What is the approach to using Angiotensin-Converting Enzyme (ACE) inhibitors in patients with acute tubular injury?

From the Guidelines

ACE inhibitors should be temporarily discontinued in patients with acute tubular injury until renal function stabilizes, as recommended by the most recent and highest quality study 1. This approach is crucial to prevent further renal deterioration and to allow for the recovery of the kidneys. The use of ACE inhibitors in patients with acute tubular injury can worsen renal function due to their effects on glomerular filtration pressure and the potential for hyperkalemia 1. When the patient's condition improves and renal function begins to recover, ACE inhibitors can be cautiously reintroduced at lower doses with close monitoring of kidney function, blood pressure, and electrolytes (particularly potassium) 1. Some key considerations for the management of ACE inhibitors in patients with acute tubular injury include:

• Monitoring serum creatinine and electrolyte levels before and after initiating ACE inhibitor therapy 1
• Establishing a tolerable upper limit for serum creatinine levels above which the medication should be discontinued 1
• Identifying and correcting reversible vascular disease, such as renal artery stenosis, to improve tolerance to ACE inhibitors 1
• Avoiding the use of ACE inhibitors in patients with frank hypotension or volume depletion, as these conditions can increase the risk of acute renal failure 1
• Considering the use of alternative medications, such as Ang II receptor antagonists, in patients who are unable to tolerate ACE inhibitors 1. It is essential to weigh the potential benefits of ACE inhibitors, including their renoprotective effects, against the potential risks of worsening renal function in patients with acute tubular injury 1. By carefully managing ACE inhibitors and monitoring renal function, healthcare providers can optimize the care of patients with acute tubular injury and improve outcomes.

From the Research

Approach to Using ACE Inhibitors in Acute Tubular Injury

The use of Angiotensin-Converting Enzyme (ACE) inhibitors in patients with acute tubular injury requires careful consideration of the potential benefits and risks.

• ACE inhibitors can be beneficial in patients with heart failure and reduced ejection fraction, but their use in patients with acute tubular injury is more complex 2.
• A study published in 1992 found that ACE inhibitors can cause acute renal failure in patients without renal artery stenosis, particularly in those with overt volume depletion, hypotension, and pre-existing chronic renal insufficiency 3.
• The mechanism of acute tubular injury caused by ACE inhibitors is not fully understood, but it is thought to involve the inhibition of angiotensin II production, which can lead to a decrease in glomerular filtration rate and an increase in renal vascular resistance 3.
• Other factors that can contribute to the development of acute tubular injury in patients taking ACE inhibitors include the use of diuretics, non-steroidal anti-inflammatory drugs, and the presence of diabetes mellitus 3.

Management of Acute Kidney Injury

The management of acute kidney injury (AKI) in patients taking ACE inhibitors involves prompt recognition of the condition and withdrawal of the offending agent.

• Measures to prevent AKI include optimization of volume status and avoidance of nephrotoxic medications 4.
• Crystalloids are preferred over colloids for most patients, and hydroxyethyl starches should be avoided 4.
• The optimal timing of renal replacement therapy in critically ill patients with AKI is unclear, but it is an area of active investigation 4.

Comparison of Different ACE Inhibitors

Different ACE inhibitors have varying efficacy and safety profiles in patients with heart failure.

• A network meta-analysis published in 2016 found that enalapril was associated with a significant reduction in systolic blood pressure, but also with a higher incidence of cough and gastrointestinal discomfort 5.
• Ramipril was associated with the lowest incidence of all-cause mortality, while lisinopril was associated with the highest incidence of all-cause mortality 5.
• The choice of ACE inhibitor should be individualized based on the patient's specific clinical characteristics and comorbidities 5.

Drug-Induced Acute Kidney Injury

Drug-induced acute kidney injury is a common cause of AKI, and ACE inhibitors are one of the many medications that can cause this condition.

• The mechanism of drug-induced AKI involves the inherent nephrotoxicity of the drug, as well as its transport and handling by the kidneys 6.
• Other medications that can cause AKI include aminoglycosides, tenofovir, and cisplatin 6.
• The recognition and management of drug-induced AKI require a thorough understanding of the medications that can cause this condition and the mechanisms by which they do so 6.