Correction of Hyponatremia by Tolvaptan Before Left Ventricular Assist Device Implantation

Imamura, Teruhiko; Kinugawa, Koichiro; Shiga, Taro; Kato, Naoko; Endo, Miyoko; Inaba, Toshiro; Maki, Hisataka; Hatano, Masaru; Yao, Atsushi; Hirata, Yasunobu; Nishimura, Takashi; Kyo, Shunei; Ōno, Minoru; Nagai, Ryozo

doi:10.1536/ihj.53.391

Cited by 13 publications

(13 citation statements)

References 17 publications

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“…[1][2][3][4][5][6][7][8][9][10] In contrast, we sometimes experience TLV-non-responders in our daily clinical practice. 11) We previously proposed a novel predictor of responsiveness to TLV, ie, the baseline urine aquaporin-2 (U-AQP2) level relative to the plasma AVP (P-AVP) level, which may indicate a preserved vasopressin type 2 receptor (V2R)-related signaling pathway in the principal cells of the renal collecting duct.…”

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Tolvaptan Prolongs Blockage of the Vasopressin Type II Receptor Over 24 Hours in Responders With Stage D Heart Failure

2016

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SummaryThe urine aquaporin-2 (U-AQP2) level relative to the plasma arginine vasopressin (P-AVP) level is a novel predictor of the responsiveness to the vasopressin type 2 receptor (V2R) antagonist tolvaptan (TLV). However, little has been reported about the concentration-time profile of U-AQP2 after TLV treatment. We evaluated 24 patients with decompensated stage D heart failure (HF) who had received 3.75 mg/day of TLV on a de novo basis for > 7 days to treat congestion refractory to conventional diuretics. Seventeen patients were TLV-responders, whose 24-hour urine volume (UV) increased after TLV initiation; the other 7 patients were TLV-non-responders. The U-AQP2 of the TLV-responders, corrected for the urine creatinine concentration, decreased significantly at 4 hours after TLV administration without returning to the day-1 morning level on the morning of day-7. The TLV-non-responder U-AQP2 levels remained low even before the TLV treatment. On the morning of day-7, the TLV-responder U-AQP2/P-AVP ratio was comparable to that of the TLV-non-responders. Among 18 patients (11 responders and 7 non-responders), the day-7 TLV trough concentration was 64 ± 62 ng/mL and was negatively correlated with the estimated glomerular filtration rate (eGFR). TLV has antagonistic effects on the V2R over 24 hours in TLV-responders with advanced heart failure and chronic kidney disease, probably due to persistently elevated blood TLV concentration. The unresponsiveness to TLV in the TLV-non-responders is not attributable to malabsorption. (Int Heart J 2016; 57: 41-46)

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Tolvaptan Prolongs Blockage of the Vasopressin Type II Receptor Over 24 Hours in Responders With Stage D Heart Failure

2016

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“…[3][4][5][6][7] We also reported the effi cacy and safety of TLV in (1) amelioration of congestion even in stage D HF patients and (2) improvement of renal function by converting ongoing diuretics to TLV. 8,9) With respect to serum sodium concentration (S-Na), various studies in Europe and the United States have demonstrated the effi cacy of TLV to improve hyponatremia with little chance of hypernatremia, ie, S-Na > 145 mEq/L (eg, 1.7% of hypernatremia in the EVEREST study and 0% in the QUEST study). 2,6,[10][11][12] In Japan, we can administer TLV to HF patients to treat their congestion regardless of baseline S-Na as long as hypernatremia or rapid increases in S-Na do not develop.…”

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Urine Sodium Excretion After Tolvaptan Administration Is Dependent Upon Baseline Serum Sodium Levels

et al. 2014

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SummarySeveral studies have demonstrated that tolvaptan (TLV) can improve hyponatremia in advanced heart failure (HF) patients with rare chance of hypernatremia. However, changes in serum sodium concentrations (S-Na) in patients with or without hyponatremia during TLV treatment have not been analyzed.Ninety-seven in-hospital patients with decompensated HF who had received TLV at 3.75-15 mg/day for 1 week were enrolled. Among 68 "responders", who had achieved any increases in urine volume (UV) during the fi rst day, urinary sodium excretion during 24 hours (U-NaEx 24 ) increased signifi cantly during one week of TLV treatment along with higher baseline S-Na (P < 0.05 and r = 0.325). Considering a cut-off value (S-Na, 132 mEq/L; AUC, 0.711) for any increases in U-NaEx 24 , we defi ned "hyponatremia" as S-Na < 132 mEq/L. In hyponatremic responders (n = 25), S-Na increased signifi cantly, although 1 week was not suffi cient for normalization (125.8 ± 5.0 versus 128.9 ± 4.3 mEq/L, P < 0.05), along with unchanged U-NaEx 24 (2767 ± 2703 versus 2972 ± 2950 mg/day, NS). In contrast, in normonatremic responders (n = 43), S-Na remained unchanged (136.6 ± 3.1 versus 137.4 ± 2.9 mEq/L, NS) along with increased UNaEx 24 (2201 ± 1644 versus 4198 ± 3550 mg/day, P < 0.05).TLV increased S-Na only in hyponatremic responders by way of pure aquaresis, but increased U-NaEx 24 only in normonatremic responders, which explains the scarcity of hypernatremia. Epithelial Na-channels in the distal nephrons, whose repression by TLV increases urinary sodium excretion, may be attenuated by reduced ATP-supply in worse hemodynamics under hyponatremia. (Int Heart J 2014; 55: 131-137) Key words: Heart failure, Vasopressin, Urine osmolality T he orally active vasopressin antagonists vaptans provide potential effects to treat chronic water-retaining disorders. 1) Among them, the vasopressin type 2 (V2) receptor antagonist tolvaptan (TLV) has been available for patients with heart failure (HF) with symptomatic congestion or hyponatremia.2) TLV has been demonstrated to ameliorate congestion, stabilize hemodynamics, and improve renal function without any signifi cant adverse effects.3-7) We also reported the effi cacy and safety of TLV in (1) amelioration of congestion even in stage D HF patients and (2) improvement of renal function by converting ongoing diuretics to TLV. 8,9) With respect to serum sodium concentration (S-Na), various studies in Europe and the United States have demonstrated the effi cacy of TLV to improve hyponatremia with little chance of hypernatremia, ie, S-Na > 145 mEq/L (eg, 1.7% of hypernatremia in the EVEREST study and 0% in the QUEST study). 2,6,[10][11][12] In Japan, we can administer TLV to HF patients to treat their congestion regardless of baseline S-Na as long as hypernatremia or rapid increases in S-Na do not develop. However, no studies have examined the effi cacy and safety of TLV in patients with normonatremia thus far. Therefore, we have analyzed and compared the effect of TLV on S-Na between patients with and witho...

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“…Recently, TLV has been demonstrated to be advantageous in the correction of hyponatremia, 11,12) stabilization of hemodynamic state, 13) and amelioration of congestion without a worsening of renal function. 14) Administration of TLV along with discontinuation of trichlormethiazide successfully reversed his hyponatremia and renal dysfunction.…”

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Successful Conversion From Thiazide to Tolvaptan in a Patient With Stage D Heart Failure and Chronic Kidney Disease Before Heart Transplantation

et al. 2013

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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...

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Correction of Hyponatremia by Tolvaptan Before Left Ventricular Assist Device Implantation

Cited by 13 publications

References 17 publications

Tolvaptan Prolongs Blockage of the Vasopressin Type II Receptor Over 24 Hours in Responders With Stage D Heart Failure

Tolvaptan Prolongs Blockage of the Vasopressin Type II Receptor Over 24 Hours in Responders With Stage D Heart Failure

Urine Sodium Excretion After Tolvaptan Administration Is Dependent Upon Baseline Serum Sodium Levels

Successful Conversion From Thiazide to Tolvaptan in a Patient With Stage D Heart Failure and Chronic Kidney Disease Before Heart Transplantation

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