Prerenal acute kidney injury: Clinical sciences

Acute kidney injury, or AKI for short, is a sudden, potentially reversible decline in kidney function, resulting in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste such as ammonia and uric acid.

You can split AKI into three causes depending on the location of the injury. Prerenal AKI is when the cause of the injury occurs before the kidneys, intrinsic AKI means the injury is within the kidneys, and postrenal AKI refers to injury after the kidneys.

Focusing on prerenal AKI, its causes can be grouped into four main categories, which include medication-induced renal autoregulation impairment, hypovolemia, systemic vasodilation, and interstitial volume overload.

Now, if your patient presents with a chief concern suggesting AKI, first perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, which might include dialysis access. Finally, put your patient on continuous vital sign monitoring and cardiac telemetry, and if needed, provide supplemental oxygen!

Here’s a clinical pearl to keep in mind! Look out for life-threatening complications of AKI such as hyperkalemia, volume overload, or metabolic acidosis, and start emergent hemodialysis right away if needed!

Okay, now let’s go back to the ABCDE assessment and take a look at stable patients. First, obtain a focused history and physical exam. Patients with AKI may report nonspecific symptoms, like fatigue and malaise, or urinary symptoms, such as reduced urine output or hematuria. They may have just started a new medication or have a known chronic medical condition, such as congestive heart failure, multiple myeloma, or systemic lupus erythematosus.

Physical exam might reveal blood pressure abnormalities, a rash, or periorbital or peripheral edema. With these findings, suspect AKI, and then order a basic metabolic panel, and measure their urine output.

Okay, now let’s use the information obtained from these investigations to assess the criteria for AKI! These criteria include a rise in serum creatinine of 0.3 milligrams per deciliter or more over 48 hours; a rise of serum creatinine 1.5 times more than baseline in the last 7 days, or urine output less than 0.5 milliliters per kilogram per hour for six hours. If your patient meets any of these criteria, diagnose AKI!

Next, order labs including urine sodium and creatinine levels, so you can calculate the fractional excretion of sodium, or FENa, which reflects renal handling of sodium. Divide the product of the urinary sodium and serum creatinine by the product of the urinary creatinine and the serum sodium, then, multiply the dividend by 100. A FENa between 1 and 2 percent is considered normal. However, if FENa is outside this range, you’ll need to investigate further by correlating it with the BUN to creatinine ratio, and urine sodium levels.

If the patient’s BUN to creatinine ratio is less than 20 to 1, urine sodium is greater than 20 milliequivalents per liter, and the FENa is greater than 2 percent, consider an alternative diagnosis, such as postrenal or intrinsic AKI.

On the other hand, if your patient’s BUN to creatinine ratio is greater than 20 to 1, urine sodium is less than or equal to 20 milliequivalents per liter, and the FENa is less than 1 percent, diagnose prerenal AKI.