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Acute kidney injury: Clinical practice

Acute kidney injury: Clinical practice


1 / 4 complete

USMLE® Step 1 style questions USMLE

3 questions

USMLE® Step 2 style questions USMLE

4 questions

A 38-year-old woman comes to the emergency department for evaluation of altered mental status that began five hours ago. She is accompanied by her husband. Past medical history is notable for asthma and diffuse scleroderma. On arrival, her temperature is 37.6°C (99.7°F) and blood pressure is 183/121 mmHg. On physical examination, the patient is oriented to self but neither time nor place. Diffuse thickening of the skin is observed, and contractures are present in the bilateral fingers. Laboratory testing is obtained, and results are as follows:  

 Laboratory value  Result 
 Hemoglobin  10.7 g/dL 
 Leukocyte Count  7,300/mm3 
 Platelet Count  80,000/mm3 
 Blood Urea Nitrogen  35 mg/dL 
 Creatinine, Serum  2.0 mg/dL 
Which of the following is the next best step in the management of this patient’s condition?


Content Reviewers:

Rishi Desai, MD, MPH

With acute kidney injury, or AKI, there’s a decrease in kidney function that typically happens over a few days.

This leads to the retention of urea and other nitrogenous waste products- such as ammonia and uric acid and dysregulation of extracellular volume and electrolytes.

The most commonly used diagnostic criteria for AKI are the Kidney Disease: Improving Global Outcomes or KDIGO guidelines.

The KDIGO guidelines define AKI as an increase in serum creatinine of at least 0.3 milligrams per deciliter within 48 hours or as an increase in serum creatinine by 1.5 times the baseline serum creatinine within the last 7 days or when the urine volume has been less than 0.5 milliliters per kilogram per hour for six hours.

Based on these criteria, there are three stages of AKI, where stage 1 is mild and stage 3 is severe AKI.

In stage 1 AKI, there’s an increase in serum creatinine to 1.5 to 1.9 times the baseline serum creatinine or an increase in serum creatinine by 0.3 milligrams per deciliter or a decrease in urine output to below 0.5 milligrams per kilogram per hour for 6 to 12 hours.

In stage 2 AKI, there’s an increase in serum creatinine to 2 to 2.9 times the baseline serum creatinine or a decrease in urine output to less than 0.5 milligrams per kilogram per hour for more than 12 hours.

In stage 3 AKI, there’s an increase in serum creatinine to 3 times the baseline serum creatinine or an increase in serum creatinine to more than 4 milligrams per deciliter or a decrease in urine output to less than 0.3 milligrams per kilogram per hour for more than 24 hours or anuria- meaning less than 100 milliliters per day of urine- for more than 12 hours or where renal replacement therapy has been initiated.

All individuals are classified according to whichever criteria places them in the most severe stage of injury.

Once diagnosed, the causes of AKI can be split into prerenal, intrarenal, and post-renal causes.

In prerenal AKI, there’s decreased blood flow into the kidneys.

This can happen in hypovolemic states like an acute hemorrhage, gastrointestinal losses- like with diarrhea and vomiting, renal losses- like with diuretics or osmotic diuresis in hyperglycemia, dermal losses- like with burns and finally sequestration of fluid- also known as third-spacing- like with acute pancreatitis or sepsis.

On the clinical examination, there’s tachycardia, hypotension, reduced skin turgor, and cool extremities.

Now, prerenal AKI can also happen with hypervolemic states where there’s a low effective circulating volume.

One example is severe systolic heart failure leading to pump failure, and when this happens, it’s called cardiorenal syndrome. In this situation, there are signs of heart failure, like hypotension, fatigue, dyspnea, and peripheral edema.

Another hypervolemic situation due to a low effective circulating volume is hypoalbuminemia from decompensated liver disease. When that leads to AKI, it’s called hepatorenal syndrome.

The individual has hypotension and signs of liver disease like splenomegaly, caput medusae, ascites, and peripheral edema.

Additionally, some medications such as NSAIDs, ACE-inhibitors, ARBs, cyclosporine and iodinated contrast can damage renal blood vessels - leading to ischemia and causing prerenal AKI.

Next, there’s intrarenal AKI which is due to damage to the tubules, the glomerulus, or the kidney interstitium, which is the space between tubules or vascular damage.

The most common cause of intrarenal AKI is acute tubular necrosis or ATN, which causes damage to the tubules due to ischemia.

Often ATN is due to ischemia from a prerenal acute kidney injury.

The other way tubules can necrose is via nephrotoxins such as aminoglycosides antibiotics, methotrexate, heavy metals like lead, myoglobin from damaged muscles - like in rhabdomyolysis, ethylene glycol, radiocontrast dye, and uric acid. Typically, the individual has been exposed to a nephrotoxin and has associated symptoms.

For example, if they’ve been exposed to ethylene-glycol, the individual might also be confused and have dilated pupils, whereas if the cause is myoglobinuria - they may have had a recent crush injury.

Another type of intrarenal AKI is glomerular disease, which is anything that damages the glomeruli.

Glomerular disease can cause isolated gross hematuria- like immunoglobulin A nephropathy.

It can also cause signs of nephrotic syndrome, such as peripheral or periorbital edema, even ascites- this can happen with membranous nephropathy or membranoproliferative glomerulonephritis.

Labs here show proteinuria that’s above 3.5 grams per day, protein-to-creatinine ratio greater than 3 grams per gram, hypoalbuminemia that’s typically less than 3.5 grams per deciliter and hyperlipidemia, with levels of low-density lipoprotein or LDL above 130 milligrams per deciliter and levels of triglycerides above 150 milligrams per deciliter.

On urinalysis, specifically microscopy, there is lipiduria, which is identified based on the presence of fat droplets.

Or it can present signs of nephritic syndrome, such as arterial hypertension and peripheral edema- this can happen with systemic Lupus erythematosus.

Labs here show moderate proteinuria- between 1 and 3 grams per day and on urinalysis, there are more than 5 dysmorphic red blood cells per microliter and also red cell casts.

Finally, it can also present with signs and symptoms of a more severe systemic condition, such as malaise, arthralgia and fever- like with Goodpasture disease.

Another cause of intrarenal AKI is acute interstitial nephritis, which is inflammation of the interstitium over the course of days to weeks.

This is thought to be a type I or type IV hypersensitivity reaction, and is typically a response to a medication like NSAIDs, penicillin, and diuretics, such as thiazide diuretics, like chlorothiazide. Early symptoms include fever and rash.

Now, vascular damage can be caused by renal artery stenosis, which is when one or both renal arteries are narrowed.

This can be caused by atherosclerosis in older individuals and by fibromuscular dysplasia, which is a noninflammatory and nonatherosclerotic condition that usually affects the internal carotids and renal arteries in younger individuals.

Symptoms include persistent arterial hypertension despite taking antihypertensive medications and sometimes peripheral edema.

Finally, there’s postrenal AKI, which is due to an obstruction to the outflow of urine from the kidneys which causes a buildup of urine and pressure that backs up into the kidney.

This is most frequently due to benign prostatic hyperplasia or prostatic cancer in a male, both of which lead to compression of the urethra. This can lead to frequent urination but a slow urinary stream.

Other causes include intra-abdominal tumors that compress the ureter- in which case the individual can present with unintentional weight loss and fatigue.

Finally, there are kidney stones that can get stuck in either ureter or in the urethra.

Now, if only one ureter is obstructed, called unilateral obstruction, and the other kidney is working fine, then renal function is usually preserved.

But if both ureters are obstructed- like when there are stones in both ureters, called bilateral obstruction, or if the urethra gets blocked, then we’ve got a recipe for postrenal AKI.

With obstructive ureteral kidney stones, the individual has renal colic along with anuria if both ureters are completely obstructed.

With urethral stones, the individual has pain in the urethra and anuria.

Now, additional labs include creatinine levels in order to calculate the estimated glomerular filtration rate or eGFR, BUN, CBC, and electrolytes to check for hyperkalemia.

Hyperkalemia can develop because when the individual is oliguric, potassium isn’t effectively removed from the blood.

Also, if the individual is hyperventilating, this can be a sign of metabolic acidosis, so an ABG is also done.

AKI can lead to severe metabolic acidosis where the pH dips below 7.1, because acid excretion is impaired when there’s a low eGFR.

Next, urinalysis- both dipstick and microscopic examination of the urine sediment and urine sodium excretion are done to help calculate the fraction of sodium excreted to sodium filtered, or FENa.