What causes Intrinsic Acute Kidney Injury (AKI)?

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Last updated: June 20, 2025View editorial policy

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From the Guidelines

Intrinsic Acute Kidney Injury (AKI) is primarily caused by direct damage to the kidney tissue, with the most common causes being acute tubular necrosis (ATN) due to ischemia or nephrotoxic injury, as well as other conditions such as acute interstitial nephritis, glomerulonephritis, and vascular disorders. The pathophysiology of intrinsic AKI involves direct cellular damage to kidney structures, resulting in decreased filtration capacity, tubular dysfunction, and inflammatory responses that further compromise kidney function 1.

Causes of Intrinsic AKI

  • Acute tubular necrosis (ATN) due to ischemia or nephrotoxic injury
  • Acute interstitial nephritis, often medication-induced by antibiotics, NSAIDs, or proton pump inhibitors
  • Glomerulonephritis, an immune-mediated inflammation of the glomeruli
  • Vascular disorders such as vasculitis, malignant hypertension, or thrombotic microangiopathies
  • Nephrotoxic injury from substances harmful to the kidneys, including medications (aminoglycosides, NSAIDs, certain antibiotics like vancomycin, chemotherapeutic agents), contrast media used in imaging studies, heavy metals, and myoglobin released during rhabdomyolysis 1

Prevention Strategies

  • Maintaining adequate hydration
  • Avoiding nephrotoxic medication combinations
  • Appropriate dosing of medications in patients with reduced kidney function
  • Prompt treatment of conditions that may lead to kidney hypoperfusion
  • Evaluation of nephrotoxins as a plausible cause of AKI and selection of less nephrotoxic drugs when possible 1

Clinical Considerations

Intrinsic AKI can have a significant impact on patient morbidity and mortality, with increased healthcare costs 1. Early identification and management of the underlying cause of AKI are critical to improve patient outcomes. A thorough history, physical examination, and laboratory analysis, including serum creatinine and urine microscopy, are essential for the diagnosis and management of intrinsic AKI 1.

From the Research

Causes of Intrinsic Acute Kidney Injury (AKI)

Intrinsic AKI refers to damage that occurs within the kidney itself, as opposed to prerenal or postrenal causes. The following are some of the key causes of intrinsic AKI:

  • Ischemia: reduced blood flow to the kidneys, which can be caused by a variety of factors such as dehydration, blood loss, or cardiac arrest 2, 3
  • Nephrotoxicity: exposure to substances that are toxic to the kidneys, such as certain medications or toxins 2, 4
  • Acute tubular necrosis: a condition in which the tubules of the kidney become damaged, often due to ischemia or nephrotoxicity 4
  • Inflammation: inflammation within the kidney can cause damage and lead to AKI 3
  • Infectious diseases: certain infections, such as sepsis, can cause intrinsic AKI 5

Pathophysiology of Intrinsic AKI

The pathophysiology of intrinsic AKI is complex and involves the interaction of multiple cell types and molecular mechanisms. Some of the key factors involved include:

  • Renal ischemia and reperfusion injury: this can cause damage to the kidney tissue and lead to AKI 3, 6
  • Inflammation and oxidative stress: these can contribute to tissue damage and dysfunction in the kidney 3, 6
  • Maladaptive repair: after an injury, the kidney may undergo maladaptive repair, which can lead to chronic kidney disease 2

Medical Causes of Intrinsic AKI

There are several medical causes of intrinsic AKI, including:

  • Nephrotoxic medications: certain medications, such as antibiotics or chemotherapy agents, can be toxic to the kidneys and cause AKI 4
  • Sepsis: sepsis can cause intrinsic AKI by leading to inflammation and oxidative stress in the kidney 3, 5
  • Cardiac surgery: cardiac surgery can cause intrinsic AKI due to renal ischemia and reperfusion injury, as well as other factors such as inflammation and oxidative stress 6

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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