MBBS · General Medicine

Acute kidney injury

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Acute kidney injury — on-site reading

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Acute kidney injury (AKI), previously called acute renal failure, is a sudden decrease in kidney function that develops within seven days, as shown by an increase in serum creatinine or a decrease in urine output, or both.
Causes of AKI are classified as either prerenal (due to decreased blood flow to the kidney), intrinsic renal (due to damage to the kidney itself), or postrenal (due to blockage of urine flow). Prerenal causes of AKI include sepsis, dehydration, excessive blood loss, cardiogenic shock, heart failure, cirrhosis, and certain medications such as ACE inhibitors or NSAIDs. Intrinsic renal causes of AKI include glomerulonephritis, lupus nephritis, acute tubular necrosis, certain antibiotics, and chemotherapeutic agents. Postrenal causes of AKI include kidney stones, bladder cancer, neurogenic bladder, enlargement of the prostate, narrowing of the urethra, and certain medications such as anticholinergics.
The diagnosis of AKI is made based on a person's signs and symptoms, along with laboratory tests measuring serum creatinine and urine output. Other tests include urine microscopy and urine electrolytes. Renal ultrasound can be obtained when a postrenal cause is suspected. A kidney biopsy may be obtained when intrinsic renal AKI is suspected, and the cause is unclear.
AKI is seen in 10–15% of people admitted to the hospital and in more than 50% of people admitted to the intensive care unit. AKI may lead to several complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, effects on other organ systems, and death. People who have experienced AKI are at increased risk of developing chronic kidney disease in the future. Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy.

How this connects to General Medicine

Molecular investigation links DNA variation and gene regulation to RNA, proteins and cellular function. Assays measure selected molecular features with finite sensitivity and specificity; a detected variant or transcript does not automatically establish biological causation or a clinical diagnosis.

Text credit: Wikipedia contributors, “Acute kidney injury”, original article · authors & revision history · CC BY-SA 4.0. Unmodified opening extract, accessed 24 September 2026. This Wikipedia-derived section is provided under CC BY-SA 4.0; the independent MedAtlas notes and design are separate works.

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Acute kidney injury · visual study map

Scalable vector illustration. Labeled conceptual map, not a precise anatomical, histological or diagnostic image.
TOPIC LEARNING MAP · NOT AN ANATOMICAL PLATE01 · BackgroundAcute kidney injury (AKI), previouslycalled acute renal failure, is a suddendecrease in kidney function…02 · Main conceptCauses of AKI are classified as eitherprerenal (due to decreased blood flow tothe kidney), intrinsic renal…03 · Related processPrerenal causes of AKI include sepsis,dehydration, excessive blood loss,cardiogenic shock, heart failure,…04 · Study connectionIntrinsic renal causes of AKI includeglomerulonephritis, lupus nephritis,acute tubular necrosis, certain…Acute kidney injuryRead the full text below the visual · all reading is on this website

The wording in this learning map is adapted from the attributed Wikipedia background section below (CC BY-SA 4.0).

Study foundation 01

What the underlying subject studies

Internal medicine integrates the patient history, examination and selected investigations to explain symptoms across interacting organ systems. A diagnosis is a testable clinical hypothesis, not a result inferred from one symptom or diagram.

Study foundation 02

How mechanisms and evidence connect

Build a mechanistic differential by distinguishing structural, infectious, inflammatory, metabolic, genetic, vascular and medication-related processes as relevant. Consider time course, comorbidities and warning findings.

Study foundation 03

How to develop a sound explanation

For revision, connect normal physiology to possible dysfunction, characteristic patterns and the tests that may discriminate between alternatives. Actual diagnosis and therapy must follow current supervised clinical practice.

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