Association between pulse pressure and progression of chronic kidney disease.

The aim of this study was to investigate the association between pulse pressure (PP) and chronic kidney disease (CKD) progression among the general population in Japan. We conducted a population-based cohort study of the residents of Iki Island, Nagasaki, Japan, from 2008 to 2018. We identified 1042 participants who had CKD (estimated glomerular filtration rate(eGFR) < 60 mL/min/1.73 m2 or the presence of proteinuria) at baseline. Cox's proportional hazard model was used to evaluate the association between PP and progression of CKD. During a 4.66-year mean follow-up, there were 241 cases of CKD progression (incident rate: 49.8 per 1000 person-years). A significant increase existed in CKD progression per 10 mmHg of PP elevation, even when adjusted for confounding factors [adjusted hazard ratio 1.17 (1.06-1.29) p < 0.001]. Similar results were obtained even after dividing PP into quartiles [Q2: 1.14 (0.74-1.76), Q3: 1.35 (0.88-2.06), Q4: 1.87 (1.23-2.83) p = 0.003 for trend]. This trend did not change significantly irrespective of baseline systolic or diastolic blood pressures. PP remained a potential predictive marker, especially for eGFR decline. In conclusion, we found a significant association between PP and CKD progression. PP might be a potential predictive marker for CKD progression.

Usefulness of the blood pressure classification in the new 2017 ACC/AHA hypertension guidelines for the prediction of new-onset chronic kidney disease.

The aim of this study was to determine whether the blood pressure (BP) classification recommended in the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) hypertension guidelines is useful for the prediction of chronic kidney disease (CKD) in adults. We conducted a retrospective cohort study using annual health check data in Iki City, Nagasaki, Japan. A total of 3269 adults without CKD, who were not on BP-lowering medication, were included in the present analysis. BP was classified as: normal (systolic BP (SBP) <120 mmHg and diastolic BP (DBP) <80 mmHg), elevated BP (120 ≤ SBP < 130 and/or DBP < 80), stage 1 hypertension (130 ≤ SBP < 140 and/or 80 ≤ DBP < 90), and stage 2 hypertension (SBP ≥ 140 mmHg and/or DBP ≥ 90 mmHg). The primary outcome of the study was new-onset CKD. The effects of BP on the development of CKD were evaluated using Cox's proportional hazards modelling. During a mean follow-up of 4.8 years, 472 (14.4%) participants developed CKD. The incidence (per 1000 person-years) of new-onset CKD was higher in individuals with elevated BP. After adjustment for other risk factors, there were significant associations between elevated BP and new-onset CKD: hazard ratio 1.11 (95% confidence interval 0.87-1.42) in elevated BP, 1.25 (1.01-1.54) in stage 1 hypertension, and 1.45 (1.18-1.79) in stage 2 hypertension, compared with the reference group with normal BP (P < 0.001 for trend). Thus, the findings of this study confirm the definition of hypertension (≥130/80 mmHg) recommended by the 2017 ACC/AHA guidelines for the management of hypertension to be useful for the prediction of new-onset CKD.

Living-donor kidney transplant in T-cell and B-cell flow cytometry crossmatch-positive patients.

OBJECTIVES: Complement-dependent cytotoxic crossmatch is an important indicator for kidney transplant. However, there is controversy about treatment for flow cytometry crossmatch-positive cases. MATERIALS AND METHODS: This was a retrospective study of 127 living-donor kidney transplant recipients from May 2007 to July 2011. We divided patients into 115 flow cytometry crossmatch T-cell and B-cell-negative cases, and 12 T-cell and B-cell-positive cases. Both groups were given 20 mg basiliximab the day of surgery and 4 days after surgery. Common oral immunosuppressive agents used were tacrolimus, mycophenolate mofetil, and methylprednisolone. Flow cytometry crossmatch T-cell and B-cell-negative recipients started immunosuppression 7 days before surgery, T-cell and B-cell-positive recipients started immunosuppression 14 days before surgery. T-cell and B-cell-positive patients also received 200 mg rituximab 1 week before surgery, had 3 plasma exchange sessions before transplant, and received intravenous immunoglobulin 20 g/day during surgery and after surgery for 5 days. We measured flow-panel reactive antibodies of T-cell and B-cell-positive patients just before surgery to check desensitization efficiency. We evaluated patient survival, graft survival, graft function, and frequency of rejection and infectious diseases. RESULTS: Patient survival and graft survival were 100% in both groups. Flow cytometry crossmatch T-cell and B-cell-positive cases had no rejection events, but T-cell and B-cell-negative groups developed rejection. There was no statistical difference in the incidence of infection and graft function. Flow-panel reactive antibody demonstrated improvement in all T-cell and B-cell-positive cases. CONCLUSIONS: In living-donor kidney transplant, flow cytometry crossmatch T-cell and B-cell-positive patients are still considered to be at high risk. Although this is a short-term outcome, all T-cell and B-cell-positive patients in this study achieved excellent results with appropriate preoperative and postoperative treatment.