EFFECT OF ACE INHIBITORS ON RENAL SALT REGULATION

Main Article Content

Hussain Obaid Almutairi
Mustafa Hussain Sabie
Mohammed Mughabbish Thafrani
Ahmed Ibrahim Alkhawaji
Mohammad Ahmed Motwwam
Reem Naif Almutairi
Turki Falah Almutairi
Jassim Mohammad Alrasheedi
Haitham Ali Muharraq
Turki Mansour Mohammed Alsaad
Manal Ali Hakami
Heba Omar Abdulrahman Melebary
Azhar Habib Alhayek
Fatima Hussain Asiri

Keywords

ACE inhibitors, Renal salt regulation, renal hemodynamic, congestive heart failure

Abstract

Introduction: ACE inhibitors are currently among the most widely prescribed classes of antihypertensive medications. Their application has expanded to include the long-term care of patients with congestive heart failure (CHF) and both diabetic and nondiabetic nephropathies, in addition to their effectiveness in managing hypertension. The use of ACE inhibitor therapy has been linked to a syndrome known as "functional renal insufficiency" and/or hyperkalemia, despite the fact that it typically improves renal blood flow (RBF), sodium excretion rates in CHF, and the rate at which renal damage progresses in chronic renal disease. Treatment with furosemide and ACE inhibitors together may be used to treat dilutional hyponatremia. The correction of azotemia and an increase in low serum sodium values can occur when ACE inhibitor doses are carefully titrated to prevent severe hypotension. The primary causes of these effects are decreased thirst and ADH release.


 Aim of the study: This article discusses the uses of ACE inhibitors and provides guidance on how to manage side effects, and renal salt regulation such as hyperkalemia and deteriorating renal function.


 Methodology: The study is a comprehensive research of PUBMED since the year 1990 to 2019.


 Conclusion: Angiotensin-converting enzyme (ACE) inhibitors have a wide range of effects on renal hemodynamics, depending on the kidneys' underlying physiologic and pathologic conditions. It's still debatable whether ACE inhibitors should be used to treat renovascular hypertension. ACE inhibition has the potential to impair the angiotensin II-mediated autoregulation of GFR and worsen renal function, particularly in individuals with bilateral renal artery stenosis or stenosis of a single kidney. As long as ACE inhibitor and diuretic dosages are adjusted to prevent systemic hypotension and sodium and fluid depletion, ACE inhibitors can generally be started cautiously and used safely in CHF patients.


There are no overt adverse effects of ACE inhibitors on the kidneys' ability to handle salt and water. However, the patient's capacity to enhance sodium reabsorption and retain water is compromised during severe dehydration and salt deprivation. As a result, in these circumstances, ACE inhibitors should be stopped or used carefully.

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