.3 ± 5.8 years) and had a higher prevalence of adult polycystic kidney disease (APKD) and hepatitis C virus (HCV) liver disease (42.2 vs. 10.2%), p < 0.01. In the non-ESA group, HCV+ patients had a lower prevalence of APKD (2.2 vs. 38.4%) and hepatic cysts (2.2 vs. 19.2%), but significantly higher endogenous erythropoietin levels (55.8 ± 37.1 vs. 30.9 ± 38.4 mU/ml). No significant differences in anemia, iron metabolism, insulin, IGF-1 and renin were found between non-ESA and control groups. Non-ESA patients had a significantly higher number of renal (90.6 vs. 36.5%) and hepatic cysts (12.5 vs. 3.4%), and these were also larger in size (3.3 ± 2.4 vs. 1.5 ± 0.8 cm). In the multivariate Cox analysis, independent predictor factors for absence of anemia in HD patients were number of renal cysts >10 cysts (95% CI 1.058-1.405; p = 0.00), HCV+ liver disease (95% CI 1.147-1.511; p = 0.05) and time on RRT (95% CI 1.002-1.121; p = 0.05). CONCLUSIONS: The absence of anemia in HD patients is not infrequent. Its frequency is higher in men and younger patients with long-term RRT, in patients with HCV+ liver disease and in APKD. It is associated with increased endogenous erythropoietin production and the presence of renal and hepatic cysts.

Effect of allopurinol in chronic kidney disease progression and cardiovascular risk.

BACKGROUND AND OBJECTIVES: 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. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: 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. RESULTS: 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. CONCLUSIONS: 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.