With aging, the kidney undergoes inexorable and progressive changes in structural and functional performance. These aging-related alterations are more obvious and serious in diabetes mellitus (DM). Renal accelerated aging under DM conditions is associated with multiple stresses such as accumulation of advanced glycation end products (AGEs), hypertension, oxidative stress, and inflammation. The main hallmarks of cellular senescence in diabetic kidneys include cyclin-dependent kinase inhibitors, telomere shortening, and diabetic nephropathy-associated secretory phenotype. Lysosome-dependent autophagy and antiaging proteins Klotho and Sirt1 play a fundamental role in the accelerated aging of kidneys in DM, among which the autophagy-lysosome system is the convergent mechanism of the multiple antiaging pathways involved in renal aging under DM conditions. Metformin and the inhibitor of sodium–glucose cotransporter 2 are recommended due to their antiaging effects independent of antihyperglycemia, besides angiotensin-converting enzyme inhibitors/angiotensin receptor blockers. Additionally, diet intervention including low protein and low AGEs with antioxidants are suggested for patients with diabetic nephropathy (DN). However, their long-term benefits still need further study. Exploring the interactive relationships among antiaging protein Klotho, Sirt1, and autophagy-lysosome system may provide insight into better satisfying the urgent medical needs of elderly patients with aging-related DN.

Background/Aims: There is a strong correlation between non-dipping status and cardiovascular events in chronic kidney disease (CKD) patients. Our study is designed to identify the effect of evening administration of antihypertensive drugs to hypertensive CKD patients. Methods: A comprehensive search of Medline, Embase, the Chinese Biomedical Literature Database, Wanfang Data, Chinese National Knowledge Infrastructure, and the Cochrane Central Register of Controlled Trials was performed in July 2014. Concurrent controlled or crossover trials (including randomized and non-randomized experimental trials) designed to evaluate the effects of evening- versus morning-dosing hypertensive drug regimens on clinical outcomes in CKD patients with hypertension were included. All statistical analyses were performed using the RevMan software, which is available free from the Cochrane Collaboration. Results: Seven trials involving 1277 patients were identified, and the randomized controlled trials (RCTs) and non-randomized controlled trials (non-RCTs) were classified into two groups. Taking at least one blood pressure-lowering medication at bedtime was not shown to reduce total death (P=0.056) or cardiovascular death (P=0.059) but was shown to reduce total events (P<0.001) and major cardiovascular events (P<0.001) in both RCTs and non-RCTs. Compared with a morning dosing regimen, taking antihypertensive drug in the evening significantly lowered nighttime systolic blood pressure (SBP) (P<0.0001) and diastolic blood pressure (P<0.05) in patients in the RCTs but did not affect blood pressure in patients in the non-RCTs (P<0.05). There is limited evidence from one non-RCT that taking an antihypertensive drug (benazepril 10 mg) in the evening did not increase adverse events (P=0.72) or withdrawals due to adverse events (P=0.64). Conclusions: A regimen of antihypertensive drugs in the evening should be considered for CKD patients with hypertension to lower nighttime blood pressure and help prevent total events and cardiovascular mortality. More studies are needed to verify the results of this study. i 2015 S. Karger AG, Basel

Chronic kidney disease (CKD) is a worldwide health problem for which effective therapeutic methods are still lacking. Traditional Chinese medicine (TCM) has been indicated as an effective alternative treatment for kidney disease. In this study, a clinically effective therapy, yiqihuoxue (YQHX) formula, was administrated to adenine-induced kidney disease rats for 6 weeks. We found that the adenine rats displayed a significant reduction in renal function as evidenced by the increased levels of serum creatinine (Scr), blood urea nitrogen (BUN), and 24-h urinary albumin level, which were attenuated by the YQHX treatment. The glomerulosclerosis, interstitial fibrosis, arteriolosclerosis, interstitial inflammation, and tubular dilatation were reversed by the YQHX treatment in the adenine rats. Furthermore, the hepatic damage characterized by increased levels of aspartate aminotransferase and alanine aminotransferase and inflammatory cell infiltration was improved by YQHX. In addition, the number of apoptotic cells in the adenine rats was obviously reduced by the YQHX treatment as manifested by the lower expression level of cleaved caspase-3 protein. Moreover, the YQHX treatment downregulated the expression levels of fibronectin, type I collagen, α-smooth muscle actin, and TGF-β1 in the adenine rats. Furthermore, autophagy was activated by the YQHX treatment, which manifested as an increased LC3-II and Beclin-1 expression levels and a decreased p62 level. In conclusion, the YQHX formula might retard the progression of kidney disease by activating autophagy.