Yuko Mutsuyoshi

Background: We evaluated the anti-SARS-CoV-2 spike antibody response following seven doses of the BNT162b2 messenger RNA COVID-19 vaccine in patients undergoing hemodialysis and investigated factors associated with antibody levels after the fifth, sixth, and seventh doses. Methods: Forty patients were recruited in the analysis of this single-center, prospective, longitudinal study. Changes in anti-SARS-CoV-2 spike antibody levels between the second and seventh doses were evaluated. Factors independently associated with the antibody levels after the fifth, sixth, and seventh doses were determined by multiple linear regression analyses. Results: The antibody level was significantly higher 4 weeks after the third dose than 4 weeks after the second dose (17,000 [interquartile range (IQR), 9916–30,500] vs. 2372 [IQR, 896–4206] AU/mL, p < 0.001). The level was also significantly higher 4 weeks after the fourth dose than 4 weeks after the third dose (27,000 [IQR, 10,453–46,500] vs. 17,000 [IQR, 9916–30,500] AU/mL, p < 0.05). However, the levels 4 weeks after the fifth, sixth, and seventh doses were not significantly different from the level 4 weeks after the fourth dose. The antibody level 1 week before vaccination was correlated with the antibody level 4 weeks after vaccination at the fifth dose (standard coefficient [β] = 0.736, p < 0.001), sixth dose (β = 0.601, p < 0.001), and seventh dose (β = 0.717, p < 0.001). Conclusions: The antibody level increased between the second and fourth doses and then plateaued through the seventh doses in hemodialysis patients. The pre-vaccination antibody level was associated with the post-vaccination antibody level at the fifth, sixth, and seventh doses in this population.

Background: Intradialytic hypotension (IDH) is a critical pathological condition associated with all-cause mortality in patients undergoing hemodialysis (HD). However, few studies have investigated IDH-related changes in hepatic and cerebral regional tissue oxygen saturation (rSO₂). This study investigated IDH-induced changes in hepatic and cerebral rSO₂. Methods: Hepatic and cerebral rSO₂ during HD were measured using an INVOS 5100C oxygen saturation monitor, and their percentage (%) changes during the development of IDH were analyzed. Ninety-one patients undergoing HD were investigated, including twenty with IDH. Results: In patients with IDH, % changes in hepatic and cerebral rSO₂ decreased at the onset of IDH. Additionally, the % change in hepatic rSO₂ was significantly larger than that in cerebral rSO₂ (p < 0.001). In patients without IDH, no significant differences were found between the % changes in hepatic and cerebral rSO₂ at the time of the lowest systolic blood pressure during HD. Multivariable linear regression analysis showed that the difference between the % changes in cerebral and hepatic rSO₂ was significantly associated with the development of IDH (p < 0.001) and the ultrafiltration rate (p = 0.010). Conclusions: Hepatic and cerebral rSO₂ significantly decreased during the development of IDH, and hepatic rSO₂ was more significantly decreased than cerebral rSO₂ at the onset of IDH.

Background: Intradialytic hypotension (IDH) is a critical pathological condition associated with all−cause mortality in patients undergoing hemodialysis (HD). However, few studies have investigated IDH-related changes in hepatic and cerebral regional tissue oxygen saturation (rSO2). This study investigated IDH-induced changes in hepatic and cerebral rSO2. Methods: Hepatic and cerebral rSO2 during HD were measured using an INVOS 5100C oxygen saturation monitor, and their percentage (%) changes during IDH development were analyzed. Ninety-one patients undergoing HD were investigated, including 20 with IDH development. Results: In patients with IDH, % changes in hepatic and cerebral rSO2 decreased at IDH onset. Additionally, the % change in hepatic rSO2 was significantly larger than those in cerebral rSO2 (P < 0.001). In patients without IDH, no significant differences were found between the % changes in hepatic and cerebral rSO2 at time of the lowest systolic blood pressure during HD. Multivariable linear regression analysis showed that the difference between the % change in cerebral and hepatic rSO2 was significantly associated with IDH development (P < 0.001) and ultrafiltration rate (P = 0.010). Conclusion: Hepatic and cerebral rSO2 significantly decreased in IDH development and hepatic rSO2 was more largely decreased than cerebral rSO2 at IDH onset.

Near-infrared spectroscopy has been used to measure regional oxygen saturation (rSO₂), and intradialytic tissue rSO₂ measurements have been playing an important role in evaluating changes in tissue oxygenation in various clinical settings of hemodialysis (HD) therapy. However, few reports have described changes in hepatic oxygenation associated with body fluid management in overhydrated HD patients. We herein report an HD patient with congestive heart failure (CHF) that had improved systemic and tissue oxygenation, including in the brain and liver, during HD with ultrafiltration. A 73-year-old man undergoing HD was admitted to our hospital with CHF. After admission, HD with ultrafiltration was performed to adequately manage his body fluid excess. Because of deterioration of systemic oxygenation on admission, we monitored his percutaneous arterial oxygen saturation (SpO₂) using a pulse oximeter and regional oxygen saturation (rSO₂) in the brain and liver using an INVOS 5100c oxygen saturation monitor during HD. At HD initiation, his cerebral and hepatic rSO₂ levels were relatively low, at 43.2% and 34.1%, respectively, in addition to the SpO₂ of 88%. During HD with ultrafiltration, systemic oxygenation evaluated by SpO₂ and tissue oxygenation by cerebral and hepatic rSO₂ improved. Interestingly, the hepatic rSO₂ ratio, defined as the ratio of rSO₂ values at t (min) during HD and the initial rSO₂ value before HD, increased larger than the cerebral rSO₂ ratio during HD. After the adjustment of body fluid condition under the maintained SpO₂ values, we confirmed the hepatic and cerebral SO₂ ratio again during HD, and these two values changed nearly in the same manner. Throughout our experience, in this case, we confirmed a remarkable increase in hepatic rSO₂ ratio relative to cerebral rSO₂ ratio under a CHF status during HD, and these differences disappeared after the adjustment of the body fluid status.

Background: Proteinase 3-antineutrophil cytoplasmic antibody has been reported to be positive in 5–10% of cases of renal injury complicated by infective endocarditis; however, histological findings have rarely been reported for these cases. Case presentation: A 71-year-old Japanese man with a history of aortic valve replacement developed rapidly progressive renal dysfunction with gross hematuria and proteinuria. Blood analysis showed a high proteinase 3-antineutrophil cytoplasmic antibody (163 IU/ml) titer. Streptococcus species was detected from two separate blood culture bottles. Transesophageal echocardiography detected mitral valve vegetation. Histological evaluation of renal biopsy specimens showed necrosis and cellular crescents in glomeruli without immune complex deposition. The patient met the modified Duke criteria for definitive infective endocarditis. On the basis of these findings, the patient was diagnosed with proteinase 3-antineutrophil cytoplasmic antibody-positive necrotizing crescentic glomerulonephritis complicated by Streptococcus infective endocarditis. His renal disease improved, and his proteinase 3-antineutrophil cytoplasmic antibody titer normalized with antibiotic monotherapy. Conclusion: Few case reports have described histological findings of proteinase 3-antineutrophil cytoplasmic antibody-positive renal injury complicated with infective endocarditis. We believe that an accumulation of histological findings and treatments is mandatory for establishment of optimal management for proteinase 3-antineutrophil cytoplasmic antibody-positive renal injury complicated with infective endocarditis.