ICU Map

Acute Kidney Injury

From confirming AKI to classifying it by mechanism.

RecognizeAssessDecideDifferentialInterveneReassess
Rising Creatinine / Falling Urine Output
Assessment StepConfirm AKI
A rise in serum creatinine or a fall in urine output meeting KDIGO criteria, compared against the patient's known baseline.
Assessment StepReview medications and imaging exposure
Nephrotoxins, recent IV contrast, NSAIDs, ACE inhibitors/ARBs, and any recent episode of hypotension.
Assessment StepAssess volume status and bladder
A bedside bladder scan or Foley catheter excludes obstruction quickly; also assess for hypovolemia versus volume overload.
Decision PointClassify by mechanism
Prerenal, intrinsic, and postrenal causes are distinguished by perfusion status, urinalysis/sediment, and imaging.
Differential Branches (3)
1Branch
Physiologic MechanismPrerenalExplore Topic
Renal hypoperfusion from hypovolemia, hypotension, or heart failure — typically reversible with restoration of perfusion.
2Branch
Physiologic MechanismIntrinsic (e.g. acute tubular necrosis)Explore Topic
Direct injury to the tubules, glomeruli, or interstitium — from prolonged hypoperfusion, nephrotoxins, or an inflammatory process.
3Branch
Physiologic MechanismPostrenal
Urinary tract obstruction — confirm with a bladder scan and renal ultrasound.

An educational representation of clinical reasoning, not a diagnostic algorithm or personalized medical advice — always apply clinical judgment and institutional protocols.

Caution

Escalate — Red Flags & Critical Warnings

  • Hyperkalemia with ECG changes, refractory pulmonary edema, or severe uncorrectable acidosis in the setting of AKI — these are indications for urgent renal replacement therapy regardless of the creatinine trend.
  • Anuria with flank pain, or a solitary/transplanted kidney — obtain an urgent renal ultrasound to exclude obstruction.

Related Bedside Clinical Problems (23)

Bedside Presentations
Acute Hypercapnia & Ventilatory Failure

Triaging rising PaCO2: distinguishing acute uncompensated acidemia from chronic compensation, identifying central vs pump vs dead-space failure, and titrating noninvasive ventilation.

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Acute Hypotension & Undifferentiated Shock

Rapid bedside hemodynamic categorization: confirming MAP < 65 mmHg, assessing peripheral perfusion, POCUS cardiac/IVC profiling, and differentiating hypovolemic, distributive, cardiogenic, and obstructive etiologies.

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Refractory Shock Despite High-Dose Vasopressors

Advanced multimodal hemodynamic rescue: second-line vasopressors (vasopressin, angiotensin II), inotropic augmentation, stress-dose steroids, metabolic correction, and mechanical circulatory support evaluation.

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Linked Deep-Dive Topics (5)

Reference Knowledge
Acute Kidney Injury in Critical Carerenal

Sepsis-AKI microcirculatory decoupling, KDIGO staging, Furosemide Stress Test (FST), urine microscopy, and the AEIOU dialysis threshold framework.

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Continuous Renal Replacement Therapy (CRRT)renal

Principles of convection vs diffusion, filtration fraction, delivered effluent dosing (20–25 mL/kg/h), Regional Citrate Anticoagulation, and citrate toxicity.

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Shock: Foundational Critical Care Frameworkcardiovascular

Cellular dysoxia, DO2/VO2 physiology, the 4 shock phenotypes, dynamic fluid responsiveness (PLR/PPV) vs fluid tolerance (VExUS), and vasoactive pharmacology.

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Acid-Base Disorders: Comprehensive Critical Care Approachrenal

Stepwise 6-step interpretation algorithm, compensation formulas, albumin-corrected anion gap, delta ratio, and Stewart physicochemical (SID) principles.

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Severe Hyperkalemia in Critical Illnessrenal

Nernst resting potential mechanics, ECG progression, the 3-step resuscitation framework (Stabilize, Shift, Eliminate), and post-dialysis rebound kinetics.

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