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Background Chronic kidney disease (CKD) is age-related disease, and decreased renal function is associated with the premature aging of T cells and increased incidence of other age-related diseases. However, the relationship between T cell senescence and CKD progression remains unclear. Here, we investigated the relationship between T cell senescence, as indicated by decreased thymic output and increased proportion of highly differentiated CD28− T cells, and CKD progression. Results A total of 175 patients with non-dialysis-dependent CKD were enrolled in this study. Thymic output was assessed based on the CD45RA+CD31+CD4+ cell (recent thymic emigrant [RTE]) counts (RTEs) (/mm3) and the proportion of RTE among CD4+ T cells (RTE%). Highly differentiated T cells were assessed based on the proportion of CD28− cells among CD4+ T cells (CD28−/CD4+) and CD28− cells among CD8+ T cells (CD28−/CD8+). The primary outcome was estimated glomerular filtration rate (eGFR) decline of ≥40% or initiation of renal replacement therapy. The association between T cell senescence and renal outcomes was examined using Cox proportional hazards models and restricted cubic splines. The median age was 73 years, 33% were women, and the median eGFR was 26 mL/min/1.73 m2. The median RTEs, RTE%, CD28−/CD4+, and CD28−/CD8+ were 97.5/mm3, 16.2, 5.3, and 49.7%, respectively. After a median follow-up of 1.78 years, renal outcomes were observed in 71 patients. After adjusting for age, sex, eGFR, proteinuria, diabetes, and cytomegalovirus seropositivity, decreased RTEs, which corresponded to decreased thymic output, significantly and monotonically increased the risk of poor renal outcome (p = 0.04), and decreased RTE% and increased highly differentiated CD28−/CD4+ T cells also tended to monotonically increase the risk (p = 0.074 and p = 0.056, respectively), but not CD28−/CD8+ T cells. Conclusions Decreased thymic output in CKD patients, as well as increased highly differentiated CD4+ T cells, predicted renal outcomes. Thus, the identification of patients prone to CKD progression using T cell senescence, particularly decreased RTE as a biomarker, may help to prevent progression to end-stage kidney disease.

Background Peritonitis is a serious and potentially fatal complication of peritoneal dialysis. We report a case of fatal peritonitis caused by Mycobacterium mageritense that was detected for the first time in peritonitis. Case presentation A male patient in his 60 s undergoing peritoneal dialysis was admitted for catheter diversion with exit-site renewal. The patient had a refractory exit-site infection. Mycobacterial culture was not performed at the exit site prior to admission. After the surgery, the patient developed a fever, and a cloudy effluent was observed. Various antibiotics, including anti-tuberculosis drugs, were administered; however, his symptoms did not improve. The catheter was removed on the thirty-seventh day of admission. Bacteria positive for Ziehl–Neelsen staining were found in the peritoneal sample collected during the surgery. Since nontuberculous mycobacteria were considered the cause of peritonitis, the patient was administered imipenem/cilastatin, amikacin, and clarithromycin. However, he died of septic shock on the fifty-first day after admission. Mycobacterium mageritense was detected in the ascites culture after death. Conclusion This is, to our knowledge, the first report of peritonitis caused by Mycobacterium mageritense. In patients undergoing peritoneal dialysis, when a refractory exit-site infection is observed, mycobacterial culture is necessary to prevent the development of peritonitis.

Background Blood purification therapy is a treatment method, wherein many patients gather in the same space to receive regular treatments, possibly increasing the risk of contracting the coronavirus disease 2019 (COVID-19) through contact, droplet, and aerosol. We experienced a nosocomial outbreak and evaluated the clinical characteristics of COVID-19 infection in patients undergoing blood purification therapy. Methods We retrospectively analyzed 28 patients who underwent blood purification therapy at the dialysis center of our hospital from April 2, 2020, to April 29, 2020. Logistic regression analysis was performed to identify clinical factors related to COVID-19 for 18 patients who were tested using real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Results Of the 28 patients, seven were COVID-19 positive, as confirmed by RT-PCR. The median age was 77 years, 22 patients were male (79%), four patients had acute kidney injury (14%), and six patients were bedridden (21%). All infected patients had been admitted to the wards where the nosocomial outbreak had occurred. Logistic regression analysis revealed that being bedridden (odds ratio 13.33, 95% confidence interval 1.05–169.56, p

Background Idiopathic membranous nephropathy (MN) is one of the major glomerulonephritis that cause nephrotic syndrome. The phospholipase A2 receptor (PLA2R) has recently been identified as an endogenous antigen of idiopathic MN. Thrombotic thrombocytopenic purpura (TTP) is a disorder characterized by schistocytes, hemolytic anemia, thrombocytopenia, and organ dysfunction which occurs as a result of thrombi. Patients with acquired TTP have autoantibodies against a disintegrin and metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13). These autoantibodies act as an inhibitor and cause ADAMTS13 deficiency. Idiopathic MN and acquired TTP are usually considered as independent autoimmune diseases. We experienced a patient who developed TTP during the conservative treatment of idiopathic MN, with the coexistence of ADAMTS13 inhibitor and anti-PLA2R antibody. Case presentation A 73-year-old man presented with thrombocytopenia, hemolytic anemia, disturbance of consciousness, and acute kidney injury after 4-year course of biopsy-proven idiopathic MN. ADAMTS13 activity was undetectable and the ADAMTS13 inhibitor was identified. Additionally, he was positive for anti-PLA2R antibody. The patient did not have any diseases that could cause secondary thrombotic microangiopathy, and he was diagnosed with acquired TTP. Steroid therapy and plasma exchange were initiated and the acquired TTP resolved. MN achieved remission 3 months after the anti-PLA2R antibody disappeared. Conclusions This is the first reported case of acquired TTP developed during conservative treatment of idiopathic MN, with both ADAMTS13 inhibitor and anti-PLA2R antibody positive at the onset of the TTP. The present case suggests that idiopathic MN might be associated with the development of some cases of acquired TTP.

Background Management of diabetic kidney disease (DKD) to prevent end-stage kidney disease (ESKD) has become a major challenge for health care professionals. This study aims to investigate the characteristics of patients with DKD when they are first referred to a nephrologist and the subsequent prognoses. Methods A total of 307 patients who were referred to our department from October 2010 to September 2014 at Osaka General Medical Center were analyzed. Independent risk factors associated with renal replacement therapy (RRT) and cardiovascular composite events (CVE) following their nephrology referral were later identified using Cox proportional hazards analysis. Results Of 307 patients, 26 (8.5%), 67 (21.8%), 134 (43.6%), and 80 (26.1%) patients were categorized as having chronic kidney disease (CKD) stages 3a, 3b, 4, and 5, respectively. The median estimated glomerular filtration rate (eGFR) and urinary protein levels were 22.3 mL/min/1.73 m2 and 2.83 g/gCr, respectively, at the time of the nephrology referral. During the follow-up period (median, 30 months), 121 patients required RRT, and more than half of the patients with CKD stages 5 and 4 reached ESKD within 60 months following their nephrology referral; 30% and Conclusion Patients with DKD were referred to nephrologist at CKD stage 4. Although almost half of the patients with CKD stage 5 at the time of nephrology referral required RRT within one-and-a-half years after the referral, kidney function of patients who were referred to nephrologist at CKD stage 3 and 4 were well preserved.

Aim School urine screening has been established in several countries of Asia, including Japan, Korea and Taiwan. In Osaka prefectural schools, the urine screening system had some problematic issues including an unclear referral procedure for students with abnormal urinary findings. Therefore, the school urine screening system was reviewed and restructured in 2004. The aim of this study was to assess the improvement in school urine screening through evaluation of the restructured Osaka prefectural school urinary screening system. Methods The Osaka prefectural school urinary screening system was reviewed, mainly considering two points. One was the incorporation of standard urinary protein/creatinine ratio measurement instead of the traditional urine dipstick and urine sediment tests; the second point was that all students requiring further examination were referred to regional nephrologists. Results After restructuring, the number of students who were referred to a medical institute for detailed examinations decreased to 10%, although the number of students newly diagnosed with kidney disease and the types of diagnosis did not change. The positive predictive value of screening increased to about 8 times the value before the system restructuring. The reductions enabled students who required further examination to be referred to regional nephrologists and has contributed to a decreased cost for these examinations. Conclusion Incorporating urinary protein/creatinine ratio measurement into the school urinary screening system, and updating the guiding principles, including referral to nephrology specialists, has enabled the school urinary screening system in Osaka Prefecture to become more efficient and have better cost performance.

Background Idiopathic membranous nephropathy (MN) is one of the major glomerulonephritis that cause nephrotic syndrome. The phospholipase A2 receptor (PLA2R) has recently been identified as an endogenous antigen of idiopathic MN. Thrombotic thrombocytopenic purpura (TTP) is a disorder characterized by schistocytes, hemolytic anemia, thrombocytopenia, and organ dysfunction which occurs as a result of thrombi. Patients with acquired TTP have autoantibodies against a disintegrin and metalloprotease with thrombospondin type 1 motif 13 (ADAMTS13). These autoantibodies act as an inhibitor and cause ADAMTS13 deficiency. Idiopathic MN and acquired TTP are usually considered as independent autoimmune diseases. We experienced a patient who developed TTP during the conservative treatment of idiopathic MN, with the coexistence of ADAMTS13 inhibitor and anti-PLA2R antibody. Case presentation A 73-year-old man presented with thrombocytopenia, hemolytic anemia, disturbance of consciousness, and acute kidney injury after 4-year course of biopsy-proven idiopathic MN. ADAMTS13 activity was undetectable and the ADAMTS13 inhibitor was identified. Additionally, he was positive for anti-PLA2R antibody. The patient did not have any diseases that could cause secondary thrombotic microangiopathy, and he was diagnosed with acquired TTP. Steroid therapy and plasma exchange were initiated and the acquired TTP resolved. MN achieved remission 3 months after the anti-PLA2R antibody disappeared. Conclusions This is the first reported case of acquired TTP developed during conservative treatment of idiopathic MN, with both ADAMTS13 inhibitor and anti-PLA2R antibody positive at the onset of the TTP. The present case suggests that idiopathic MN might be associated with the development of some cases of acquired TTP.