What is the management plan for a patient presenting to the Emergency Room with intrarenal Acute Kidney Injury (AKI) with Acute Tubular Necrosis (ATN) due to the use of Angiotensin-Converting Enzyme Inhibitors (ACE-i) and Hydrochlorothiazide (HCTZ) diuretic, presenting with nausea?

From the Guidelines

The immediate management plan for a patient presenting to the Emergency Room with intrarenal Acute Kidney Injury (AKI) with Acute Tubular Necrosis (ATN) due to the use of Angiotensin-Converting Enzyme Inhibitors (ACE-i) and Hydrochlorothiazide (HCTZ) diuretic, presenting with nausea, should be to discontinue both medications and provide supportive care, as recommended by the most recent and highest quality study 1. The decision to discontinue these medications is based on the consideration of their potential nephrotoxicity and the need to individualize treatment in patients with Acute Kidney Disease (AKD) 1.

Key Management Steps:

• Discontinue ACE-i and HCTZ diuretic to prevent further kidney injury
• Initiate intravenous fluid resuscitation with isotonic saline to restore intravascular volume and improve renal perfusion, typically starting with a 1-2L bolus followed by maintenance fluids based on clinical response
• Monitor fluid status carefully to avoid volume overload
• Administer antiemetics such as ondansetron 4mg IV every 8 hours as needed or metoclopramide 10mg IV every 6 hours for nausea, avoiding medications with significant renal clearance
• Daily laboratory monitoring should include serum creatinine, BUN, electrolytes, and urine output
• Strict intake and output measurements are essential

Additional Considerations:

• Nephrology consultation is recommended for management guidance and to determine if renal replacement therapy might be needed for severe cases with significant uremia, hyperkalemia, or volume overload unresponsive to medical management
• Patient education should focus on medication safety, explaining the mechanism of kidney injury from combined ACE inhibitors and diuretics, especially during volume-depleted states
• For follow-up, arrange nephrology appointments at 1-2 weeks after discharge, then monthly until renal function stabilizes
• Primary care follow-up within 1 week of discharge is also important to reassess blood pressure control with alternative antihypertensives such as calcium channel blockers (amlodipine 5-10mg daily) or beta-blockers (metoprolol 25-100mg twice daily) that pose less risk to compromised kidneys, as supported by previous guidelines 1.

From the FDA Drug Label

CLINICAL PHARMACOLOGY Hydrochlorothiazide blocks the reabsorption of sodium and chloride ions, and it thereby increases the quantity of sodium traversing the distal tubule and the volume of water excreted. Pharmacodynamics Acute antihypertensive effects of thiazides are thought to result from a reduction in blood volume and cardiac output, secondary to a natriuretic effect, although a direct vasodilatory mechanism has also been proposed. OVERDOSAGE The most common signs and symptoms observed are those caused by electrolyte depletion (hypokalemia, hypochloremia, hyponatremia) and dehydration resulting from excessive diuresis. If digitalis has also been administered, hypokalemia may accentuate cardiac arrhythmias. In the event of overdosage, symptomatic and supportive measures should be employed.

The management plan for a patient presenting with intrarenal Acute Kidney Injury (AKI) with Acute Tubular Necrosis (ATN) due to the use of Angiotensin-Converting Enzyme Inhibitors (ACE-i) and Hydrochlorothiazide (HCTZ) diuretic, presenting with nausea, should include:

• Discontinuation of the offending agents (ACE-i and HCTZ)
• Correction of dehydration and electrolyte imbalance
• Supportive measures for nausea and other symptoms
• Monitoring of renal function and electrolyte levels 2 2

From the Research

Management Plan for Intrarenal Acute Kidney Injury (AKI) with Acute Tubular Necrosis (ATN)

• The management of a patient presenting with intrarenal AKI with ATN due to the use of Angiotensin-Converting Enzyme Inhibitors (ACE-i) and Hydrochlorothiazide (HCTZ) diuretic involves identifying and correcting reversible causes, preventing further kidney injury, and performing supportive therapy 3.
• It is essential to evaluate the patient's medical and social history, laboratory studies, and perform tests such as renal biopsy and ultrasonography to determine the cause of AKI 3.
• The use of ACE-i after AKI is associated with lower risks of all-cause mortality, recurrent AKI, and progression to incident CKD 4.
• However, ACE-i use is also associated with a higher risk of hyperkalemia, which requires close clinical monitoring 4.
• The continued administration of ACE-i during an episode of AKI or initiation of these agents prior to discharge may be safe and not impede kidney recovery following AKI 5.
• In patients with AKI, ACE-i or ARB therapy appears to be associated with lower mortality but a higher risk of hospitalization for a renal cause, suggesting a potential benefit of ACE-i or ARB use after AKI 6.

Diagnostic Approach

• Simple laboratory parameters such as urine sodium (UNa), urine specific gravity (USG), and renal failure index (RFI) can be used to differentiate pre-/intrarenal AKI and identify the etiology of AKI 7.
• These parameters are not confounded by medication or comorbidities and can be easily determined using serum and spot urine 7.
• The evaluation of these parameters can help guide therapy and improve patient outcomes 7.

Symptomatic Management

• Nausea, a common symptom in patients with AKI, should be managed symptomatically to prevent further dehydration and electrolyte imbalances.
• The patient's volume status and electrolyte levels should be closely monitored and managed accordingly 3.