Prerenal acute kidney injury: Clinical sciences

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Introduction0:00–0:54

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.

Unstable Patient0:54–1:40

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.

Stable Patient1:40–2:27

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.

Assess criteria for AKI2:27–3:02

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.

Labs3:02–3:43

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.

Consider alternative diagnosis 3:43–4:02

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.

Prerenal AKI 4:02–4:17

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.
Okay, now, your next step is to assess the underlying causes! If your patient reports using certain medications, such as NSAIDs, or renin angiotensin aldosterone system inhibitors such as ACE inhibitors, or ARBs, diagnose Prerenal AKI due to Medication-Induced Renal Autoregulation Impairment.

Assess underlying causes 4:17–4:24

Medication-induced Renal Autoregulation Impairment 4:24–4:59

As far as treatment goes, you provide supportive care for AKI which can include giving IV hydration, diuresis, and correction of electrolyte and acid-base disturbances.
More importantly, remember to discontinue any offending medications. Okay, onto our next underlying cause.

Hypovolemia 4:59–5:31

Your patient may report vomiting, diarrhea, bleeding, or a history of shock. The physical exam might reveal hypotension, dry mucous membranes, and poor skin turgor.
With these findings, diagnose prerenal AKI due to hypovolemia. The treatment focuses on supportive care for AKI and addressing the underlying cause of hypovolemia.
Back to our underlying causes of prerenal AKI. Next, some patients might report having symptoms of an infection, like a cough or fever, or, the patient may have a history of recent allergen exposure, like peanut ingestion, and are having difficulty breathing.

Systemic Vasodilation 5:31–6:22

The physical exam will reveal warm dry flushed skin, and a normal capillary refill time. With these findings, diagnose prerenal AKI due to systemic vasodilation, which can occur in conditions such as sepsis and anaphylaxis.
Treatment also focuses on supportive care for AKI and treating the underlying condition. Also, don’t forget intravascular volume resuscitation with IV fluids and vasopressors if the patient is in shock.

Volume Overload 6:22–7:45

Let’s wrap this up with our last underlying cause! Lastly, your patient might complain of shortness of breath, with a history of heart failure, or cirrhosis.
Both heart failure and cirrhosis can lead to significant volume overload due to third spacing, and an abnormal accumulation of fluid in the interstitial spaces between cells, causing swelling.
This in turn decreases the effective circulating blood volume, decreasing blood flow to the kidneys. In heart failure, this occurs due to a drop in cardiac output, while in cirrhosis, this happens due to splanchnic venous pooling and systemic vasodilation.
The physical examination might show jugular venous distension, respiratory crackles, ascites, or lower extremity edema. These findings are highly suggestive of prerenal AKI due to interstitial volume overload.
Treatment consists of supportive care for AKI and treating the underlying cause. Additionally, you might need to correct extravascular volume overload, by administering intravenous albumin, which will create an osmotic gradient to draw fluid intravascularly, and then begin cautious diuresis, all of which will improve kidney perfusion.

Review7:45–8:46

Alright, as a quick recap... Prerenal AKI occurs when the cause of renal injury is before the kidneys.
The diagnosis of prerenal AKI is confirmed if the 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.
Once you’ve diagnosed prerenal AKI, your next step is to determine the underlying cause to guide your management. For Prerenal AKI due to Medication-Induced Renal Autoregulation Impairment, provide supportive care for AKI and discontinue offending medications.
If they are hypovolemic or have systemic vasodilation, treat the underlying cause and address intravascular volume expansion with fluids, as well as vasopressors if needed.
Finally, if your patient has volume overload due to heart failure or cirrhosis, you’ll need to address the underlying cause