Acute kidney injury

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You’re looking at a short reference article from Explain Medicine (one of four distinct learning formats available in Clinical Odyssey). Try it out, and have fun improving your clinical skills.

Medicine

Last updated on:
October 19^th, 2021

Medicine

Last updated on:
October 19^th, 2021

Hi there!

You’re looking at a short reference article from Explain Medicine (one of four distinct learning formats available in Clinical Odyssey). Try it out, and have fun improving your clinical skills.

Clinicals - History

Fact	Explanation
Introduction	Acute kidney injury (AKI) occurs when a sudden decrease in kidney function causes the accumulation of the products of metabolism; it can be classified into prerenal AKI, intrinsic AKI, and postrenal AKI. Prerenal AKI is a consequence of renal hypoperfusion; and postrenal AKI is due to obstruction of the urinary tract. Both are a consequence of extrarenal disease. Intrinsic AKI represents true kidney disease, and can be categorized by the component of the kidney that is primarily affected: tubular, glomerular, interstitial, or vascular. Importantly, prerenal AKI can precipitate intrinsic AKI, if prolonged severe hypoperfusion causes ischemic injury to the renal tubules; this is termed acute tubular necrosis (ATN).
No symptoms	Most patients with mild to moderate AKI are asymptomatic. Such individuals are diagnosed with AKI only after laboratory testing.
Prerenal AKI: reduced fluid intake	Reduced fluid intake causes intravascular volume depletion, and may also impact renal arterial pressures. Renal perfusion is correspondingly lowered, resulting in a reduced glomerular filtration rate (GFR) and prerenal AKI.
Prerenal AKI: volume depletion	Severe volume loss can occur due to vomiting, diarrhea, diuretic overuse, burns, or hemorrhage. The intravascular volume depletion and resulting reduction in renal arterial blood pressures then gives rise to prerenal AKI.
Prerenal AKI: medications	Medications such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARB), and nonsteroidal anti-inflammatory drugs (NSAIDs) can cause prerenal AKI due to volume depletion or impairment of renal perfusion.
Prerenal AKI: heart failure	Prerenal AKI can occur as a consequence of heart failure; this is termed “cardiorenal syndrome.”
Prerenal AKI: liver failure	Liver failure can give rise to prerenal AKI; this is termed “hepatorenal syndrome.”
Prerenal AKI: vascular causes	Vascular conditions causing renal hypoperfusion (e.g., renovascular disease, hemolytic uremic syndrome, etc.) can give rise to prerenal AKI.
Intrinsic AKI: glomerular disease	All glomerular diseases can give rise to intrinsic AKI—especially (but not exclusively) those giving rise to nephritic syndrome. Rheumatological conditions (e.g., systemic lupus erythematosus) and autoimmune disorders (e.g. Goodpasture's syndrome) can also give rise to intrinsic AKI. Their symptoms should be looked for.
Intrinsic AKI: medications	Antibiotics such as aminoglycosides, acyclovir, phenytoin, interferon, proton pump inhibitors (PPI), and NSAIDs can cause ATN and acute interstitial nephritis (AIN).
Intrinsic AKI: contrast agent use	Use of an intravascular contrast agent (as an adjunct for imaging studies) can result in contrast-induced AKI, a form of intrinsic AKI. Risk factors include co-existing chronic kidney disease (CKD), diabetes mellitus, NSAID therapy, a low circulatory volume, and the use of a large amount of contrast.
Postrenal AKI: voiding symptoms	Symptoms such as urgency, hesitancy, intermittent flow, anuria, or polyuria may indicate postrenal AKI. In this, an obstruction to the urinary flow causes increased intra-tubular pressure and a correspondingly decreased GFR. The obstruction can be at any level of the urinary system, from the renal tubule to the urethra. Benign prostatic hypertrophy (BPH) is the most common such etiology.

Introduction

Acute kidney injury (AKI) occurs when a sudden decrease in kidney function causes the accumulation of the products of metabolism; it can be classified into prerenal AKI, intrinsic AKI, and postrenal AKI. Prerenal AKI is a consequence of renal hypoperfusion; and postrenal AKI is due to obstruction of the urinary tract. Both are a consequence of extrarenal disease. Intrinsic AKI represents true kidney disease, and can be categorized by the component of the kidney that is primarily affected: tubular, glomerular, interstitial, or vascular. Importantly, prerenal AKI can precipitate intrinsic AKI, if prolonged severe hypoperfusion causes ischemic injury to the renal tubules; this is termed acute tubular necrosis (ATN).

No symptoms

Most patients with mild to moderate AKI are asymptomatic. Such individuals are diagnosed with AKI only after laboratory testing.

Prerenal AKI: reduced fluid intake

Reduced fluid intake causes intravascular volume depletion, and may also impact renal arterial pressures. Renal perfusion is correspondingly lowered, resulting in a reduced glomerular filtration rate (GFR) and prerenal AKI.

Prerenal AKI: volume depletion

Severe volume loss can occur due to vomiting, diarrhea, diuretic overuse, burns, or hemorrhage. The intravascular volume depletion and resulting reduction in renal arterial blood pressures then gives rise to prerenal AKI.

Prerenal AKI: medications

Medications such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARB), and nonsteroidal anti-inflammatory drugs (NSAIDs) can cause prerenal AKI due to volume depletion or impairment of renal perfusion.

Prerenal AKI: heart failure

Prerenal AKI can occur as a consequence of heart failure; this is termed “cardiorenal syndrome.”

Prerenal AKI: liver failure

Liver failure can give rise to prerenal AKI; this is termed “hepatorenal syndrome.”

Prerenal AKI: vascular causes

Vascular conditions causing renal hypoperfusion (e.g., renovascular disease, hemolytic uremic syndrome, etc.) can give rise to prerenal AKI.

Intrinsic AKI: glomerular disease

All glomerular diseases can give rise to intrinsic AKI—especially (but not exclusively) those giving rise to nephritic syndrome. Rheumatological conditions (e.g., systemic lupus erythematosus) and autoimmune disorders (e.g. Goodpasture's syndrome) can also give rise to intrinsic AKI. Their symptoms should be looked for.

Intrinsic AKI: medications

Antibiotics such as aminoglycosides, acyclovir, phenytoin, interferon, proton pump inhibitors (PPI), and NSAIDs can cause ATN and acute interstitial nephritis (AIN).

Intrinsic AKI: contrast agent use

Use of an intravascular contrast agent (as an adjunct for imaging studies) can result in contrast-induced AKI, a form of intrinsic AKI. Risk factors include co-existing chronic kidney disease (CKD), diabetes mellitus, NSAID therapy, a low circulatory volume, and the use of a large amount of contrast.

Postrenal AKI: voiding symptoms

Symptoms such as urgency, hesitancy, intermittent flow, anuria, or polyuria may indicate postrenal AKI. In this, an obstruction to the urinary flow causes increased intra-tubular pressure and a correspondingly decreased GFR. The obstruction can be at any level of the urinary system, from the renal tubule to the urethra. Benign prostatic hypertrophy (BPH) is the most common such etiology.

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