Impact of Remote Ischemic Preconditioning Conducted in Living Kidney Donors on Renal Function in Donors and Recipients Following Living Donor Kidney Transplantation: A Randomized Clinical Trial.

Although remote ischemic preconditioning (RIPC) has been shown to have renoprotective effects, few studies have assessed the effects of RIPC on renal function in living kidney donors. This study investigated whether RIPC performed in living kidney donors could improve residual renal function in donors and outcomes in recipients following kidney transplantation. The donors were randomized into a control group (n = 85) and a RIPC group (n = 85). The recipients were included according to the matched donors. Serum creatinine (sCr) concentrations and estimated glomerular filtration rate (eGFR) were compared between control and RIPC groups in donors and recipients. Delayed graft function, acute rejection, and graft failure within one year after transplantation were evaluated in recipients. sCr was significantly increased in the control group (mean, 1.13; 95% confidence interval (CI), 1.07-1.18) than the RIPC group (1.01; 95% CI, 0.95-1.07) (p = 0.003) at discharge. Donors with serum creatinine >1.4 mg/dL at discharge had higher prevalence of chronic kidney disease (n = 6, 26.1%) than donors with a normal serum creatinine level (n = 8, 5.4%) (p = 0.003) after one year. sCr concentrations and eGFR were similar in the RIPC and control groups of recipients over the one-year follow-up period. Among recipients, no outcome variables differed significantly in the RIPC and control groups. RIPC was effective in improving early renal function in kidney donors but did not improve renal function in recipients.

Impact of the serum albumin level on acute kidney injury after cerebral artery aneurysm clipping.

BACKGROUND: Although hypoalbuminemia is a known risk factor for acute kidney injury (AKI) following surgery, little is known about its effects following aneurysm clipping surgery. We aimed to investigate the predictors of AKI and overall mortality and assessed the relationship between preoperative albumin and postoperative outcomes after aneurysm clipping surgery. METHODS: This study included 2,339 patients who underwent aneurysm clipping surgery. According to the criteria updated by the Kidney Disease: Improving Global Outcomes (KDIGO), patients were classified into AKI and no AKI group. Independent AKI predictors were analyzed by multivariate methods, and the influence of AKI on the outcome variables was assessed with by propensity score matching analysis. Survival in relation to AKI was analyzed using the Kaplan-Meier method. RESULTS: The total proportion of patients who developed AKI was 1.9%. The cutoff value of preoperative albumin for predicting AKI was 3.9 g/dL. Multivariate analyses showed that preoperative albumin≤ 3.9 g/dL, aneurysmal subarachnoid hemorrhage, male sex, phenylephrine use, and hemoglobin were associated with postoperative AKI development. In multivariate analysis, mortality was increased in AKI patients (p< 0.01). After propensity score matching, preoperative albumin≤ 3.9 g/dL was significantly related to AKI and overall mortality. CONCLUSION: Preoperative albumin≤ 3.9 g/dL is associated with postoperative AKI and mortality.

Early postoperative albumin level following total knee arthroplasty is associated with acute kidney injury: A retrospective analysis of 1309 consecutive patients based on kidney disease improving global outcomes criteria.

Hypoalbuminemia has been reported to be an independent risk factor for acute kidney injury (AKI). However, little is known about the relationship between the albumin level and the incidence of AKI in patients undergoing total knee arthroplasty (TKA). The aim of our study was to assess incidence and risk factors for AKI and to evaluate the relationship between albumin level and AKI following TKA.The study included a retrospective review of medical records of 1309 consecutive patients who underwent TKA between January 2008 and December 2014. The patients were divided into 2 groups according to the lowest serum albumin level within 2 postoperative days (POD2_alb level < 3.0 g/dL vs ≥3.0 g/dL). Multivariate logistic regression analysis was used to assess risk factors for AKI. A comparison of incidence of AKI, hospital stay, and overall mortality in the 2 groups was performed using propensity score analysis.Of 1309 patients, 57 (4.4%) developed AKI based on Kidney Disease Improving Global Outcomes criteria. Factors associated with AKI included age (odds ratio [OR] 1.05; 95% confidence interval [CI] 1.01-1.09; P = 0.030), diabetes (OR 3.12; 95% CI 1.65-5.89; P < 0.001), uric acid (OR 1.51; 95% CI 1.26-1.82; P < 0.001), beta blocker use (OR 2.65; 95% CI 1.48-4.73; P = 0.001), diuretics (OR 16.42; 95% CI 3.08-87.68; P = 0.001), and POD2_alb level < 3.0 g/dL (OR 1.92; 95% CI 1.09-3.37; P = 0.023). After propensity score analysis, POD2_alb level<3.0 g/dL was associated with AKI occurrence (OR 1.82; 95% CI 1.03-3.24, P = 0.041) and longer hospital stay (P = 0.001).In this study, we demonstrated that POD2_alb level<3.0 g/dL was an independent risk factor for AKI and lengthened hospital stay in patients undergoing TKA.

The Antiallodynic Effects of Nefopam Are Mediated by the Adenosine Triphosphate-Sensitive Potassium Channel in a Neuropathic Pain Model.

BACKGROUND: Nefopam hydrochloride is a centrally acting compound that induces antinociceptive and antihyperalgesic properties in neuropathic pain models. Previous reports have shown that activation of adenosine triphosphate (ATP)-sensitive and calcium-activated potassium (KATP and KCa2+) channels has antiallodynic effects in neuropathic pain. In the present study, we evaluated the relationship between potassium channels and nefopam to determine whether the antiallodynic effects of nefopam are mediated by potassium channels in a neuropathic pain model. METHODS: Mechanical allodynia was induced by spinal nerve ligation (SNL) in rats, and the paw withdrawal threshold (PWT) was evaluated by the use of von Frey filaments. Nefopam was administered intraperitoneally before or after SNL. We assessed the relationship between nefopam and intrathecal injection of the KCa2+ channel antagonists apamin and charybdotoxin, and the KATP channel blocker glibenclamide to assess their abilities to reverse the antiallodynic effects of nefopam. In addition, we evaluated whether the KATP channel opener pinacidil had antiallodynic effects and promoted the antiallodynic effects of nefopam. RESULTS: Administration of nefopam before and after SNL induced significant antiallodynic effects (P < .01, respectively), which were significantly reduced by glibenclamide (P < .01). Pinacidil improved the antiallodynic effects of nefopam (P < .01); however, apamin and charybdotoxin had little effects on the antiallodynic properties of nefopam. CONCLUSIONS: The antiallodynic effects of nefopam are increased by a KATP channel agonist and reversed by a KATP channel antagonist. These data suggest that the KATP channel is involved in the antiallodynic effects of nefopam in a neuropathic pain model.