RESUMEN
The cardiorenal syndrome is a complex entity in which a primary heart dysfunction causes kidney injury (Types 1 and 2) and vice versa (Types 3 and 4), being either acute or chronic events, or maybe the result of a systemic disease that involves both organs (Type 5). Approximately 49% of heart failure cases present some grade of kidney dysfunction, significantly increasing morbidity and mortality rates. Its pathogenesis involves a variety of hemodynamic, hormonal and immunological factors that in the majority of cases produce fluid overload; the diagnosis and treatment of such constitutes the disease's management basis. Currently, a clinical based diagnosis is insufficient and the use of biochemical markers, such as natriuretic peptides, or lung and heart ultrasound is required. These tools, along with urinary sodium levels, allow the evaluation of therapy effectiveness. The preferred initial decongestive strategy is based on a continuous infusion of a loop diuretic with a step-up dosing regimen, aiming for a minimal daily urine volume of 3 liters, with the possibility to sequentially add potassium sparing diuretics, thiazide diuretics and carbonic anhydrase inhibitors to reach the diuresis goal, leaving ultrafiltration as a last resource due to its higher rate of complications. Finally, evidence-based therapy should be given to improve quality of life, decrease mortality, and delay the deterioration of kidney and heart function over the long term.
El síndrome cardiorrenal es una entidad compleja en la que la disfunción primaria cardíaca produce daño renal (tipos 1 y 2) y viceversa (tipos 3 y 4) y los episodios pueden ser agudos o crónicos o bien efecto de una enfermedad sistémica que afecta a ambos órganos (tipo 5). Hasta 49% de los pacientes con insuficiencia cardíaca muestra algún grado de disfunción renal, lo que aumenta de manera significativa la morbilidad y mortalidad. Su patogenia incluye diversos factores hemodinámicos, hormonales e inmunológicos que en la mayor parte de los casos producen sobrecarga hídrica, y cuyo diagnóstico y tratamiento son la base de su atención. En la actualidad, el diagnóstico clínico es insuficiente y se requieren marcadores bioquímicos, como péptidos natriuréticos, o el uso de ultrasonido pulmonar y cardíaco; estas herramientas, junto con la medición del sodio urinario, también permiten vigilar la efectividad terapéutica. De modo inicial se prefieren las medidas descongestivas con diuréticos de asa en infusión continua a dosis escalonadas para alcanzar una diuresis mínima de 3 L por día, con la posibilidad de agregar diuréticos ahorradores de potasio, tiazidas e inhibidores de la anhidrasa carbónica de modo secuencial para alcanzar el objetivo; como último recurso se recurre a la ultrafiltración en virtud de su mayor tasa de complicaciones. Por último, se debe indicar tratamiento con base en la evidencia para mejorar la calidad de vida, reducir la mortalidad y retrasar el deterioro de la función renal y cardíaca a largo plazo.
Asunto(s)
Síndrome Cardiorrenal , Insuficiencia Cardíaca , Síndrome Cardiorrenal/diagnóstico , Síndrome Cardiorrenal/terapia , Insuficiencia Cardíaca/tratamiento farmacológico , Insuficiencia Cardíaca/terapia , Hemodinámica , Humanos , Calidad de Vida , Ultrafiltración/efectos adversosRESUMEN
OBJECTIVE: Modified ultrafiltration (MUF) reduces some of the complications associated with cardiopulmonary bypass (CPB) in pediatric cardiac surgery. However, we have observed hypokalemia and hypomagnesemia in children when MUF is used. Such alterations may elicit severe arrhythmias in the postoperative period. To date, no studies have focused on the effects MUF may have in plasma levels of potassium (K) and magnesium (Mg). The objective of our study was to determine if there is any variation in plasma levels of K (plK) and Mg (plMg) after MUF in children undergoing cardiac surgery with CPB. PATIENTS: Sixteen children scheduled for cardiac surgery with CBP and MUF were prospectively studied. Anesthetic, CPB and MUF management were standardized for all patients, the latter lasting for 10 minutes. RESULTS: Plasma K average levels before and after MUF were 4.16 mmol/L and 3.58 mmol/L, respectively. The average plasma Mg levels before and after MUF were 4.82 mmol/L and 4.81 mmol/L, respectively. CONCLUSIONS: The plasma level of K is reduced by 13.7% after MUF (p<0.0001). The reduction in Mg at the same period of time was not statistically significant (p<0.970).