Acute renal injury (AKI) - prerenal, intrarenal, postrenal causes

This article doesn't meet WikiLectures quality standards.

This article seems to not fulfill most of the items on our Editorial Process checklist. As such, it's going to be deleted soon. To the author of this article: if you still work on this article, make sure to replace this template with the Under construction template. However, be aware that if you don't make any changes to the article after that soon enough, the article will still be deleted. To find out what you need to do to improve this article, read Help:Editorial process. Feel free to ask for help on Forum:Support. To see how articles on WikiLectures should look like, check out articles in Category:Finished articles. For more information, contact the user who inserted this template, you can find them in the Page History (under the "Actions" button). Last user who modified this page: ShadyMedic

Scheme of Acute Kidney Injury Symptoms

Definition of Acute Kidney Injury

Acute Kidney Injury (AKI) is a sudden decline in renal function, resulting in impaired excretion of nitrogenous waste products, disregulation of fluid and electrolyte balance, and reduced urine output. It is potentially reversible, particularly when promptly recognized and treated.

AKI is characterized by:

• Rising serum creatinine
• Elevated blood urea nitrogen (BUN)
• Azotemia (accumulation of nitrogenous waste products)
• Often oliguria

Diagnostic Criteria

AKI is defined by any of the following:

• Increase in serum creatinine ≥ 0.3 mg/dL within 48 hours, or
• Increase in serum creatinine to ≥ 1.5 times baseline within 7 days, or
• Urine output < 0.5 mL/kg/hour for ≥ 6 hours

Classification of AKI

AKI is classified according to the site of the underlying disturbance into:

1. Prerenal AKI
2. Intrinsic (Intrarenal) AKI
3. Postrenal AKI

Prerenal Acute Kidney Injury

Pathophysiology

Prerenal AKI results from reduced renal perfusion, leading to a decrease in glomerular capillary hydrostatic pressure and reduced glomerular filtration rate (GFR), without intrinsic kidney damage.

Key mechanisms include:

• Decreased renal blood flow
• Reduced effective circulating volume
• Alterations in afferent or efferent arteriolar tone (afferent arteriole vasoconstriction and efferent arteriole vasodilation)

Common causes include:

• Hypovolemia (hemorrhage, dehydration, burns)
• Reduced cardiac output (heart failure, cardiogenic shock)
• Systemic vasodilation (sepsis)
• Renal artery stenosis

Drug-induced Prerenal AKI

Renal autoregulation depends on:

• Prostaglandin-mediated afferent arteriolar vasodilation
• Angiotensin II–mediated efferent arteriolar vasoconstriction

Therefore:

• NSAIDs inhibit prostaglandin synthesis → afferent vasoconstriction → ↓ GFR
• ACE inhibitors inhibit angiotensin II → efferent vasodilation → ↓ GFR

Prerenal AKI is reversible if renal perfusion is restored promptly; prolonged hypoperfusion may progress to ischemic acute tubular necrosis.

Intrarenal Acute Kidney Injury

Intrarenal AKI is caused by direct damage to renal parenchyma, including tubules and interstitium.

1. Acute Tubular Necrosis (ATN)

Acute tubular necrosis is the most common cause of intrinsic AKI.

Etiology

• Ischemic injury (prolonged prerenal AKI, shock, sepsis)
• Nephrotoxic injury, including:
  • Aminoglycoside antibiotics
  • Heavy metals
  • Endogenous toxins (myoglobin in rhabdomyolysis, hemoglobin in hemolysis, uric acid)

Pathophysiology

• Tubular epithelial cell necrosis and detachment
• Tubular obstruction by cellular debris
• Back-leak of filtrate
• Reduced GFR

2. Inflammatory and Vascular Causes of Intrarenal AKI

• Acute interstitial nephritis (often drug-induced or infectious)
• Glomerulonephritis
• Renal vasculitis
• Thrombotic microangiopathies, including:
  • Hemolytic Uremic Syndrome (HUS) – commonly associated with Shiga toxin–producing E. coli

Postrenal Acute Kidney Injury

Pathophysiology

Postrenal AKI results from obstruction of urinary outflow, leading to:

• Increased intratubular pressure
• Decreased GFR
• Azotemia and oliguria

Causes of Postrenal AKI

• Ureteral obstruction
  • Nephrolithiasis
  • Tumors
  • Retroperitoneal fibrosis or masses
• Bladder outlet obstruction
  • Benign prostatic hyperplasia
  • Prostate carcinoma
• Urethral obstruction

Clinical Course and Outcome

AKI is potentially reversible, especially prerenal and postrenal forms. However:

• Severe or prolonged AKI may require renal replacement therapy (dialysis)
• Untreated AKI may progress to uremia
• Intrarenal AKI, especially ATN, may lead to chronic kidney disease

Reference

1. Kumar V, Abbas AK, Aster JC.Robbins and Cotran Pathologic Basis of Disease.10th ed. Philadelphia: Elsevier; 2021. Chapter: The Kidney (Acute Kidney Injury).
2. McPhee SJ, Hammer GD.Pathophysiology of Disease: An Introduction to Clinical Medicine. 7th ed. New York: McGraw-Hill Education; 2014. Chapter: Acute Kidney Injury.
3. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J.Harrison’s Principles of Internal Medicine.21st ed. New York: McGraw-Hill Education; 2022. Section: Acute Kidney Injury.