A 62-year-old man with a history of hypertension, well-controlled diabetes, and coronary artery disease presents with shortness of breath. A history is obtained, with pertinent positives including orthopnea and leg swelling. His blood pressure is 146/94 mmHg with a heart rate of 84 beats per minute. The patient has an S3 on cardiac auscultation, bilateral rales are heard along the lung bases, and there is pitting edema around the ankles. Laboratory tests are ordered, which show a creatinine of 2.4 mg/dL (baseline 1.0 mg/dL).
What is the next step in managing this patient’s renal failure?
A. IV fluids: IV furosemide. The most important treatment of AKI is managing the underlying condition, which in this case is heart failure. The patient has a suggestive history and physical examination of CHF, and he is fluid overloaded. It might be surprising that prerenal AKI (caused by decreased blood flow to the kidneys) could occur in the setting of hypervolemia. However, even though the patient has ample blood volume, the effective arterial volume is decreased due to heart failure and poor cardiac output (i.e., large blood volume but poor flow). Therefore the kidneys are receiving less blood flow and responding the same way as they would in the setting of hypovolemia. Diuresis with IV furosemide would correct the patient’s volume overload, allowing the heart’s function to improve and increase blood flow to the kidneys. This is often called cardio-renal syndrome.
(A) Although IV fluids are used to treat prerenal AKI caused by hypovolemia, in this case it would worsen the AKI because it would further exacerbate his heart failure. (B) Starting an NSAID would decrease the GFR further due to afferent arteriole vasoconstriction, worsening the patient’s prerenal AKI and potentially precipitating ATN. (C) Corticosteroids may be used in AIN if the kidneys fail to respond to the withdrawal of the offending agent, although there is mixed evidence as to the efficacy.