Approach to acute kidney injury: Clinical sciences

Acute kidney injury, or AKI, refers to a sudden decline in kidney function that results in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste, such as ammonia and uric acid.

If your patient presents with chief concerns suggesting AKI, perform an ABCDE assessment to determine if they are unstable or stable.

If unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access, which might include dialysis access, and put your patient on continuous vital sign monitoring and cardiac telemetry!

Finally, if you identify hyperkalemia, metabolic acidosis, volume overload, or symptomatic uremia, start emergent hemodialysis!

Now, let’s go back to the ABCDE assessment and look at stable patients. In these individuals, obtain a focused history and physical exam, which is going to help you differentiate different types of AKI.

First, let’s focus on prerenal AKI. Prerenal AKI is typically associated with reduced urine output, sometimes in combination with nonspecific symptoms, including malaise, fever, and vomiting.

Additionally, your patient might have a history of congestive heart failure or cirrhosis, or they might report starting a new medication, such as NSAIDs.

The physical exam might reveal signs of cardiovascular involvement, including blood pressure abnormalities, weak peripheral pulses, and tachycardia. Also, you might notice peripheral edema or signs of dehydration, like dry mucous membranes! With these findings, consider prerenal AKI.

Next, order a basic metabolic panel or BMP and urinalysis with microscopy, measure the patient’s urine output or UOP over time, and check renal ultrasound!

In all types of AKI, labs will reveal a rise in serum creatinine of 0.3 milligrams per deciliter or more over 48 hours; a rise of serum creatinine 1.5 times the baseline or more in the last 7 days, or urine output less than 0.5 milliliters per kilogram per hour for six hours.

In prerenal AKI, the BUN-to-creatinine ratio will be greater than 20 to 1, and urine sodium will be less than 20 milliequivalents per liter.

Next, calculate FENa, which refers to the fractional excretion of sodium, and check the percentage of sodium filtered by kidneys into the urine.

In prerenal AKI, the kidneys filter less sodium to maintain intravascular volume, so the FENa will be below 1%.

Now, here’s a clinical pearl! FENa is not reliable in oliguric individuals with chronic kidney disease because this condition is associated with an impaired ability to concentrate urine and varying baseline plasma sodium levels. In other words, FENa values will not adequately reflect the changes in acute kidney injury.

Similarly, FENa is not reliable in oliguric patients who are taking diuretics because these medications promote sodium excretion, causing FENa to be elevated.

Additionally, urine microscopy might reveal hyaline casts, while the renal ultrasound will show normal kidneys and parenchyma with no hydronephrosis. With these findings, diagnose prerenal AKI, so be sure to assess the underlying cause.

First, let’s focus on hypovolemia, which is typically associated with vomiting, profuse diarrhea, or acute blood loss.

If the physical exam reveals hypotension, dry mucous membranes, and poor skin turgor, diagnose hypovolemia!

Next up is systemic vasodilation, which might be associated with symptoms of infection, like fever, cough, and rash. History could also reveal a recent allergen exposure, such as a bee sting, and difficulty breathing. If the exam reveals warm, dry flushed skin and normal capillary refill, diagnose systemic vasodilation!

Now, moving on to interstitial volume overload, which is typically seen in conditions associated with third spacing of fluids, like congestive heart failure or cirrhosis. If the exam reveals signs of volume overload, including jugular venous distension, ascites, and peripheral edema, diagnose interstitial volume overload.

Finally, once you rule out previous causes, consider medication-induced renal autoregulation impairment, which is associated with NSAIDs and renin angiotensin aldosterone system inhibitors, such as ACE inhibitors. If the physical exam is normal, diagnose medication-induced renal autoregulation impairment.

Next up is intrinsic AKI, which is typically associated with nonspecific signs and symptoms!

For example, history might reveal reduced urine output, bloody urine, or systemic symptoms, like fatigue, malaise, and fever. Additionally, patients might report taking nephrotoxic medications or having chronic conditions, like systemic lupus erythematosus or malignancy.

Similarly, the physical exam is nonspecific and might reveal blood pressure abnormalities, rash, or periorbital and peripheral edema. In this case, consider intrinsic AKI, so order a basic metabolic panel and urinalysis with microscopy, assess the patient’s urine output over time, and check renal ultrasound!

Again, your patient will have lab findings suggestive of AKI, which 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 the baseline or more in the last 7 days, or urine output less than 0.5 milliliters per kilogram per hour for six hours. With intrinsic AKI, the BUN-to-creatinine ratio is less than 20 to 1, and urine sodium is greater than 20 milliequivalents per liter.

In intrinsic AKI, kidneys fail to reabsorb the sodium from filtered urine, meaning more sodium gets excreted into the urine, causing FENa to be greater than 2 percent.

The urinalysis and microscopy will often reveal RBC-, WBC-, or tubular epithelial casts.

Finally, if the renal ultrasound shows normal kidneys with normal parenchyma and no hydronephrosis, diagnose intrinsic AKI, which can occur due to glomerular and non-glomerular causes.

First, let’s focus on glomerular causes, which include proliferative glomerulonephritis and non-proliferative glomerulopathy.

Proliferative glomerulonephritis is often associated with fever, joint pain, and frankly bloody or dark-colored urine! These individual will typically present with facial or peripheral edema and hypertension, and their urinalysis will show hematuria, dysmorphic RBCs, and RBC casts.

With these findings, diagnose proliferative glomerulonephritis, more specifically, a nephritic pattern of glomerular injury, which is commonly seen in poststreptococcal glomerulonephritis, IgA nephropathy, and ANCA-associated glomerulonephritis.