Rapid and sensitive detection of NGAL for the prediction of acute kidney injury via a polydopamine nanosphere/aptamer nanocomplex coupled with DNase I-assisted recycling amplification

The Analyst ◽  
2020 ◽  
Vol 145 (10) ◽  
pp. 3620-3625
Author(s):  
Yiting Hu ◽  
Xie-an Yu ◽  
Ying Zhang ◽  
Ran Zhang ◽  
Xuefei Bai ◽  
...  

A rapid and sensitive method for NGAL detection has been developed to predict acute kidney injury and evaluate the protective effect of drug on renal disease.

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Zhiya Deng ◽  
Maomao Sun ◽  
Jie Wu ◽  
Haihong Fang ◽  
Shumin Cai ◽  
...  

AbstractOur previous studies showed that silent mating-type information regulation 2 homologue-1 (SIRT1, a deacetylase) upregulation could attenuate sepsis-induced acute kidney injury (SAKI). Upregulated SIRT1 can deacetylate certain autophagy-related proteins (Beclin1, Atg5, Atg7 and LC3) in vitro. However, it remains unclear whether the beneficial effect of SIRT1 is related to autophagy induction and the underlying mechanism of this effect is also unknown. In the present study, caecal ligation and puncture (CLP)-induced mice, and an LPS-challenged HK-2 cell line were established to mimic a SAKI animal model and a SAKI cell model, respectively. Our results demonstrated that SIRT1 activation promoted autophagy and attenuated SAKI. SIRT1 deacetylated only Beclin1 but not the other autophagy-related proteins in SAKI. SIRT1-induced autophagy and its protective effect against SAKI were mediated by the deacetylation of Beclin1 at K430 and K437. Moreover, two SIRT1 activators, resveratrol and polydatin, attenuated SAKI in CLP-induced septic mice. Our study was the first to demonstrate the important role of SIRT1-induced Beclin1 deacetylation in autophagy and its protective effect against SAKI. These findings suggest that pharmacologic induction of autophagy via SIRT1-mediated Beclin1 deacetylation may be a promising therapeutic approach for future SAKI treatment.


Author(s):  
Yon-Suk Kim ◽  
Si-Heung Sung ◽  
Yujiao Tang ◽  
Eun-Ju Choi ◽  
Young-Jin Choi ◽  
...  

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Cheol Ho Park ◽  
Bin Lee ◽  
Myeonggil Han ◽  
Woo Joong Rhee ◽  
Man Sup Kwak ◽  
...  

AbstractSodium-glucose cotransporter 2 inhibitors, which are recently introduced as glucose-lowering agents, improve cardiovascular and renal outcomes in patients with diabetes mellitus. These drugs also have beneficial effects in various kidney disease models. However, the effect of SGLT2 inhibitors on cisplatin-induced acute kidney injury (AKI) and their mechanism of action need to be elucidated. In this study, we investigated whether canagliflozin protects against cisplatin-induced AKI, depending on adenosine monophosphate-activated protein kinase (AMPK) activation and following induction of autophagy. In the experiments using the HK-2 cell line, cell viability assay and molecular analysis revealed that canagliflozin protected renal proximal tubular cells from cisplatin, whereas addition of chloroquine or compound C abolished the protective effect of canagliflozin. In the mouse model of cisplatin-induced AKI, canagliflozin protected mice from cisplatin-induced AKI. However, treatment with chloroquine or compound C in addition to administration of cisplatin and canagliflozin eliminated the protective effect of canagliflozin. Collectively, these findings indicate that canagliflozin protects against cisplatin-induced AKI by activating AMPK and autophagy in renal proximal tubular cells.


2021 ◽  
pp. 201-204
Author(s):  
Shashikantha Shashikantha ◽  
Sohil Sharda. ◽  
Bernice Robert ◽  
Gangurde Bhushan Daulatrao

INTRODUCTION: Acute kidney injury is a common occurrence in ICU admissions causing increased morbidity and mortality. Present study aimed to determine the causes and prognostic factors of acute kidney injury in intensive care unit. MATERIAL AND METHODS: This Hospital based Cross sectional Study was conducted at a tertiary care Hospital and Research Center, including 100 patients aged >18 years with Acute Kidney Injury admitted in ICU from the period of October 2018 to June 2020. Patients with chronic renal disease, previous renal transplantation, congenital renal disease were excluded from the study. RESULTS: Most of the patients (63%) were aged above 50 years. Diabetes was found in 55% and hypertension in 26% of AKI cases. Most common cause identied were sepsis, CLD, renal, CNS and CVD. Hypotension occurred in 48% patients, while oliguria occurred in 45% patients. Ventilatory support was required by 43% patients, while 31% patients required haemodialysis. Mortality rate in AKI was 51%. Mortality was signicantly associated with advanced age, presence of Diabetes, and RIFLE criteria. Spot urine <40 meq/L, hyperkalemia, serum creatinine >4 mg/dl, blood urea >100 mg/dl and acidosis were associated with higher mortality. CONCLUSION: Continuous monitoring parameters like Spot Fe Na, Serum Potasium and pH especially in patients at risk, like elderly patients with diabetes, those with sepsis, can help in early identication and appropiate management, thus reduce the incidence or severity of AKI.


2020 ◽  
Vol 19 (3) ◽  
pp. 270-276
Author(s):  
Jianying Wang ◽  
Xiaoting Yu

Acute kidney injury is a severe complication of sepsis. We have shown a protective effect of Platycodin D on sepsis induced acute kidney injury in an animal model that employs cecal ligation and puncture. Cecal ligation and puncture induced a series of degenerative changes in kidney, such as edema, hyperemia, and expansion in glomerular capillary, and inflammatory cells infiltration that were attenuated by Platycodin D. Also, rise in proinflammatory cytokine levels in septic rats was blunted by Platycodin D. Furthermore, Platycodin D administration reduced rise in serum levels of kidney injury markers-blood urea nitrogen and serum creatinine-in septic rats. Moreover, Platycodin D administration also suppressed the cell apoptosis in kidney that was associated with enhanced B-cell lymphoma 2 protein and reduced cleaved cysteine-aspartic protease-3 and BCL2-associated X protein. Lastly, Platycodin D administration attenuated sepsis-induced increase of phospho (p)-extracellular signal-regulated kinase, p-c-Jun NH2-terminal kinase, and p-p38. In conclusion, Platycodin D demonstrated protective effect against sepsis induced acute kidney injury through inactivation of mitogen activated protein kinase pathways, thus providing promising therapeutic strategy for the treatment of sepsis.


Renal disease may occur de novo during pregnancy and pregnancy may occur in women with pre-existing renal disease. The chapters in this section consider the causes and implications of acute kidney injury that may occur during pregnancy and the likely outcomes of pregnancy in women with pre-existing chronic kidney disease, including the possible maternal and foetal complications of preterm delivery and pre-eclampsia (PET). There is a high incidence of PET in women with renal disease during pregnancy and importance of diagnosis and safe treatment of hypertension during pregnancy is discussed. The authors present the current theories of the pathogenesis of PET and highlight the importance of prophylactic treatment with aspirin to reduce the risk of PET. Pregnancy is increasingly common following renal transplantation and this group requires special consideration. They may have other concurrent medical conditions that need to be considered during pregnancy, or they may be at higher risk of other medical complications e.g. urinary tract infection with potential implications for maternal health and foetal wellbeing. It is important to facilitate preconception counselling for women with pre-existing renal disease to discuss optimal timing of pregnancy, make necessary adjustments to medications, and to discuss the likely outcomes for mother and baby. Managing renal disease during pregnancy requires the input of nephrologists, obstetricians, midwives, and often other healthcare professionals which is optimally delivered in a multi-disciplinary antenatal clinic with an expertise in this area.


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