It is difficult to evaluate heart failure in hemodialysis patients because of high concentrations of BNP and NT-proBNP. The concentration changes of these peptides were measured in 26 hemodialysis patients from post-hemodialysis on the weekend to pre-hemodialysis at the beginning of the next week. The time course of NT-proBNP after hemodialysis completely corresponded to the logarithmic curve. Therefore, NT-proBNP kinetic analysis was performed using the single-compartment model and the elimination rate constant and half-life were determined. The elimination rate constant was estimated using NT-proBNP, body mass index (BMI) and estimated glomerular filtration rate (eGFR) using multiple regression analysis. The half-lives of NT-proBNP and BNP were 15.3±2.7 hours and 27.2±10.5 minutes, respectively. The BNP half-life got shorter in association with the severity of heart failure, but there was no significant change in the NT-proBNP half-life. This study indicates the formula for conversion between the NT-proBNP in hemodialysis patients and that in individuals with normal renal function. The converted NT-proBNP has a good relationship with the evaluation of heart failure by echocardiography. Thus, it is possible to evaluate heart failure by using NT-proBNP in hemodialysis patients as in individuals with normal renal function.

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In general hemodialysis sessions, blood flow rate (QB) has been controlled at around 200 mL/min because of several technical problems including apprehension about an increase in venous return and cardiac overload in the early days. We estimated cardiac output by ultrasound cardiography with changing QB during dialysis sessions. In 33 patients, QB change (400 mL/min, 200 mL/min, 400 mL/min) did not alter single stroke volume, heart rate, and their product (an indicator of cardiac output). Diameter of the inferior vena cava also showed no significant difference by QB increase. From this investigation, high QB may not consistently increase cardiac overload and cause heart failure in patients receiving hemodialysis without valve diseases.

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A 67-year-old man had been under hemodialysis since June 2010 because of chronic renal failure with unproven etiology. He had drunk alcohol at about 80 g/day. He had experienced appetite loss since March 2011. In mid-April, his fatigue had gotten worse and blood gas analysis showed remarkable hypoglycemia (30 mg/dL) and acidemia (pH 7.19) at an outpatient clinic. Although hemodialysis was started, it was stopped and he was injected with 20 g of glucose and transported to our hospital. Blood gas analysis at our hospital revealed pH 7.351, pCO₂ 29.1 torr, pO₂ 104.4 torr, HCO₃⁻ 16.1 mmol/L, and high anion-gap metabolic acidosis (anion-gap 23.9 mmol/L). Recognizing his disorientation and ataxia with anamnesis indicating that he could not have had a sufficient diet, we diagnosed Wernicke’s encephalopathy. Regarding the metabolic acidosis, we considered that alcoholic acidosis from an excessive intake of alcohol and lactic acidosis from a lack of vitamin B₁ (thiamine) had synergistically induced it. After admission, supplying glucose and vitamin B₁, his symptoms and metabolic acidosis clearly improved. We compared the serum vitamin B₁ level of 20 patients under maintenance hemodialysis in our hospital before and after hemodialysis. However, there was no significant difference (30.4±6.7 ng/mL and 30.2±7.2 ng/mL, respectively). On the other hand, a study has demonstrated a case that underwent 40% decrease in the serum vitamin B₁ level, so the possibility of removing vitamin B₁ with hemodialysis has been indicated. In addition, several cases of Wernicke’s encephalopathy in non-alcoholic patients on hemodialysis have been reported. We should consider the lack of vitamin B₁ and Wernicke’s encephalopathy when we recognize consciousness disturbance or metabolic acidosis in patients on maintenance hemodialysis, whether they are drinkers or not.

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