RESUMEN
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)
Asunto(s)
Humanos , Soluciones para Hemodiálisis/farmacología , Diálisis Renal/métodos , Insuficiencia Renal/terapia , Fósforo/administración & dosificación , Hipofosfatemia/tratamiento farmacológico , Resultado del Tratamiento , Fósforo/farmacocinéticaRESUMEN
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.
Asunto(s)
Soluciones para Hemodiálisis/química , Fosfatos/administración & dosificación , Diálisis Renal , Algoritmos , Enema , Humanos , Hipofosfatemia/terapia , Fosfatos/análisis , Soluciones/químicaRESUMEN
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.