Effect of intrarenal renin-angiotensin-aldosterone system on renal function in patients after cardiac surgery

Peiyuan Niu1,2,3, Xuejing Ren1,2,3, Meihao Wu1,2,3

  • 1Department of Nephrology, Henan Provincial People's Hospital; People's Hospital of Zhengzhou University, People's Hospital of Henan University, Zhengzhou, Henan, China.

Medicine
|April 1, 2022
PubMed

Insights

Increased intrarenal renin-angiotensin system (RAS) activation after cardiac surgery is linked to acute kidney injury (AKI). Urinary angiotensinogen (uAGT) may predict AKI occurrence and severity, suggesting RAS inhibition as a potential treatment.

Area of Science:

  • Nephrology
  • Cardiology
  • Surgical Science

Background:

  • Cardiac surgery with cardiopulmonary bypass is associated with acute kidney injury (AKI).
  • The role of the intrarenal renin-angiotensin system (RAS) in post-cardiac surgery AKI is not fully understood.
  • Intrarenal RAS activation may contribute to the decline in renal function following these procedures.

Purpose of the Study:

  • To investigate the influence of intrarenal RAS activation on renal function decrease in patients undergoing cardiac surgery.
  • To determine if urinary angiotensinogen (uAGT) can serve as a biomarker for predicting AKI after cardiac surgery.
  • To explore the potential of inhibiting intrarenal RAS as a therapeutic strategy.

Main Methods:

  • Observational study involving 24 patients with AKI and 21 controls without AKI after cardiac surgery.
  • Measurement of urinary angiotensinogen (uAGT) at baseline, and 0 and 12 hours post-surgery.
  • Collection of clinical and laboratory data to assess renal function and patient outcomes.

Main Results:

  • All patients exhibited intrarenal RAS activation post-surgery.
  • Patients who developed AKI showed significantly higher uAGT levels at 0 and 12 hours post-surgery compared to the non-AKI group.
  • A positive correlation was observed between RAS activation at 0 hours and the decrease in renal function at 48 hours (r=0.654, P=.001).

Conclusions:

  • Intrarenal RAS activation is significantly elevated in patients developing AKI after cardiac surgery.
  • Urinary angiotensinogen (uAGT) shows promise as a predictive biomarker for AKI occurrence and severity.
  • Targeting intrarenal RAS activation may represent a future therapeutic avenue for preventing or treating post-cardiac surgery AKI.

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
540
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
868
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
516
Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
33.8K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
954
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
82