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en: Lower mortality in calcimimetic users compared to non-users in dialysis patients with serum parathyroid hormone levels within the target range.

en: Lower serum parathyroid hormone (PTH) levels are reported to improve mortality and fracture incidence in patients using calcimimetics. We investigated the prognosis of calcimimetic users and non-users with similar PTH levels within the target range. This retrospective study compared 2-year all-cause mortality and the incidence of any fracture in dialysis patients between calcimimetic users (n = 131) and non-users (n = 294) with PTH levels between 60 and 240 pg/mL using a propensity score-matched model. Kaplan-Meier survival curves censored by PTH level, calcimimetic use, and other factors were compared; then, adjusted Cox proportional hazards regression analysis was performed. After matching, mortality was significantly lower in calcimimetic users than in non-users (n = 130; hazard ratio [HR] 0.243, 95% confidence interval [CI] 0.073-0.801, P = 0.022, log-rank test). The PTH levels of users and non-users were 142.4 ± 49.4 and 132.7 ± 48.0 pg/mL, respectively (P = 0.127). Cox regression analysis demonstrated that mortality was significantly lower in users than in non-users (adjusted HR 0.260, 95% CI 0.071-0.947, P = 0.041). Calcimimetic use had no effect on fracture incidence. These findings suggest that, among dialysis patients with PTH levels between 60 and 240 pg/mL, mortality risk was significantly lower among calcimimetic users than in non-users. However, fracture risk was not significantly different between these groups.

en: Scientific Reports

ja: Scientific Reports


en: Improved survival with high albumin leakage in patients with protein-energy wasting and inflammation on hemodialysis and online hemodiafiltration.

en: Albumin leakage (Alb-L) and serum albumin (S-Alb) levels are predictors of mortality in dialysis patients. Because protein-energy wasting (PEW) and inflammation reduce hepatic albumin synthesis, we hypothesized that mortality would differ based on Alb-L and/or S-Alb levels, depending on the presence of PEW and inflammation. This retrospective study included 738 super high-flux hemodialysis (SHF HD) and online hemodiafiltration (OHDF) patients. Three-year all-cause mortality was compared in patients without PEW and inflammation (Group 1) and with PEW and/or inflammation (Group 2) using a propensity score matching model and Cox regression analysis with adjustment. In Group 2, mortality in patients with "high Alb-L" or "high S-Alb" was significantly lower in comparison to low groups, but not in Group 1. In Group 2, mortality in the "high Alb-L" and "high S-Alb (3.5 ± 0.2 g/dL)" group was lower than in other groups, including Group 1, except for the "high Alb-L" and "low S-Alb (3.2 ± 0.2 g/dL)" group, which had no deaths. In SHF HD and OHDF patients with PEW and/or inflammation, "high Alb-L" with normoalbuminemia to mild hypoalbuminemia improved survival to a level similar to patients without PEW and inflammation. Additionally, Alb-L and/or S-Alb had little impact on mortality in patients without PEW and inflammation.


en: Ability of NAD and Sirt1 to epigenetically suppress albuminuria.

en: The time for diabetic nephropathy (DN) to progress from mild to severe is long. Thus, methods to continuously repress DN are required to exert long-lasting effects mediated through epigenetic regulation. In this study, we demonstrated the ability of nicotinamide adenine dinucleotide (NAD) and its metabolites to reduce albuminuria through Sirt1- or Nampt-dependent epigenetic regulation. We previously reported that proximal tubular Sirt1 was lowered before glomerular Sirt1. Repressed glomerular Sirt1 was found to epigenetically elevate Claudin-1. In addition, we reported that proximal tubular Nampt deficiency epigenetically augmented TIMP-1 levels in Sirt6-mediated pathways, leading to type-IV collagen deposition and diabetic fibrosis. Altogether, we propose that the Sirt1/Claudin-1 axis may be crucial in the onset of albuminuria at the early stages of DN and that the Nampt/Sirt6/TIMP-1 axis promotes diabetic fibrosis in the middle to late stages of DN. Finally, administration of NMN, an NAD precursor, epigenetically potentiates the regression of the onset of DN to maintain Sirt1 and repress Claudin-1 in podocytes, suggesting the potential use of NAD metabolites as epigenetic medications for DN.

en: Clinical and Experimental Nephrology

ja: Clinical and Experimental Nephrology


en: Development of adult T-cell leukemia/lymphoma during immunosuppressive Therapy for human T-cell leukemia virus type 1 associated arthropathy

ja: リウマチ様関節炎に対する免疫抑制療法中に発症した成人T細胞性白血病/リンパ腫の1例

en: A 64-year-old woman presented with lower leg edema, fever, and bilateral joint pain, involving the wrists, fingers, and knees, in April 201X. Serological test results were negative for rheumatoid factor, antinuclear antibody, and anti-cyclic citrullinated peptide antibody. A diagnosis of remitting seronegative symmetrical synovitis with pitting edema syndrome, a type of seronegative rheumatoid arthritis, was made and prednisolone was administered. The joint pain was refractory to prednisolone therapy. In February, 201X+2, the patient presented with right cervical lymphadenopathy. The CT scan revealed swelling of the cervical, axillary, and inguinal lymph nodes bilaterally and rapidly enlarged. In April, 18F-fluorodeoxyglucose PET/CT scan showed an abnormal collection in the enlarged lymph nodes. The patient subsequently developed hoarseness with dyspnea and attended our department. Blood test results showed high levels of lactate dehydrogenase (547U/L) and soluble interleukin‐2 receptor (34200 IU/L) and were positive for anti-human T-cell leukemia virus type1 (HTLV‐1) antibody. Biopsy of the right cervical lymph node showed proliferation of abnormal lymphoid cells positive for CD3, CD4, and CD25 and negative for CD7. Monoclonal integration of HTLV‐1 proviral DNA was detected in the lymph node. A diagnosis of adult T-cell leukemia/lymphoma (ATLL), lymphoma type was made. The pain involving multiple joints was attributed to HTLV‐1associated arthropathy. Immunosuppressive therapy for HTLV‐1 carrier status may have played a role in the development of ATLL.

en: Shikoku Acta Medica

ja: 四国医学雑誌