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Acute Kidney Injury (AKI)

Definition:
An abrupt loss of kidney function characterized by (1):
- Increase in serum creatinine (SCr) of β‰₯0.3 mg/dL within 48 hours
- β‰₯50% increase in baseline SCr within 7 days
- Urine output of <0.5 mL/kg/hr for 6 hours

Staging (based on SCr or urine output):

Stage Increase in Baseline Creatinine Increase in Creatinine Urine Output
1 1.5 times β‰₯0.3 mg/dL <0.5 mL/kg/hr for 6-12 hours
2 2.0-2.9 times N/A <0.5 mL/kg/hr for β‰₯12 hours
3 3.0 times β‰₯4.0 mg/dL <0.3 mL/kg/hr for β‰₯24 hours

Results in retention of nitrogenous waste, electrolyte, acid-base, and volume abnormalities.

Epidemiology

  • Incidence:
  • 5% of hospital admissions and 30% of ICU admissions have AKI.
  • 25% develop AKI while hospitalized; 50% of these cases are iatrogenic.
  • AKI during hospitalization is associated with >4-fold increased risk of death (2).

Etiology and Pathophysiology

Categories:

  • Prerenal (reduced renal perfusion, typically reversible):
    Causes: hypovolemia (GI losses, diuretics, hemorrhage), hypotension, renal artery stenosis, burns, heart/liver failure. Prolonged/severe can lead to ischemic acute tubular necrosis (ATN).

  • Intrarenal (intrinsic kidney injury):
    Causes: ATN (due to ischemia or nephrotoxins such as aminoglycosides, NSAIDs, contrast), glomerulonephritis (GN), acute interstitial nephritis (AIN), vasculitis, cholesterol embolization, uric acid nephropathy, multiple myeloma.

  • Postrenal (obstruction of urinary collecting system):
    Causes: extrinsic compression (BPH, carcinoma, pregnancy), intrinsic obstruction (calculus, tumor, clot, strictures), neurogenic bladder.

Genetics

  • No known genetic pattern.

Risk Factors

  • Chronic kidney disease (CKD), diabetes, hypertension, heart failure, liver failure
  • Advanced age, female gender, African American ethnicity
  • Nephrotoxic medications: NSAIDs, ACE inhibitors, ARBs, cyclosporine, tacrolimus, aminoglycosides, platinum chemo
  • Radiocontrast exposure (intravascular)
  • Hypovolemia (diuretics, hemorrhage, GI losses)
  • Sepsis, surgery, rhabdomyolysis, burns
  • Solitary kidney, BPH, malignancy (e.g., multiple myeloma)

General Prevention

  • Maintain adequate renal perfusion with isotonic fluids, vasopressors if needed
  • Avoid nephrotoxic agents

Commonly Associated Conditions

  • Hyperkalemia, hyperphosphatemia, hypercalcemia, hyperuricemia
  • Hydronephrosis, BPH, nephrolithiasis, CHF, uremic pericarditis, cirrhosis, malignant hypertension, vasculitis, sepsis, burns, rhabdomyolysis, internal bleeding, dehydration

Diagnosis

Clinical Presentation

  • Often asymptomatic until severe loss of function
  • Oliguria can be present but is neither specific nor sensitive

History

  • Medication review; changes in oral intake, urine output, body weight
  • Prerenal: thirst, orthostasis, vomiting, diarrhea, bleeding
  • Intrarenal: nephrotoxic meds, contrast, toxins
  • Postrenal: colicky flank pain radiating to groin (ureteric obstruction), nocturia, frequency, hesitancy (prostatic disease), suprapubic/flank pain (bladder distension)
  • Uremic symptoms: lethargy, altered mental status, nausea, vomiting, metallic taste

Physical Exam

  • Uremic signs: altered mental status, seizures, myoclonus, pericardial friction rub, neuropathies
  • Prerenal signs: tachycardia, low JVP, orthostatic hypotension, dry mucous membranes, decreased skin turgor
  • Intrinsic renal signs: pruritic rash, livedo reticularis, subcutaneous nodules, ischemic digits despite good pulses
  • Postrenal signs: suprapubic distension, flank pain, enlarged prostate

Diagnostic Tests & Interpretation

Initial Tests

  • Compare to baseline renal function (creatinine and GFR)【1】【2】
  • Urinalysis: dipstick for blood and protein; microscopy for cells, casts, crystals
  • Sterile pyuria with WBC casts β†’ suggest AIN
  • Proteinuria, hematuria, nephritic sediment (RBCs and RBC casts) β†’ GN or vasculitis
  • Casts:
    • Transparent hyaline β†’ prerenal
    • Pigmented granular/muddy brown β†’ ATN
    • WBC casts β†’ AIN
    • RBC casts β†’ GN
  • Urine eosinophils β‰₯1% β†’ suggest AIN (low sensitivity)
  • Urine electrolytes in oliguric state:
  • FENa <1% β†’ prerenal etiology
  • FENa >2% β†’ intrinsic cause
  • On diuretics: use FEurea instead
    • FEurea <35% β†’ prerenal
    • FEurea >50% β†’ intrinsic disease
  • CBC, BUN, serum creatinine, electrolytes (Ca/Mg/P), ABG/VBG
  • Labs often show ↑ potassium, phosphate, magnesium, uric acid; ↓ hemoglobin, calcium
  • Calculate creatinine clearance (CrCl) for dosing

Imaging

  • Renal ultrasound: first-line to exclude postrenal causes, assess kidney size, stones
  • Doppler renal US: assess renal artery stenosis/thrombosis
  • Abdominal x-ray (KUB): calcifications, stones, kidney size
  • Novel biomarkers (research): urinary IL-18, NGAL, KIM-1, plasma cystatin C, TIMP-2, IGFBP7【3】

Follow-Up Tests & Special Considerations

  • CK for rhabdomyolysis; immunologic testing if GN/vasculitis suspected
  • Advanced imaging:
  • US effective as CT for obstruction
  • Noncontrast CT for nephrolithiasis
  • Radionuclide renal scan for perfusion, GFR, obstruction
  • MRI: increased T2 signal in acute interstitial nephritis
  • Avoid gadolinium contrast in at-risk patients; hydrate before/after if necessary

Diagnostic Procedures

  • Cystoscopy + retrograde pyelogram for bladder tumors, hydronephrosis, obstruction
  • Kidney biopsy: last resort; evaluate intrinsic AKI causes (AIN, GN, vasculitis, rejection)

Treatment

General Measures

  • Identify/correct prerenal and postrenal causes
  • Stop nephrotoxic drugs; renally dose others
  • Strict monitoring of intake/output and weight
  • Optimize cardiac output to maintain renal perfusion
  • Nutrition optimization and infection treatment
  • Remove obstruction (Foley, suprapubic catheter, nephrostomy)

Indications for Renal Replacement Therapy (RRT)

  • Volume overload, severe hyperkalemia, metabolic acidosis refractory to treatment
  • Advanced uremic complications (pericarditis, encephalopathy, bleeding)
  • Pulmonary edema

Medications

  • First Line:
  • Treat underlying cause; correct electrolytes (especially hyperkalemia)
  • Judicious fluid challenge in oliguric, non-overloaded patients
  • Furosemide: not preventive but used for volume overload/hyperkalemia; stress test predictive
  • Fenoldopam: equivocal evidence, not recommended (1)[C]
  • Hyperkalemia management: IV calcium gluconate, sodium bicarbonate (if acidemic), insulin + glucose, nebulized albuterol, Kayexalate/furosemide, dialysis if refractory

  • Fluid restriction in oliguric patients to avoid hyponatremia

  • Second Line:

  • Tamsulosin/selective Ξ±-blockers for BPH-related obstruction
  • Dihydropyridine calcium channel blockers may protect posttransplant ATN

Prevention Strategies

  • Isotonic IV fluids, once-daily aminoglycoside dosing, lipid amphotericin B, iso-osmolar contrast media
  • Contrast-induced AKI risk lowered by hydration protocols:
  • Inpatients: isotonic saline 1 mL/kg/hr 6-12 hr before, during, after procedure
  • Outpatients: isotonic saline 3 mL/kg/hr 1 hr preprocedure, then 1–1.5 mL/kg/hr 4-6 hr during/after

Referral Indications

  • Nephrology: possible RRT, persistent oliguria/anuria, refractory BUN/Cr elevation, structural renal disease, transplant patients
  • Urology: obstructive nephropathy

Surgery/Procedures

  • Relieve obstruction: retrograde ureteral catheters, percutaneous nephrostomy
  • Hemodialysis catheter placement

Complementary & Alternative Medicine

  • Many herbal/dietary supplements potentially nephrotoxic (aristolochic acid, ochratoxin A, cat's claw, Chinese yew, St. John's wort, etc.)

Admission and Nursing Considerations

  • Treat life-threatening complications: hyperkalemia, acidosis, volume overload, advanced uremia
  • Monitor strict intake/output, daily weights
  • Urinary catheter for accurate urine output measurement; remove ASAP to reduce CAUTI risk
  • Stabilize renal function before discharge; dialysis if needed

Ongoing Care and Follow-Up

  • Nephrology follow-up if persistent renal impairment or proteinuria

Diet

  • Total caloric intake: 20-30 kcal/kg/day (1)
  • Sodium restriction: 2 g/day (unless hypovolemic)
  • Potassium restriction: 2-3 g/day if hyperkalemic
  • Phosphate binders may be considered if hyperphosphatemic (no proven benefit in AKI)
  • Avoid magnesium- and aluminum-containing compounds

Patient Education

  • Maintain adequate hydration
  • Avoid nephrotoxic drugs such as NSAIDs and aminoglycosides

Prognosis

  • Prerenal and postrenal AKI with short duration β†’ good recovery rates
  • Recovery after RRT more likely with higher baseline GFR, sepsis/surgery-related ATN
  • Poorer recovery with preexisting heart failure

Complications

  • Death, sepsis, infection, CKD
  • Seizures, paralysis, peripheral edema, CHF, arrhythmias
  • Uremic pericarditis, bleeding, hypotension, anemia, hyperkalemia, uremia

Clinical Pearls

  • AKI classification: prerenal (decreased perfusion), intrarenal (intrinsic damage, mostly ATN), postrenal (obstruction)
  • Emergent hemodialysis indications: severe hyperkalemia, refractory metabolic acidosis, volume overload, uremic complications
  • ATN management is supportive; no proven therapies to accelerate recovery
  • Fluid management key in prerenal and intrinsic AKI

References

  1. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int. 2012;(Suppl 2):1-138.
  2. Gonsalez SR, et al. Acute kidney injury overview: from basic findings to new prevention and therapy strategies. Pharmacol Ther. 2019;200:1-12.
  3. Gameriero J, et al. Acute kidney injury: from diagnosis to prevention and treatment strategies. J Clin Med. 2020;9(6):1704.

See Also

  • Chronic Kidney Disease
  • Acute Glomerulonephritis
  • Hepatorenal Syndrome
  • Hyperkalemia
  • Benign Prostatic Hyperplasia (BPH)
  • Renal Insufficiency
  • Reye Syndrome
  • Rhabdomyolysis
  • Sepsis

ICD10 Codes

  • N17.0 Acute kidney failure with tubular necrosis
  • N17.1 Acute kidney failure with acute cortical necrosis
  • N17.8 Other acute kidney failure