Saori Minato

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.

Purpose: We compared the efficacy of teneligliptin versus linagliptin for glycemic control and renoprotection in patients with advanced-stage diabetic kidney disease. Patients and Methods: Changes in the glycated hemoglobin (HbA1c), fasting blood glucose concentration, urine albumin-to-creatinine ratio (UACR), and estimated glomerular filtration rate (eGFR) during a 12-month period were retrospectively analyzed after switching from linagliptin to teneligliptin in 13 patients with advanced-stage diabetic kidney disease (teneligliptin group). Thirteen propensity score-matched patients who were treated with linagliptin alone served as controls (linagliptin group). Results: The HbA1c, fasting blood glucose concentration, and UACR did not change during the 12-month study period in either group. The annual change rate in the eGFR did not differ between before and after baseline in either group. Conclusion: Switching from linagliptin to teneligliptin may not improve glycemic control, reduce urinary protein excretion, or ameliorate the rate of renal function decline in patients with advanced-stage diabetic kidney disease. These results suggest that teneligliptin may not be more advantageous for glycemic control and renoprotection compared with linagliptin in patients with advanced-stage diabetic kidney disease.

Background: We investigated the effects of roxadustat on the anemia, iron metabolism, peritoneal membrane function, and residual renal function; and determined the factors associated with the administration of roxadustat in patients who were undergoing peritoneal dialysis.Methods: We retrospectively analyzed the changes in hemoglobin, serum ferritin, transferrin saturation (TSAT), 4-h dialysate/plasma creatinine, and renal weekly urea clearance over the 24 weeks following the change from an erythropoiesis-stimulating agent (ESA) to roxadustat in 16 patients who were undergoing peritoneal dialysis and had anemia (Roxadustat group). Twenty-three peritoneal dialysis patients who had anemia and continued ESA served as a control group (ESA group).Results: There were no significant differences in hemoglobin, serum ferritin, TSAT, 4-h dialysate/plasma creatinine, or renal weekly urea clearance between the two groups at baseline. The hemoglobin concentration was significantly higher in the Roxadustat group than in the ESA group after 24 weeks (11.6 ± 1.0 g/dL vs. 10.3 ± 1.1 g/dL, p < 0.05), whereas the ferritin concentration and TSAT were significantly lower (139.5 ± 102.0 ng/mL vs. 209.2 ± 113.1 ng/mL, p < 0.05; and 28.1 ± 11.5% vs. 44.8 ± 10.4%, p < 0.05, respectively). The changes in 4-h dialysate/plasma creatinine and renal weekly urea clearance did not differ between the two groups. Linear regression analysis revealed that the serum potassium concentration correlated with the dose of roxadustat at 24 weeks (standard coefficient = 0.580, p = 0.019).Conclusion: Roxadustat may improve the anemia and reduce the serum ferritin and TSAT of the peritoneal dialysis patients after they were switched from an ESA, without association with peritoneal membrane function or residual renal function.

Keiji Hirai, Susumu Ookawara, Junki Morino, Saori Minato, Shohei Kaneko, Katsunori Yanai, Hiroki Ishii, Momoko Matsuyama, Taisuke Kitano, Mitsutoshi Shindo, Haruhisa Miyazawa, Kiyonori Ito, Yuichirou Ueda, Tatsuro Watano, Shinji Fujino, Kiyoka Omoto, Yoshiyuki Morishita. Kidney Research and Clinical Practice 2020;39:441-50. https://doi.org/10.23876/j.krcp.19.126

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.

Background: We investigated the relationship between serum total carbon dioxide (CO2) and bicarbonate ion (HCO3-) concentrations in pre-dialysis chronic kidney disease (CKD) patients and devised a formula for predicting low bicarbonate (HCO3- < 24 mmol/L) and high bicarbonate (HCO3- >= 24 mmol/L) using clinical parameters. Methods: In total, 305 samples of venous blood collected from 207 pre-dialysis patients assessed by CKD stage (G1 + G2, 46; G3, 50; G4, 51; G5, 60) were investigated. The relationship between serum total CO2 and HCO3- concentrations was analyzed using Pearson's correlation coefficient. An approximation formula was developed using clinical parameters correlated independently with HCO3- concentration. Diagnostic accuracy of serum total CO2 and the approximation formula was evaluated by receiver operating characteristic curve analysis and a 2 x 2 table. Results: Serum total CO2 correlated strongly with HCO3- concentration (r = 0.91; P < 0.001). The following approximation formula was obtained by a multiple linear regression analysis: HCO3- (mmol/L) = total CO2- 0.5 x albumin - 0.1 x chloride - 0.01 x (estimated glomerular filtration rate + blood glucose) + 15. The areas under the curves of serum total CO2 and the approximation formula for detection of low bicarbonate and high bicarbonate were 0.981, 0.996, 0.993, and 1.000, respectively. This formula had superior diagnostic accuracy compared with that of serum total CO2 (86.6% vs. 81.3%). Conclusion: Serum total CO2 correlated strongly with HCO3- concentration in pre-dialysis CKD patients. An approximation formula including serum total CO2 showed superior diagnostic accuracy for low and high bicarbonate compared with serum total CO2.