Approach to acute kidney injury: Clinical sciences

Chapters:

Watch video only

Introduction 0:00–0:21

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 A, B, C, DE assessment to determine if they are unstable or stable.

Unstable patient 0:21–0:56

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.

Stable Patient 0:56–1:08

First, let's focus on pre-renal AKI. Pre-renal AKI is typically associated with reduced urine output, sometimes in combination with non-specific symptoms, including malaise, fever, and vomiting.

Prerenal AKI 1:08–3:40

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 BP abnormalities, weak peripheral pulses, and tachycardia.
Also, you might notice peripheral edema or signs of dehydration, like dry mucous membranes. With these findings, consider pre-renal 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 mg per deciliter or more over 48 hours, a rise of serum creatinine 1.5 times the baseline or more in the last seven days, or urine output less than 0.5 mL per kilogram per hour for six hours.
In pre-renal 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 FINA, which refers to the fractional excretion of sodium, and check the percentage of sodium filtered by the kidneys into the urine.
In pre-renal AKI, the kidneys filter less sodium to maintain intravascular volume, so the FA 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, FINA values will not adequately reflect the changes in acute kidney injury. Similarly, PENA is not reliable in oliguric patients who are taking diuretics because these medications promote sodium excretion, causing PENA 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 pre-renal 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.

Hypovolemia 3:40–3:57

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.

Systemic vasodilation 3:57–4:20

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.

Interstitial volume overload 4:20–4:41

If the exam reveals signs of volume overload, including jugular venous distention, 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.

Medication-induced renal autoregulation impairment 4:41–5:04

If the physical exam is normal, diagnose medication-induced renal autoregulation impairment. Next up is intrinsic AKI, which is typically associated with non-specific signs and symptoms.

Intrinsic AKI 5:04–6:55

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 erythematosis or malignancy.
Similarly, the physical exam is non-specific and might reveal BP 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 mg per deciliter or more over 48 hours, a rise of serum creatinine 1.5 times the baseline or more in the last seven days, or urine output less than 0.5 mL per kilogram per hour for six hours.
With intrinsic AKI, the BUN to creatinine ratio is less than 20:1, and urine sodium is greater than 20 millequivalents per liter.
In intrinsic AKI, kidneys fail to reabsorb the sodium from filtered urine, meaning more sodium gets excreted into the urine, causing FA to be greater than 2%.
The urinalysis and microscopy will often reveal red blood cell, white blood cell, 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.

Glomerular causes 6:55–8:12

Proliferative glomerulonephritis is often associated with fever, joint pain, and frankly bloody or dark colored urine. These individuals will typically present with facial or peripheral edema and hypertension, and their urinalysis will show hematuria, dysmorphic red blood cells, and red blood cell casts.
With these findings, diagnose proliferative glomerulonephritis, more specifically, a nephritic pattern of glomerular injury, which is commonly seen in post-streptococcal glomerulonephritis, IgA nephropathy, and anka associated glomerulonephritis.
On the flip side, non-proliferative glomerulopathy is usually associated with unintentional weight gain and foamy urine.
In this case, the exam will typically reveal periorbital or peripheral edema and sometimes hypertension. If the urinalysis reveals proteinuria.
Diagnose non-proliferative glomerulopathy, more specifically, a nephrotic pattern of glomerular injury, which is commonly seen in focal segmental glomerulosclerosis and membranous nephropathy.
Moving on to non-glomerular causes, starting with acute tubular necrosis or ATN, which is usually associated with current or recent shock, like in sepsis.

Non-glomerular causes 8:12–10:30

Sometimes there might be no shock, but your patient might report taking nephrotoxic medications, including amino glycosides and vancomycin, or exposure to nephrotoxic substances like radiocontrast dye.
Finally, if the urine microscopy shows muddy brown granular casts and renal tubular epithelial cells, diagnose ATN. Next up is acute interstitial nephritis or AIN, which is typically characterized by fever and rash.
In some cases, the patient might report taking antibiotics or immune checkpoint inhibitors. Finally, if the urine microscopy reveals white blood cells, white blood cell casts with or without eosinophilia, diagnose AIN.
Now, let's focus on intratubular renal obstruction, which is usually seen in individuals with multiple myeloma and tumor lysis syndrome, which typically occurs as a result of cytotoxic therapy.
Urinalysis with microscopy reveals red blood cells, white blood cells, and sometimes hematuria with proteinuria. With multiple myeloma, you might also see light chain casts, while in tumor lysis syndrome, you will notice uric acid crystals due to increased uric acid release.
With these findings, diagnose intratubular renal obstruction. Finally, let's go over extraglomerular vascular injuries.
In this case, history might reveal recent vascular instrumentation, such as cardiac catheterization or conditions like malignant hypertension, sepsis, or severe trauma.
If your analysis reveals hematuria, proteinuria, red blood cells, white blood cells, and no casts, diagnose extraglomerular vascular injury.
Examples of extraglomerular vascular injury include macrovascular conditions such as aortic dissection and renal vein thrombosis, but also conditions that affect microvasculature like disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and hemolytic uremic syndrome.
Finally, let's look at post-renal AKI. These patients will typically report pelvic discomfort, often in combination with slow stream or dribbling.

Post-renal AKI 10:30–11:38

In acute cases, the patient could report sudden pelvic pain and urinary retention. Additionally, history might reveal sudden flank pain and bloody urine or conditions like prostate disease and nephrolithiasis.
Next, the physical exam might reveal palpable bladder and flank tenderness. Finally, on the digital rectal exam or DRE, you might notice prostate enlargement or palpable mass.
With these findings, consider post renal AKI. So again, order basic metabolic panel and urinalysis with microscopy, assess the patient's urine output over time, and don't forget renal ultrasound.
If creatinine levels and urine output are suggestive of AKI and you find bland urine sediment in combination with obstruction and hydronephrosis on renal ultrasound, diagnose post-renal AKI.
In this case, obtain a post-void residual bladder scan. Post-void residual below 100 mL suggests upper urinary tract obstruction, so order abdominal and pelvic CT to assess the underlying cause.

Upper urinary tract obstruction 11:38–12:39

If the CT confirms hydronephrosis and shows bilateral ureteral stone, diagnose nephrolithiasis. Bilateral ureterral obstruction in healthy individuals is rare.
However, conditions like hyperuricemia and hyperparathyroidism increase the risk of kidney stones, so these individuals have a higher chance of developing bilateral obstruction.
Keep in mind that in patients with a single functioning kidney, unilateral ureteral stone can result in AKI. Next, if the CT scan reveals a solid mass surrounding or infiltrating the ureters, malignancy is likely the underlying cause.
Finally, if the CT scan reveals a mass external to the colonic lumen with fluid locculations, think of an intraabdominal abscess.
On the flip side, the post-void residual greater than 100 mL indicates lower urinary tract obstruction and urinary retention.

Lower urinary tract obstruction 12:39–14:11

In this case, assess the digital rectal exam findings because prostate enlargement and palpable mass suggest prostate disease.
If the digital rectal exam is normal, order additional imaging to rule out bladder and urethral stones. Moreover, order an abdominal X-ray to check for the presence of calcium phosphate and calcium oxalate stones, which are already opaque.
However, uric acid stones are radiolucent, so you can't identify them using X-ray. Instead, consider ultrasound, cystoscopy, or CT which can also help you identify possible tumors or anatomical abnormalities like strictures.
If imaging reveals a bladder stone or tumor, diagnose bladder outlet obstruction. And if you identify a urethral stone or urethral stricture, diagnose urethral obstruction.
Finally, if imaging findings are normal and your patient is taking anticholinergic medications like atropine or medications with known anticholinergic side effects such as antihistamines, diagnose medication-induced urinary retention.
On the flip side, if imaging findings are normal and history reveals central nervous system conditions like multiple sclerosis, autonomic neuropathy, which is common in diabetes, or a spinal cord injury, think of neurogenic bladder.
All right, as a quick recap, Acute kidney injury refers to a sudden decline in kidney function that results in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste.

Review 14:11–14:48

Important causes of pre-renal AKI include hypovolemia and systemic vasodilation, while conditions associated with intrinsic AKI include glomerular causes like proliferative glomerulonephritis and non-glomerular causes like acute tubular necrosis.
Finally, post-renal AKI can occur due to nephrolithiasis and bladder outlet or urethral obstruction.
Approach to acute kidney injury: Video and Anatomy | Osmosis