The patient was an 81-year-old female who had been receiving hemodialysis (HD) for 21 months. The patient was obese (body mass index [BMI]: 25.1±0.1); malnourished (serum albumin level: 3.3±0.03 g/dL, percentage creatinine generation rate [%CGR]: 56.0±1.8); and exhibited reductions in her muscle strength, walking speed, and ability to perform activities of daily living (which was considered to be due to frailty rather than sarcopenia). As the patient suffered frequent cramps and intradialytic hypotension, she was forced to stop receiving HD. HD removes not only uremic toxins, but also various nutrients, including water-soluble vitamins and amino acids. Therefore, there is a possibility that the amounts of nutrients removed by HD exceed those consumed via dietary intake, even after 4 hours HD (blood flow rate [QB]=200 mL/min, dialysis fluid flow rate [QD]=500 mL/min). Human energy levels are maintained by gluconeogenesis, which involves amino acid catabolism. Most amino acid catabolism involves glutamate as a reaction intermediate. In this study, the patient’s blood glutamate concentration increased after HD; nevertheless, HD removes plenty of glutamate. However, low-efficiency HD (QD: 200 mL/min, QB: 95 mL/min from 0-30 minutes, 170 mL/min from 30 to 90 minutes, 230 mL/min from 90 to 240 minutes) suppressed the increase in the patient’s blood glutamate concentration seen after HD. In other words, it suppressed gluconeogenesis. Eventually, low-efficiency HD significantly improved the patient’s nutritional status (serum albumin level: 3.6±0.1 g/dL, p=0.020; %CGR: 81.7±11.9, p=0.0024), BMI (27.1±0.22), and catabolic status. Furthermore, the number of rounds of treatment required for cramp combined with intradialytic hypotension dramatically decreased after the introduction of low-efficiency HD.

An 82-year-old female with severe renal impairment and therapy-resistant pulmonary hypertension (PH) was admitted on an emergency basis due to dyspnea. She had a history of occupational exposure to asbestos during her 20s and chronic kidney disease due to diabetic nephropathy and benign nephrosclerosis, an old myocardial infarction, and a pleural lesion that was compatible with asbestos-related disease (ARD). Laboratory tests performed upon admission revealed elevated levels of serum creatinine and brain natriuretic peptide. Hypoxia was also evident, but no pulmonary thromboembolisms were detected. Chest computed tomography demonstrated pleural thickening lesions with calcification. Ultrasound cardiography showed PH and congestion, but the patient’s left ventricular ejection fraction was within the normal range. Hemodialysis (HD) was started to reduce the burden of heart congestion and uremic toxins. However, the hypoxia persisted despite intensive care, including beraprost therapy and excess fluid removal by HD. The patient died as a result of complications (pneumonia, a myocardial infarction, and a stroke) on day 33 after admission. An autopsy revealed scattered pleural plaques (but no evidence of lung fibrosis or asbestos bodies) and marked medial thickening of the pulmonary artery. To the best of our knowledge, this is the first reported case of PH combined with ARD involving a patient with renal impairment. We consider that the patient’s asbestos exposure, renal failure, and left-sided heart disease all contributed to the development of therapy-resistant PH.