SummaryChronic kidney disease (CKD) is often complicated with advanced heart failure because of not only renal congestion and decreased renal perfusion but also prolonged use of diuretics at higher doses, which sometimes results in hyponatremia. Preoperative CKD is known to be associated with poor prognosis after heart transplantation (HTx). We experienced a stage D heart failure patient with CKD and hyponatremia who was switched from trichlormethiazide to tolvaptan. His hyponatremia was normalized, and his renal function was improved after conversion to tolvaptan. In patients with stage D heart failure, it may be useful to administer tolvaptan with a concomitant reduction in the dose of diuretics in order to preserve renal function and avoid hyponatremia before HTx. (Int Heart J 2013; 54: 48-50) Key words: Hyponatremia, Diuretics, Renal dysfunction C hronic kidney disease (CKD) and hypervolemic hyponatremia are often complicated with advanced heart failure, and are not only attributable to renal congestion and reduced renal perfusion but also to extended use of diuretics at higher doses.1-5) Heart transplantation (HTx) is the comprehensive solution for patients with stage D heart failure refractory to optimal medical therapy thus far, 6) but it is well known that preoperative CKD results in a poor prognosis after HTx.7) It is especially important to preserve preoperative renal function since postoperative immunosuppressive therapy cannot help some kinds of renal impairment. 8) We experienced a stage D heart failure patient with CKD who was administered tolvaptan (TLV) and a vasopressin type 2 (V2) receptor antagonist, along with discontinuation of trichlormethiazide. His hyponatremia normalized and his renal function improved. Furthermore, his renal function remained within an acceptable range after HTx under immunosuppressive therapy including a calcineurin inhibitor.
Case ReportThe patient was a 53-year-old male with ischemic cardiomyopathy (Figure 1, Table) who had received coronary artery bypass surgery in March 2010. His heart failure worsened even after the bypass surgery, and he eventually became dependent on intravenous infusion of inotropes regardless of maximum medical therapy including carvedilol, enalapril, spironolactone, trichlormethiazide, and furosemide in August 2010. He was transferred to our hospital as a possible candidate for HTx in September 2010. His laboratory data on admission showed 137 mEq/L of serum sodium, 1.9 mg/dL of serum total bilirubin, 1.2 mg/dL of serum creatinine, and 636 pg/mL of plasma B-type natriuretic peptide. Transthoracic echocardiography indicated an ejection fraction of 28% and left ventricular diastolic diameter of 67 mm. A hemodynamic study performed in December 2010 demonstrated that mean right atrial pressure was 2 mmHg, mean pulmonary capillary wedge pressure was 21 mmHg, and the cardiac index was 2.2 L/minute/m 2 under continuous infusion of inotropes. He was then listed in February 2011 as a recipient of HTx. In the meantime, his serum creatinine increased...