ABSTRACT
This study aimed to investigate the clinical characteristics, prognosis, and factors for survival of patients who underwent early-start peritoneal dialysis (PD) within 24 h after catheter insertion three years after PD. This study was conducted from January 1, 2013 to December 31, 2017. All adult patients who were diagnosed with end-stage renal disease (ESRD) and underwent PD for the first time within 24 h after catheter insertion in our hospital were included. All patients with PD were followed-up until they withdrew from PD, switching to hemodialysis, were transferred to other medical centers, underwent renal transplantation, died or were lost to follow-up, or continued to undergo dialysis until the end of the study period. The follow-up observation lasted three years. The number of eligible patients was 110, and switching to hemodialysis and death were the main reasons for patients to withdraw from PD. The 1-, 2-, and 3-year technical survival rates of patients were 89.1, 79.1, and 79.1% respectively, while the 1-, 2- and 3-year survival rates were 90, 81.8, and 81.8%, respectively. The Charlson comorbidity index, age, hemoglobin, serum albumin, diabetic nephropathy, chronic glomerulonephritis, and hypertensive renal damage were independent risk factors that affected the prognosis of PD patients. Under the condition of ensuring the quality of the PD catheter insertion, early-start PD within 24 h after catheter insertion is a safe treatment approach for ESRD patients.
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Catheterization/methods , Catheters, Indwelling , Peritoneal Dialysis/methods , Kidney Failure, Chronic/therapy , Prognosis , Time Factors , Catheterization/mortality , Body Mass Index , Proportional Hazards Models , Multivariate Analysis , Risk Factors , Age Factors , Peritoneal Dialysis/mortality , Kaplan-Meier Estimate , Kidney Failure, Chronic/mortalityABSTRACT
Hypertensive renal damage generally occurs during the middle and late stages of hypertension, which is typically characterized by proteinuria and renal inflammation. Captopril, an angiotensin-converting enzyme (ACE) inhibitor, has been widely used for therapy of arterial hypertension and cardiovascular diseases. However, the protective effects of captopril on hypertension-induced organ damage remain elusive. The present study was designed to explore the renoprotective action of captopril in spontaneously hypertensive rats (SHR). The 6-week-old male SHR and age-matched Wistar-Kyoto rats were randomized into long-term captopril-treated (34 mg/kg) and vehicle-treated groups. The results showed that in SHR there was obvious renal injury characterized by the increased levels of urine albumin, total protein, serum creatinine, blood urea nitrogen, renal inflammation manifested by the increased mRNA and protein expression of inflammatory factors including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and inducible nitric oxide synthase, and enhanced nuclear factor-κB (NF-κB) activation. Captopril treatment could lower blood pressure, improve renal injury, and suppress renal inflammation and NF-κB activation in SHR rats. In conclusion, captopril ameliorates renal injury and inflammation in SHR possibly via inactivation of NF-κB signaling.
Subject(s)
Animals , Male , Rats , Proteinuria/prevention & control , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Captopril/therapeutic use , NF-kappa B/adverse effects , Hypertension/drug therapy , Nephritis/prevention & control , Antihypertensive Agents/therapeutic use , Proteinuria/etiology , Rats, Inbred SHR , Rats, Inbred WKY , Signal Transduction , Hypertension/complications , Nephritis/etiologyABSTRACT
Cisplatin is widely used in lung cancer chemotherapy, but drug resistance seriously affects its efficacy.The mechanism of cisplatin resistance is not yet clear.Now it is widely recognized that P-glycoprotein (P-glycoprotein, P-gp) expression is associated with cisplatin resistance. Inhibition of P-gp expression can overcome cisplatin resistance and improve the treatment efficacy.
ABSTRACT
In ischemic hypertrophic myocardium, contractile dysfunction can be attributed to the decreased calcium induced calcium release (CICR) in cytoplasm. This study aimed to investigate the electrophysiological properties and the expression of L calcium channel subunits in post-MI myocardium. The ischemic heart remodeling model was established in SD rats. The expressions of calcium channel subunits were determined by realtime RT-PCR. Whole cell patch clamp was used to record the electrophysiological properties of L calcium channel. The results showed that the L calcium channel agonist Bayk 8644 induced the significantly decreased CICR in the rat cardiomyocyte 6weeks after myocardial infarction (MI). In the post-MI cardiomyocytes, the amplitude of ICaL decreased dramatically and the inactivation curve of the current shifted to more negative potential. At mRNA level, the expression of the calcium channel alphalc, beta2c subunits decreased dramatically in the ventricle of post-MI rats. The expression of alpha2/delta subunit, however, remained constant.It is concluded that the abnormal expression of the L calcium channel subunits in post-MI cardiomyocytes contributes to the ICaL decrease at early stage of the ischemic remodeling in cardiomyocytes,which leads to the decreased CICR in the cell and contractile dysfunction of myocardium.