Last updated: March 2025

Acute Kidney Injury (AKI): Causes, Symptoms and Treatment Options

Article Summary

Acute kidney injury (AKI) is a sudden decline in kidney function that can occur due to various factors, including dehydration, infections, or exposure to certain medications. This condition can lead to serious health complications if not diagnosed and treated promptly. This guide provides an overview of the causes, symptoms, and treatment options for acute kidney injury.

Contents of this article






What is Acute kidney injury (AKI)

Acute kidney injury (AKI), formerly known as acute renal failure (ARF), is a sudden decline in kidney function that develops within a short period, usually within seven days. It is characterized by an increase in serum creatinine levels and/or a decrease in urine output. It disrupts metabolic homeostasis, alters electrolyte and acid-base balance, and impairs fluid regulation, which can lead to life-threatening complications.
Unlike chronic kidney disease (CKD),which is progressive and often irreversible, AKI can be potentially reversible if treated promptly, many individuals can recover normal kidney function. However, if severe damage occurs, AKI can progress to chronic kidney disease (CKD)or even end-stage renal disease (ESRD), requiring long-term dialysis or kidney transplantation.
AKI can be prerenal (due to decreased blood flow to the kidneys), intrarenal (due to damage to the kidneys themselves), or postrenal (due to blockage of urine flow from the kidneys)

Risk factors for AKI

Common factors and conditions that can increase your risk of acute kidney injury include:

Causes of Acute kidney injury (AKI)

Acute kidney injury (AKI) occurs when the kidneys suddenly lose their ability to function properly. This condition can result from multiple factors that impair blood flow to the kidneys, directly damage kidney tissues, or obstruct urine flow. The causes of AKI are classified into three main categories: prerenal, intrinsic (intrarenal), and postrenal.

Prerenal Causes

Prerenal AKI occurs when there is inadequate blood flow to the kidneys, which impairs their ability to filter waste effectively. This is often due to conditions that reduce blood volume, blood pressure, or circulation. Common prerenal causes include:

  • Low blood pressure (hypotension)
  • Severe bleeding (hemorrhage)
  • Severe dehydration
  • Heart disease or heart attack
  • Sepsis (a severe infection that spreads through the bloodstream)
  • Liver failure
  • Excessive use of NSAIDs (nonsteroidal anti-inflammatory drugs) such as aspirin, ibuprofen, or naproxen
  • Severe burns
  • Severe allergic reactions (anaphylaxis)

Intrinsic (Intrarenal) Causes

Intrinsic AKI results from direct damage to the kidney tissues. This can occur due to infections, inflammatory diseases, toxins, or prolonged lack of oxygen supply to the kidneys. Common intrinsic causes include:

  • Blood clots in the kidney blood vessels
  • Glomerulonephritis(inflammation of the kidney’s filtering units)
  • Lupus nephritis (a kidney disease caused by an autoimmune disorder)
  • Kidney infections
  • Certain medications, including chemotherapy drugs, certain antibiotics
  • Contrast dyes used in imaging tests like CT scans and MRIs
  • Alcohol or drug abuse
  • Blood vessel disorders such as vasculitis (inflammation of the blood vessels)




Postrenal Causes

Postrenal AKI occurs when there is an obstruction in the urinary tract, preventing urine from leaving the kidneys. This blockage causes urine to build up, leading to increased pressure and potential kidney damage. Common postrenal causes include:

  • Kidney stones
  • Bladder problems
  • Blood clots in or around the kidneys
  • Enlarged prostate in men
  • Bladder cancer
  • Prostate cancer
  • Pelvic radiation
  • BPH (Benign prostatic hyperplesia)

Pathophysiology oF AKI

The disease process involves two pathologic mechanism implicating the process. Impaired renal blood flow or hypotension and impared perfusion leads to renal ischemia and necrosis resulting in GFR (glomerular filtration rate) reduction and tubular damage. Epithelial cells are destroyed by nephrotoxins (exogenous and endogenous infections includes bacterials and viruses). The lumen of the tubules become obliterated by oedema and swelling of the tissue, leading to acute tubular necrosis and temporal cessation of renal functions. However, if increased breakdown of renal function persist, it leads to decreased precipitation of urine with azotemia




Signs & Symptoms of AKI

Symptoms of acute kidney injury may include:

  • Decreased urination
  • Swelling of the hands, ankles, or feet
  • Shortness of breath
  • Irregular heartbeats
  • Tiredness
  • Weakness
  • Itching
  • Chest pain or pressure
  • Confusion
  • Bone pain
  • Loss of appetite
  • Fatigue and weakness
  • Nausea and vomiting
  • Seizures or coma in severe cases

Diagnostic Investigations & Test

The diagnosis of AKI is based on specific criteria, including changes in serum creatinine levels, urine output, and clinical presentation.

  • Serum Creatinine
  • Blood Urea Nitrogen (BUN)
  • Glomerular Filtration Rate (GFR)
  • Urine Albumin-to-Creatinine Ratio (UACR)
  • Urinalysis
  • Ultrasound
  • Computed Tomography (CT) Scan
  • Magnetic Resonance Imaging (MRI)
  • Intravenous Urogram (IVU)
  • Voiding Cystourethrography
  • Retrograde Urethrography

Diagnostic Criteria for AKI

AKI is diagnosed if any of the following criteria are met within 48 hours:

  • An increase in serum creatinine by 0.3 mg/dL or more
  • An increase in serum creatinine to 50% or more from baseline within the past seven days
  • A urine output of less than 0.5 milliliters per kilogram of body weight per hour for more than six hours

Urine Output Classification

AKI can be classified based on urine output:

  • Non-oliguric AKI:Urine output remains above 400 mL per day
  • Oliguric AKI:Urine output drops below 400 mL per day
  • Anuric AKI:Urine output is less than 100 mL per day


Treatment of Acute kidney injury (AKI)

The treatment of acute kidney injury (AKI) focuses on addressing the underlying cause, managing complications, and restoring kidney function.

Fluid and Electrolyte Management

  • Intravenous (IV) Fluids:If AKI is caused by dehydration or low blood volume, IV fluid administration helps restore fluid balance and improve kidney perfusion
  • Electrolyte Correction:Medications are used to manage imbalances such as high potassium (hyperkalemia), low calcium (hypocalcemia), or metabolic acidosis
  • Diuretics such as furosemide may be used to increase urine output and reduce swelling

Medications

  • Stopping Nephrotoxic Drugs that harm the kidneys, such as certain antibiotics, NSAIDs, and contrast dyes, should be discontinued or replaced with safer alternatives.
  • Calcium Gluconate administration to stabilize the heart in cases of severe hyperkalemia.
  • Potassium-binding drug to remove excess blood potassium
  • Hemodialysis to remove waste products and toxins from the blood

Dialysis

Indications for Dialysis:

  • Severe electrolyte imbalances (e.g., life-threatening hyperkalemia)
  • Severe metabolic acidosis
  • Fluid overload unresponsive to diuretics
  • Uremic symptoms such as confusion, nausea, or seizures

Other management

  • Infections prevention
  • Obstruction Removal
  • Blood Pressure Management
  • A low-protein diet may be recommended to reduce kidney workload.
  • Sodium and potassium intake should be monitored to prevent fluid retention and electrolyte imbalances.
  • Adequate calorie intake is essential to prevent muscle breakdown and support overall recovery.

Complications of AKI

Complications of acute kidney injury may include:

  • Fluid buildup
  • Muscle weakness
  • Permanent kidney damage
  • Death

Preventions of AKI

  • Treat infections
  • Live a healthy lifestyle
  • Work with your healthcare team to manage kidney and other ongoing conditions such as diabetesand hypertension