Based on experimental and epidemiological pieces of evidence, AKI may progress to chronic kidney disease (CKD) even after a recovery period due to maladaptive repair and other underlying mechanisms such as heightened Wnt signalling, overstimulation of the renin-angiotensin-aldosterone-system (RAAS) pathway, epigenetic alterations and inhibition of hypoxia-inducible factor (HIF) dependent defences.
Certain medications, such as loop diuretics, renin angiotensin system blockers, and mineralocorticoid antagonists can seemingly cause acute kidney injury.
Associations between preoperative continuation of renin-angiotensin system inhibitor and cardiac surgery-associated acute kidney injury: a propensity score-matching analysis.
Rate and Outcome of Acute Kidney Injury Following Hip Fracture Surgery in Diabetic Older Patients Treated with Renin-Angiotensin-Aldosterone Antagonists.
Elderly, patients with chronic kidney disease (CKD) and patients with heart failure who continue using renin-angiotensin-aldosterone-system (RAAS) inhibitors, diuretics, or non-steroidal-anti-inflammatory drugs (NSAIDs) during times of fluid loss have a high risk of developing complications like acute kidney injury (AKI).
Renin-angiotensin system (RAS) inhibitors carry a risk of normotensive ischemic acute kidney injury in dehydration and concurrent nonsteroidal anti-inflammatory drug (NSAID) use.
The risk for AKI with concomitant use of VACV and renin-angiotensin system (RAS) inhibitors that can cause AKI <i>via</i> a similar mechanism to NSAIDs is also unknown.
To determine whether preoperative renin-angiotensin system (RAS) inhibitor use within 7 days of noncardiac surgery is associated with a lower incidence of postoperative acute kidney injury (AKI) in hypertensive patients.
In univariable analyses, CKD [odds ratio (OR) 2.1, 95% confidence interval (CI) 0.99-4.43] and use of renin-angiotensin system (RAS) blockers and/or diuretics (OR 3.85; 95% CI 1.15-20.15) were significantly associated with the risk of AKI.
Several pathological mechanisms have been proposed to contribute to the progression of AKI and transition to CKD/ESRD including hypoxia and microvascular rarefaction, alterations of renal resident cell phenotypes and functions, cell cycle arrest in the G2/M phase, persistent chronic inflammation, and development of interstitial fibrosis, mitochondrial fragmentation, epigenetic changes, activation of renin-angiotensin system (RAS), cell and tissue senescence.
The relative risk increase is similar across population groups, but the higher baseline risk among those taking renin-angiotensin system blockers and potassium-sparing diuretics translates into higher absolute risks of acute kidney injury and hyperkalaemia in these groups.
Here we comment on their findings, exploring the clinical utility of uAGT as a biomarker to predict AKI to CKD transition and perhaps more controversially, to discuss whether the early renin-angiotensin system blockade following AKI represents a therapeutic target.
The prognostic significance of urinary angiotensinogen as an AKI biomarker strongly suggests a role for renin-angiotensin system activation in modulating the severity of AKI and its outcomes.
Although protein loading has been established as an ideal method to investigate glomerular filtration capacity in healthy kidneys, other methods such as the antagonism of the renin-angiotensin-aldosterone system have demonstrated promise as a method to determine underlying glomerular disease in those with acute kidney injury and other comorbidities (e.g., congestive heart failure and chronic kidney disease).
The FDA now requires that AKI be listed as a potential side effect of the SGLT2 inhibitors along with cautious prescription of these drugs with other medications, such as renin-angiotensin-system antagonists, diuretics, and NSAIDs.