Notes

Acute effects of sublingual nitroglycerin in cardiovagal as well as supportive baroreflex level of responsiveness.
05). In the ileal content, the population of Salmonella spp. decreased in the BV and BCV groups and the population of Lactobacillus spp. Metabolism inhibitor increased in the BV group (P  less then  0.05). The present results indicate that feeding BV or BCV alleviates damaged egg rate and decreases intestinal pathogenic bacteria, while feeding BC benefits by reducing abdominal fat. These results suggest that the effect of BCV seems to be induced by the synergistic effect of BC and BV, and that the BCV contributes to the effective use of bamboo on the laying hen's production.
In living kidney transplantation, predicting the risk of end-stage kidney disease in the organ donors though crucial remains to be resolved. Thus, any useful biomarker to predict kidney outcome would be highly desirable to safeguard donors.

This retrospective study was conducted at Nagoya Daini Red Cross Hospital to confirm whether an increase in preserved kidney volume (PKV) was a predict marker of proteinuria. A change of PKV before and 1year after kidney donation was measured, and its association with proteinuria 3years after the donation was analyzed.

A total of 119 kidney donors who met the Japanese donor guideline were enrolled. link2 The mean age was 57.4years, 46.2% were male. The mean values of the variables before kidney donation (baseline) were BMI levels 23.4kg/m
, BSA-adjusted PKV 132.9cm
/1.73m
, and estimated glomerular filtration rate (eGFRave) 82.9mL/min/1.73m
. A positive correlation was noted between BSA-adjusted PKV and eGFRave (r = 0.61, p < 0.001). BSA-adjusted PKV increased by 19.5% 1year after donation, and the median urine protein was 0.04g/gCre. Linear regression analyses showed that change of PKV and BSA-adjusted PKV before the donation were significantly associated with proteinuria 3years after donation.

Change of PKV and BSA-adjusted PKV before donation is important factors for proteinuria after donation under the Japanese donor guidelines. Further studies are needed to confirm whether these factors are associated with renal survival after donation.
Change of PKV and BSA-adjusted PKV before donation is important factors for proteinuria after donation under the Japanese donor guidelines. Further studies are needed to confirm whether these factors are associated with renal survival after donation.
There is no evidence regarding appropriate target hemoglobin levels in chronic kidney disease (CKD) patients with an erythropoiesis-stimulating agent (ESA)-hyporesponsiveness. Therefore, we conducted a randomized controlled study in non-dialysis dependent CKD (NDD-CKD) patients with ESA-hyporesponsiveness, comparing results of intensive versus conservative treatment to maintain hemoglobin levels.

This was a multicenter, open-label, randomized, parallel-group study conducted at 89 institutions. Among NDD-CKD patients, those with ESA-hyporesponsive renal anemia were randomly assigned to an intensive treatment group, to which epoetin beta pegol was administered with target hemoglobin level of 11g/dL or higher, or conservative treatment group, in which the hemoglobin levels at enrollment (within ± 1g/dL) were maintained. The primary endpoint was the time to the first kidney composite event defined as (1) transition to renal replacement therapy (dialysis or renal transplantation); (2) reduction of estimated glomerular filtration rate (eGFR) to less than 6.0mL/min/1.73m
; or (3) reduction of eGFR by 30% or more. Secondary endpoints were kidney function (change rate in eGFR), cardiovascular (CV) events, and safety.

Between August 2012 and December 2015, 385 patients were registered, and 362 patients who met the eligibility criteria were enrolled. There was no significant difference in kidney survival or in CV events between the two groups. However, the incidences of the 3 types of kidney composite events tended to differ.

In NDD-CKD patients with ESA-hyporesponsive renal anemia, the aggressive administration of ESA did not clearly extend kidney survival or result in a significant difference in the incidence of CV events.
In NDD-CKD patients with ESA-hyporesponsive renal anemia, the aggressive administration of ESA did not clearly extend kidney survival or result in a significant difference in the incidence of CV events.
Chronic kidney disease (CKD) patients are vulnerable to hepatitis B, and immunization prior to end stage kidney disease is recommended to optimize seroconversion. link3 Our institution undertook a process improvement approach to increase hepatitis B vaccination in stage 4 and 5 CKD patients.

Four strategies were utilized such as (1) Electronic health record (EHR)-based CKD registry to identify patients, (2) EHR-based physician/nurse reminders, (3) a co-located nurse appointment for vaccine administration, and (4) information sharing and provider awareness effort. The CKD registry was utilized to identify patients with stage 4 or 5 CKD, with at least two clinic visits in the prior 2years, who had not received the hepatitis B vaccine or did not have serologic evidence of immunity. Target monthly vaccination rate was set at 75%, based on clinic leadership, nephrologist, and nurse consensus.

A total of 239 patients were included in the study period, from November 2018 to January 2019 (observation period) and from February 2019 to September 2019 (intervention period). Monthly vaccination rate improved from 48% in November 2018 to the target rate of 75% by the end of the intervention (August and September 2019). There was a statistically significant increase from the rate of vaccination at a unique patient level in the first month of the baseline period, compared to the last month of the intervention period (51 vs. 75% p = 0.03).

Utilizing a nurse-led approach to hepatitis B vaccination, coupled with EHR-based tools, along with continuous monitoring of performance, helped to improve hepatitis B vaccination among CKD stage 4 and 5 patients.
Utilizing a nurse-led approach to hepatitis B vaccination, coupled with EHR-based tools, along with continuous monitoring of performance, helped to improve hepatitis B vaccination among CKD stage 4 and 5 patients.
Serum potassium disorders, commonly observed in chronic kidney disease (CKD), are reportedly associated with higher mortality, but their impact on renal outcomes is still controversial.

The present study used the longitudinal data of the Fukushima CKD cohort study to investigate the relationships between hypokalemia and hyperkalemia and adverse outcomes such as renal outcomes and all-cause mortality in Japanese patients with non-dialysis-dependent CKD. The study involved 1330 CKD patients followed-up for 2.8years. The primary endpoint of the present study was a kidney event, defined as a combination of doubling of baseline serum creatinine and end-stage kidney disease.

Hyperkalemia (≥ 5.0mmol/L) was noted in 10.6% and hypokalemia (< 4.0mmol/L) in 16.4% of the study population. Significant U-shaped associations were observed between potassium levels and both kidney events and all-cause mortality on univariate Cox regression analyses. After adjustment for covariates, both hypokalemia and hyperkalemia were significantly associated with an increased risk of kidney events, with the lowest risk at a serum potassium of 4.0-4.4mmol/L. Compared with a reference level of 4.0-4.4mmol/L, the adjusted hazard ratio for kidney events was 2.49 (1.33-4.66) for serum potassium < 4.0mmol/L, 1.72 (1.00-2.96) for 4.5-4.9mmol/L, and 2.16 (1.15-4.06) for ≥ 5.0mmol/L. There was no significant association between serum potassium levels and mortality after multivariate adjustment.

Hypokalemia and hyperkalemia were associated with an increased risk of CKD progression, but not with mortality in Japanese patients with non-dialysis-dependent CKD.
Hypokalemia and hyperkalemia were associated with an increased risk of CKD progression, but not with mortality in Japanese patients with non-dialysis-dependent CKD.Ivabradine is a unique agent that is distinct from beta-blockers and calcium channel blockers as it reduces heart rate without affecting myocardial contractility or vascular tone. Ivabradine is a use-dependent inhibitor targeting the sinoatrial node. It is approved for use in the United States as an adjunct therapy for heart rate reduction in patients with heart failure with reduced ejection fraction. In this scenario, ivabradine has demonstrated improved clinical outcomes due to reduction in heart failure readmissions. However, there has been conflicting evidence from prospective studies and randomized controlled trials for its use in stable ischemic heart disease regarding efficacy in symptom reduction and mortality benefit. Ivabradine may also play a role in the treatment of patients with inappropriate sinus tachycardia, who often cannot tolerate beta-blockers and/or calcium channel blockers. In this review, we highlight the evidence for the nuances of using ivabradine in heart failure, stable ischemic heart disease, and inappropriate sinus tachycardia to raise awareness for its vital role in the treatment of select populations.
Cardiac rupture is a fatal complication following myocardial infarction (MI). An increase in heart rate (HR) is reportedly an independent risk factor for cardiac rupture during acute MI. However, the role of HR reduction in cardiac rupture after MI remains to be fully elucidated. We aimed to evaluate the therapeutic efficacy of HR reduction with ivabradine (IVA) on post-MI cardiac rupture in mice.

We induced MI in mice by ligating the left anterior descending coronary artery. Subsequently, we subcutaneously implanted osmotic pumps filled with IVA solution or vehicle (Veh) in the surviving MI mice at 24h postoperatively. We biochemically analyzed the myocardium on day 5, additionally observed the mice for 10days, and analyzed the rates of cardiac rupture and non-cardiac rupture death, and survival after MI.

HR was significantly lower in the IVA-treated mice, whereas blood pressure was comparable between the two groups. Compared to the Veh-treated mice, apoptosis was significantly reduced in the MI border zone in the IVA-treated mice. Although there were no differences in the infarct size of the surviving MI mice between the two groups, HR reduction with IVA significantly reduced cardiac rupture (rupture rate 26 and 8% in the Veh-treated and IVA-treated groups, respectively) and improved survival after MI.

Our findings suggest that HR reduction with IVA prevents cardiac rupture after MI. This may be particularly effective in MI patients with a high HR who are either unable to adequately tolerate β-blockers or whose HR remains high despite receiving β-blockers.
Our findings suggest that HR reduction with IVA prevents cardiac rupture after MI. This may be particularly effective in MI patients with a high HR who are either unable to adequately tolerate β-blockers or whose HR remains high despite receiving β-blockers.
Rivaroxaban, an oral anticoagulant, undergoes the metabolism mediated by human cytochrome P450 (CYP). The present study is to quantitatively analyze and compare the contributions of multiple CYPs in the metabolism of rivaroxaban to provide new information for medication safety.

The metabolic stability of rivaroxaban in the presence of human liver microsomes (HLMs) and recombinant CYPs was systematically evaluated to estimate the participation of various CYP isoforms. Furthermore, the catalytic efficiency of CYP isoforms was compared via metabolic kinetic studies of rivaroxaban with recombinant CYP isoenzymes, as well as via CYP-specific inhibitory studies. Additionally, docking simulations were used to illustrate molecular interactions.

Multiple CYP isoforms were involved in the hydroxylation of rivaroxaban, with decreasing catalytic rates as follows CYP2J2 > 3A4 > 2D6 > 4F3 > 1A1 > 3A5 > 3A7 > 2A6 > 2E1 > 2C9 > 2C19. Among the CYPs, 2J2, 3A4, 2D6, and 4F3 were the four major isoforms responsible for rivaroxaban metabolism.
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