Name: acute kidney injury: causes and kidney damage
Uploaded: 2025-06-19T09:31:14.000Z
Duration: 1 min 29 s
Channel: JoVE

Acute kidney injury or AKI is classified into prerenal, intrarenal, and postrenal causes based on the location of the injury and the underlying pathophysiology.Firstly, prerenal AKI occurs when reduced blood flow to the kidneys decreases filtration capacity without directly damaging them.If blood flow is not restored in time, prolonged reduced perfusion can lead to ischemia and intrinsic kidney damage. Common causes include hypovolemia, heart failure, and sepsis.Next, intrarenal or intrinsic AKI is caused by direct damage to kidney tissues like the glomeruli, tubules, or blood vessels, leading to acute tubular necrosis, interstitial nephritis, or glomerulonephritis.These issues cause inflammation, impaired filtration, and a reduced glomerular filtration rate or GFR, ultimately affecting kidney function.Finally, postrenal AKI arises from an obstruction in the urinary tract, which prevents urine from flowing out of the kidneys. This blockage increases pressure in the renal tubules, leading to a decline in GFR.If the obstruction is not resolved promptly, the resulting pressure can cause irreversible kidney damage.

acute kidney injury ii: pathophysiology

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity without causing direct kidney damage.Common causes include:<ul><li>Hypovolemia (e.g., due to bleeding, dehydration, or severe burns)</li><li>Decreased cardiac output, such as in heart failure or following a myocardial infarction, reduces blood flow to the kidneys, impairing filtration.</li><li>Systemic vasodilation (e.g., due to sepsis or liver failure)</li><li>Renal artery stenosis</li></ul>Pathophysiology:<ul><li>In prerenal acute kidney injury, the kidneys remain structurally intact, but there is a marked reduction in renal blood flow, leading to a low glomerular filtration rate (GFR).</li><li>The kidneys attempt to compensate by activating autoregulatory mechanisms, such as prostaglandin-mediated dilation of the afferent arteriole and angiotensin II-mediated constriction of the efferent arteriole, to preserve GFR. To maintain fluid balance, the kidneys enhance sodium and water reabsorption.</li><li>However, if perfusion is not restored promptly, prolonged low blood flow can lead to ischemic injury and may evolve into intrinsic acute kidney injury, often in the form of acute tubular necrosis (ATN).</li></ul>2. Intrarenal (Intrinsic) causesEtiology: Intrarenal acute kidney injury results from direct injury to the kidney&#8217;s internal structures, affecting the glomeruli, tubules, interstitium, or vasculature.Key causes include:<ul><li>Acute tubular necrosis (ATN) due to ischemia or nephrotoxins (e.g. certain medications or contrast agents)</li><li>Acute interstitial nephritis (AIN), often due to drug reactions or infections</li><li>Glomerulonephritis (GN), caused by immune-mediated damage</li><li>Vascular diseases, such as vasculitis or malignant hypertension</li></ul>Pathophysiology: The pathophysiology of intrarenal acute kidney injury depends on the specific site of injury:<ul><li>In acute tubular necrosis (ATN), ischemia or nephrotoxins damage the renal tubular epithelial cells, leading to cell death and sloughing of cells into the tubular lumen. This results in obstruction, a decreased GFR due to filtrate back-leak, and reduced urine output.</li><li>In acute interstitial nephritis (AIN), an immune response to medications or infections causes inflammation and edema in the renal interstitium, impairing tubular function.</li><li>In glomerulonephritis (GN), immune complexes or other factors induce inflammation and damage the glomeruli, resulting in reduced filtration, proteinuria, and hematuria.</li></ul>If treated promptly, ATN is often reversible, though severe or prolonged ATN can lead to permanent damage.3. Postrenal causesEtiology: Postrenal acute kidney injury occurs when an obstruction impedes urine flow, causing back pressure in the urinary system.Common causes include:<ul><li>Ureteral obstructions (e.g., kidney stones, strictures, tumors)</li><li>Bladder outlet obstructions (e.g., benign prostatic hyperplasia or prostate cancer)</li><li>Urethral strictures or injury</li><li>Pathophysiology: When urine flow is blocked, pressure builds in the urinary system, increasing hydrostatic pressure in the renal tubules, which reduces GFR.</li><li>Early in the obstruction, the kidneys may compensate for mild blockages. However, prolonged obstruction leads to renal ischemia, hydronephrosis (swelling of the kidneys due to urine accumulation), and tubular atrophy.</li><li>Without timely intervention, this damage may become irreversible, resulting in permanent loss of kidney function.</li></ul>

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), ...

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Medical-Surgical Nursing

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Management of Patients with Kidney Disorders

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acute kidney injury: causes and kidney damage

Acute kidney injury (AKI) can be grouped by where the problem starts in the kidney system. The three main categories are prerenal, intrarenal, and postrenal causes. This breakdown helps explain how kidney function is disrupted and supports clinical decision-making.

Prerenal acute kidney injury is the most common type. It happens when blood flow to the kidneys drops, so filtration falls even though the kidney tissue itself is not directly damaged. Common causes include hypovolemia from bleeding, dehydration, or severe burns, decreased cardiac output from heart failure or after a myocardial infarction, systemic vasodilation from sepsis or liver failure, and renal artery stenosis.

In prerenal AKI, the kidneys are still structurally intact, but renal blood flow is low and the glomerular filtration rate (GFR) decreases. The kidneys try to protect GFR by using autoregulatory responses. These include prostaglandin-mediated dilation of the afferent arteriole and angiotensin II-mediated constriction of the efferent arteriole. The kidneys also increase sodium and water reabsorption to help maintain fluid balance. If perfusion is not restored quickly, the low blood flow can cause ischemic injury and progress to intrinsic AKI, often as acute tubular necrosis (ATN).

Intrarenal, also called intrinsic, acute kidney injury comes from direct damage inside the kidney. It can affect the glomeruli, tubules, interstitium, or blood vessels. Major causes include ATN from ischemia or nephrotoxins such as certain medications or contrast agents, acute interstitial nephritis (AIN) from drug reactions or infections, glomerulonephritis (GN) from immune-mediated damage, and vascular disease such as vasculitis or malignant hypertension.

The pathophysiology of intrarenal AKI depends on the part of the kidney that is injured. In ATN, ischemia or nephrotoxins damage tubular epithelial cells, which then die and slough into the tubule. This can block flow, cause filtrate back-leak, reduce GFR, and lower urine output. In AIN, an immune response causes inflammation and edema in the renal interstitium, which interferes with tubular function. In GN, immune complexes or other factors inflame and injure the glomeruli, leading to reduced filtration, proteinuria, and hematuria. ATN is often reversible if treated early, but severe or prolonged injury can leave permanent damage.

Postrenal acute kidney injury occurs when urine cannot drain normally. The blockage may be in the ureters, bladder outlet, or urethra. Examples include kidney stones, strictures, tumors, benign prostatic hyperplasia, prostate cancer, and urethral injury or stricture.

When urine flow is blocked, pressure builds in the urinary system. This raises hydrostatic pressure in the renal tubules and lowers GFR. Mild obstruction may be partly compensated early on, but prolonged blockage can cause renal ischemia, hydronephrosis, and tubular atrophy. If the obstruction is not relieved in time, the damage may become irreversible and lead to permanent loss of kidney function.

Acute Kidney Injury: Causes and Kidney Damage

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Acute kidney injury (AKI) can be grouped by where the problem starts in the kidney system. The three main categories are prerenal, intrarenal, and postrenal causes. This breakdown helps explain how kidney function is disrupted and supports clinical decision-making. Prerenal acute kidney injury is the most common type. It happens when blood flow to the kidneys drops, so filtration falls even though the kidney tissue itself is not directly damaged. Common causes include hypovolemia from...

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key terms and concepts

Explore prerenal, intrarenal, and postrenal acute kidney injury, including common causes, kidney changes, and how reduced urine flow affects GFR.

Acute Kidney Injury: Causes and Kidney Damage | JoVE K12

JoVE Core Medical-Surgical Nursing offers comprehensive animated lessons that cover major systems of the human body, integrating anatomy and physiology with system-specific assessments. This collection encompasses disease conditions based on the body systems, detailing their pathophysiology, medical and surgical management, and nursing interventions. These lessons provide a clear and practical understanding of medical-surgical care, equipping students with essential skills for managing patient care in various clinical settings.

Acute Kidney Injury: Causes and Kidney Damage

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