Submodule
Detection and Staging
AKI is a time-dependent change in filtration and urine production. Creatinine and urine output are useful but delayed, contextual, and mechanistically incomplete markers.
- Creatinine criteria
- Urine-output criteria
- KDIGO stage
- Creatinine kinetics
- PseudoAKI
Do not accept the admission value blindly
Dilution and production matter
Obstruction and diuretics change meaning
Trend severity and duration
Diagnose change, not a number
Published KDIGO criteria define AKI by a creatinine increase of at least 0.3 mg/dL within 48 hours, at least 1.5 times baseline within seven days, or urine output below 0.5 mL/kg/h for at least six hours. Reconstruct baseline from prior records rather than assuming the admission value represents normal kidney function.
Stage by the worse expression
Creatinine and urine output can disagree. Use the more severe criterion and update stage as the trajectory changes. Verify collection, catheter patency, weight, diuretics, extracorporeal clearance, and duration before attaching meaning to oliguria or anuria.
Respect creatinine kinetics
Creatinine rises after filtration falls and is changed by muscle production, nutrition, fluid dilution, tubular secretion, assay effects, and dialysis. Standard eGFR and creatinine-clearance equations assume steady state and can misrepresent real-time clearance during injury or recovery.
Separate pseudoAKI from injury
Trimethoprim, cobicistat, cimetidine, and selected targeted therapies can inhibit tubular creatinine secretion without reducing true filtration. Use the medication timeline, urine findings, volume, electrolytes, alternative filtration markers when useful, and structural-injury clues before labeling nephrotoxicity.
Quick check
Submodule
Etiology and Diagnostic Reasoning
Perfusion, intrinsic kidney injury, and obstruction are starting categories. Real patients often have several simultaneous mechanisms that must be revised as evidence accumulates.
- Hemodynamic AKI
- Acute tubular injury
- Interstitial nephritis
- Glomerular disease
- Obstruction
Test fluid responsiveness, not edema alone
Use urine and systemic clues
Relieve early
Update the model daily
Define the hemodynamic defect
Reduced kidney perfusion can arise from volume loss, vasodilation, low cardiac output, venous congestion, intra-abdominal pressure, or altered arteriolar tone. Edema does not prove adequate effective arterial volume, and hypotension does not prove that more fluid is the correct treatment.
Recognize tubular injury
Ischemia, sepsis, pigments, and nephrotoxins can injure tubular cells. Exposure and shock timing, persistent dysfunction, granular casts, transport abnormalities, and delayed recovery support acute tubular injury, but no single sediment finding replaces the whole trajectory.
Use active sediment to redirect the workup
Pyuria and white-cell casts with a compatible drug exposure can support interstitial nephritis, although fever, rash, and eosinophilia are insensitive. Dysmorphic red cells, red-cell casts, proteinuria, hypertension, pulmonary findings, or systemic inflammation raise concern for glomerular disease and may require urgent serology and biopsy.
Relieve obstruction before it becomes irreversible
Check catheter patency and bladder retention, then image the urinary tract when obstruction is plausible. Hydronephrosis may be absent early or in selected retroperitoneal conditions. Bilateral obstruction or obstruction of a solitary functioning kidney can require urgent decompression.
Quick check
Submodule
Hemodynamics and Fluid Management
Resuscitation is an experiment with a goal and stop rule. Perfusion improves when treatment matches volume, tone, cardiac output, venous pressure, and oxygen delivery.
- Fluid responsiveness
- Balanced crystalloids
- Vasopressors
- Venous congestion
- Fluid overload
Static edema is not intravascular volume
Give a goal and stop rule
Treat the circulation, not creatinine alone
De-resuscitate when excess harms
Test whether fluid will improve flow
Fluid responsiveness is a dynamic increase in flow after a reversible preload challenge. It does not prove that another bolus is safe or necessary. Use passive leg raise or a small challenge with a measured cardiac or perfusion endpoint, while watching oxygenation and venous congestion.
Choose fluid composition intentionally
Balanced crystalloids reduce chloride exposure compared with saline in many resuscitation settings. Selection still depends on sodium and chloride, acid-base status, traumatic brain injury, medication compatibility, losses, and the resuscitation goal. No crystalloid is universally correct.
Treat vasoplegia with pressure support
After appropriate volume assessment, norepinephrine is generally first line for vasodilatory shock. Restore perfusion pressure while treating infection or another cause. More fluid can worsen edema when vascular tone, not volume, is the dominant problem.
Recognize congestion as a kidney insult
Elevated venous and intra-abdominal pressures can reduce the filtration gradient and cause kidney edema. Stop unnecessary fluid, concentrate inputs, and decongest when the phenotype supports it. Loop diuretics treat overload, not the structural kidney injury itself.
Quick check
Submodule
Medication and Exposure Stewardship
Medication review distinguishes perfusion effects, structural injury, immune reactions, crystal disease, secretion changes, and accumulation, then protects both acute safety and long-term benefit.
- Nephrotoxin timeline
- Unstable-function dosing
- Loading and maintenance doses
- Contrast-associated AKI
- Medication restart
Include OTC and contrast
Mechanism changes action
eGFR is unstable in AKI
Avoid permanent therapeutic omission
Classify the drug effect before acting
NSAIDs, RAAS drugs, antimicrobials, chemotherapy, supplements, contrast, crystals, immune reactions, and secretion inhibitors affect the kidney differently. Build a complete timeline including OTC products. Stop, substitute, monitor, or continue according to mechanism and treatment necessity rather than using a blanket nephrotoxin label.
Dose for a changing clearance
Steady-state equations can mislead during AKI. Use creatinine and urine trajectory, indication severity, volume of distribution, protein binding, nonrenal clearance, therapeutic index, levels, clinical response, and KRT prescription. A loading dose is driven mainly by distribution, while maintenance is driven mainly by clearance.
Use contrast when net benefit supports it
Creatinine rise after contrast is temporally associated but may have competing causes. Weigh the urgency and value of imaging, active AKI, hemodynamics, route and dose, alternatives, hydration when appropriate, and concurrent insults. Do not withhold a life-saving vascular study because causal risk was overstated.
Plan the restart before discharge
Temporary holds of RAAS or SGLT2 therapy may be appropriate during severe hemodynamic illness. Chronic cardiac and kidney benefit may return after stabilization. Document the reason for holding, pressure, potassium, volume, laboratory criteria, follow-up date, and responsible clinician.
Quick check
Submodule
Complications and Kidney Support
Electrolyte, acid-base, volume, uremic, and toxin complications determine urgency. Kidney replacement therapy treats failed homeostasis, not an isolated creatinine value.
- Hyperkalemia
- Acidosis
- Volume overload
- Uremia and toxins
- KRT timing and modality
ECG and kinetics matter
Bicarbonate is context specific
Diuretics treat overload, not injury
Escalate for complications
Treat hyperkalemia in separate tasks
IV calcium stabilizes the myocardium when indicated, insulin with glucose and selected adjuncts shift potassium, and kidney excretion, binders, or dialysis remove it. Confirm the sample, obtain an ECG, review drugs and tissue breakdown, monitor glucose, and expect rebound after temporary shifting.
Treat the cause of acidosis
Interpret pH, respiratory compensation, anion gap, lactate, ketones, toxins, chloride, potassium, and hemodynamics. Bicarbonate is selective, not automatic, because sodium, volume, ionized calcium, and carbon dioxide can change. Refractory life-threatening acidemia can require KRT.
Start KRT for failed homeostasis
Initiate KRT for refractory electrolyte disturbance, acidemia, pulmonary or systemic volume overload, uremic complications, or a dialyzable toxin, considering trajectory and goals. Creatinine alone is not a start threshold.
Match modality and delivered dose
Intermittent, continuous, and prolonged therapies differ in solute rate, fluid precision, hemodynamic tolerance, brain effects, anticoagulation, staffing, and access. Choose the strategy that can achieve the patient's clearance and fluid goals, then verify delivered rather than prescribed treatment.
Quick check
Submodule
Recovery, Acute Kidney Disease, and Follow-Up
Recovery is an active phase in which native clearance, drug exposure, dialysis need, chronic disease therapy, and long-term kidney and cardiovascular risk change quickly.
- Kidney recovery
- KRT liberation
- Drug redosing
- AKD
- Post-AKI follow-up
No creatinine threshold alone
Match hemodynamics and goals
Recalculate every drug
Assign laboratory and clinical ownership
Recognize recovery before creatinine catches up
Increasing urine output and native clearance can precede a clear fall in serum creatinine. Reassess antibiotic and anticoagulant doses, electrolytes, fluid, nutrition, and dialysis needs frequently so recovery does not create underexposure or over-removal.
Test readiness to stop KRT
Consider urine output, interdialytic creatinine and electrolyte trajectory, measured clearance when useful, volume control, catabolism, hemodynamics, and the remaining cause. Remove temporary vascular access when dialysis is no longer expected.
Use AKD as a bridge, not a final label
Dysfunction persisting beyond seven days and through the interval before 90 days can be described as acute kidney disease. The 2026 KDIGO update remains a public-review draft, so evolving biomarker and staging concepts should be labeled as draft until final publication.
Close the post-AKI loop
Arrange early creatinine, electrolytes, pressure, volume, and medication review, then reassess kidney function and albuminuria by three months. Review nephrotoxin avoidance, sick-day risks, diabetes and heart-failure therapy, recurrence prevention, access, and whether nephrology follow-up is needed.
Quick check
Module test
Check the connections.
Each attempt draws 10 questions from the complete 100 question bank.
Each attempt draws a fresh set and rearranges the answer choices.
References
Current clinical foundation.
Lecture material was synthesized with the following contemporary guidance. Verify local policy and current guidance before applying clinical information.