The baseline serum creatinine level, use of angiotensin-converting enzyme inhibitors or angiotensin-II receptor antagonists, red blood cell transfusion volume, and history of coronary artery disease were independent risk factors for AKI.
Cancer-related AKI is common and associated with advanced stage, chronic kidney disease, diabetes, and concomitant receipt of diuretics or angiotensin-converting enzyme inhibitors/angiotensin receptor blockers.
The preoperative renal function, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker or statin administration, volume of contrast agent, range of TBAD and false lumen involving renal artery were not associated with post-operation AKI.
No association was found between the use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers and the risk of acute kidney injury, which occurred in 25% of the cohort.
In multivariable analyses, factors found to be independently associated with AKI included: male sex (adjusted odds ratio, aOR: 1.56 95% confidence interval (CI): 1.20-2.04), hypertension (aOR1.36 95% CI 1.01-1.85), being prescribed either angiotensin-converting-enzyme inhibitors or angiotensin-II-receptor-blockers (aOR: 1.59 95% CI: 1.19-2.13), or insulin (aOR: 2.27 95% CI: 1.27-4.05), presence of proteinuria (aOR 1.27 95% CI 0.98-1.63), and low estimated glomerular filtration rate (eGFR).
Among cardiovascular drugs taken before admission, angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers and statins were those associated with lower in-hospital mortality, even after adjusting for covariates (age, hemoglobin, albumin, acute kidney injury, ADL Hierarchy Scale, NT-proBNP levels) [odds ratio (OR) = 0.46, P = .045, and OR = 0.21, P = .008, respectively].
Patients with and without AKI were matched using baseline demographics, comorbidities, proteinuria, estimated glomerular filtration rate, blood pressure, angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker (ACEI/ARB) use, and inpatient exposures linked to AKI.
Logistic regression analysis showed that the independent risk factors for AKI in patients with AMI included: age (>60 years old) (odds ratio [OR] 1.04, 95% confidence interval [CI] 1.02-1.05, P = 0.000), hypertension (OR 2.51, 95% CI 1.62-3.87, P = 0.000), chronic kidney disease (OR 3.52, 95% CI 2.01-6.16, P = 0.000), Killip class ≥3 (OR 5.22, 95% CI 3.07-8.87, P = 0.000), extensive anterior myocardial infarction (OR 3.02, 95% CI 1.85-4.93, P = 0.000), use of furosemide (OR 1.02, 95% CI 1.02-1.03, P = 0.000), non-use of angiotensin-converting enzyme inhibitors/angiotensin receptor blocker (OR 1.58, 95% CI 1.04-2.40, P = 0.032).
In univariate analysis coronary artery disease and the presence of a renal artery stenosis were both significantly associated with AKI (OR: 2.38, 3.31, respectively) as well as the use of B-blockers and angiotensin converting enzyme inhibitors (OR 3.05, 2.48, respectively).
AKI frequently occurs in hypertensive patients taking angiotensin receptor blockers or ACE inhibitors (p=0.002), and in patients with diabetes with higher glycated haemoglobin levels (p=0.033).
Here we study the association between ensuing CKD and use of RAS inhibitor including angiotensin converting enzyme inhibitor or angiotensin II type 1a receptor blocker starting after renal functional recovery in our prospectively collected observational AKI cohort.
Angiotensin II type 1 receptor, mitogen activated protein kinase (MAPK), and TACE increased, while angiotensin-converting enzyme-2 (ACE2) expression decreased in LPS-induced acute kidney injury and LPS-treated HK-2 cells.
Our findings indicated that miR-187 improved I/R-induced ischemic acute renal failure through protecting glomerular filtration barrier by blocking the expression of ACHE.
ACKR2 is important in limiting persistent inflammation, tubular loss, and renal fibrosis after ischemic acute kidney injury and, thus, can prevent progression to chronic renal disease.
We observed that the Malondialdehyde (MDA) level was increased in dose-dependent manner similar to Acsl4 gene over expression suggesting a main role of ferroptosis in hemoglobinuria mediated AKI following envenomation.
This approach will allow us to obtain preliminary data to design a large randomized trial assessing the effects of chloride-sparing hypertonic solutions on development of AKI in patients with SAH.
The levels of PTH/PTHrP receptor mRNA (corrected by beta-actin mRNA) in the kidney of GNN, GNI, CRF and ARF patients was markedly decreased by up to 35.7%, 68.5%, 77.9% and 92.2%, respectively.
Moreover, TGF-β, vimentin, fibronectin and α-smooth muscle actin, biomarkers of fibrosis, and TNFα, IL6 and endothelin-1, biomarkers of inflammation, were upregulated in I/R induced AKI, primarily in heparanase transgenic mice, suggesting an adverse role of heparanase in the pathogenesis of AKI.
Novel compound heterozygote mutations (H234Q/R1206X) of the ADAMTS13 gene in an adult patient with Upshaw-Schulman syndrome showing predominant episodes of repeated acute renal failure.
She had initially presented at 14 years of age with visual disturbance and acute renal failure and been diagnosed with thrombotic thrombocytopenic purpura on the basis of kidney biopsy findings of thrombotic microangiopathy and compatible ADAMTS13 (a disentegrin and metalloproteinase with a thrombospondin type 1 motif member 13).