Acute Kidney Injury¶
Chapter 321 | Part 9: Disorders of the Kidney and Urinary Tract
KEY CLINICAL POINTS¶
- AKI is defined by an increase in serum creatinine ≥ 0.3 mg/dL within 48 h or ≥ 1.5× baseline, or urine output <0.5 mL/kg/h for >6 h.
- Etiology is classified into prerenal (volume depletion, drugs), intrinsic (ischemia, toxins), and postrenal (obstruction) causes.
- KDIGO staging uses SCr and urine output to classify severity (Stage 1-3).
- Management includes fluid resuscitation, discontinuation of nephrotoxins, and dialysis for severe cases.
- Prognosis is poor in patients with preexisting CKD or severe complications like hyperkalemia.
1. DEFINITION & OVERVIEW¶
Acute kidney injury (AKI) is characterized by rapid decline in kidney function, leading to impaired excretion of nitrogenous waste and electrolyte imbalance. It is a clinical diagnosis, not structural, and can occur with or without parenchymal injury. KDIGO criteria define AKI as an increase in serum creatinine ≥ 0.3 mg/dL within 48 h or ≥ 1.5× baseline, or urine output <0.5 mL/kg/h for >6 h.
Table 321-1: Staging of Acute Kidney Injury Severity¶
| STAGE | SERUM CREATININE | URINE OUTPUT |
|---|---|---|
| 1 | 1.5–1.9× baseline OR ‡0.3 mg/dL increase | <0.5 mL/kg/h for 6–12 h |
| 2 | 2.0–2.9× baseline | <0.5 mL/kg/h for ‡12 h |
| 3 | 3.0× baseline OR ‡4.0 mg/dL OR initiation of RRT | <0.3 mL/kg/h for ‡24 h OR anuria ‡12 h |
1.1 Pathophysiology¶
AKI results from prerenal azotemia, intrinsic renal injury, or postrenal obstruction. Sodium balance, renin-angiotensin-aldosterone system (RAAS), and autoregulation of renal blood flow are critical in maintaining GFR. Disruption of these mechanisms leads to tubular injury, reduced filtration, and accumulation of waste products.
1.2 Clinical Spectrum¶
AKI ranges from asymptomatic to life-threatening. Early stages may present with subtle changes in urine output or electrolyte abnormalities. Severe cases can lead to uremic syndrome, cardiac arrhythmias, and multiorgan failure.
2. EPIDEMIOLOGY¶
AKI complicates 5–7% of hospital admissions and up to 30% of ICU admissions. Incidence in the US increased 4× since 1988, with ~500 per 100,000 annual cases. Morbidity is high, with >50% of ICU patients developing AKI. Long-term risks include CKD progression and cardiovascular disease.
2.1 Global Variations¶
In developing countries, AKI is more prevalent due to limited resources, infectious causes (malaria, leptospirosis), and trauma-related rhabdomyolysis. Mortality is higher in these settings due to delayed diagnosis and treatment.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
AKI is classified into prerenal (volume depletion, drugs), intrinsic (ischemia, toxins), and postrenal (obstruction) causes. Pathophysiology involves disruption of renal autoregulation, sodium balance, and tubular function. Nephrotoxins like aminoglycosides, cisplatin, and contrast agents cause direct tubular injury.
Table 321-2: Major Causes, Clinical Features, and Diagnostic Studies for Prerenal and Intrinsic AKI¶
| ETIOLOGY | CLINICAL FEATURES | LABORATORY FEATURES | COMMENTS |
|---|---|---|---|
| Prerenal azotemia | Volume depletion, NSAIDs, heart failure | BUN/creatinine >20, FeNa <1% | Response to fluid resuscitation is diagnostic |
| Sepsis-associated AKI | Sepsis, hypotension | Positive cultures, granular casts | Common in ICU, poor prognosis |
| Ischemia-associated AKI | Systemic hypotension, CKD | Granular casts, FeNa >1% | Often post-surgery or sepsis |
| Nephrotoxin-associated AKI | Toxins (drugs, contrast) | Granular casts, FeNa >1% | Delayed rise in SCr, nonoliguric |
3.1 Prerenal Azotemia¶
Caused by reduced renal perfusion (hypovolemia, heart failure, NSAIDs). Sodium reabsorption increases, leading to elevated SCr without tubular damage. Response to fluid resuscitation is diagnostic.
3.2 Intrinsic AKI¶
Includes ischemia (sepsis, surgery), toxins (drugs, contrast), and glomerular diseases (vasculitis, glomerulonephritis). Tubular necrosis, inflammation, and oxidative stress are key mechanisms.
3.3 Postrenal Obstruction¶
Caused by urinary tract obstruction (stones, tumors, catheter blockage). Leads to hydronephrosis and rapid rise in SCr. Prompt relief of obstruction is critical to prevent renal damage.
4. CLINICAL FEATURES¶
AKI presents with oliguria, anuria, or changes in urine output. Other signs include edema, hypertension, and electrolyte abnormalities. Symptoms may be subtle in early stages but progress to uremic syndrome with severe complications.
4.1 Urinary Findings¶
Urine may show red blood cells (hematuria), white blood cells (pyuria), casts (granular, RTE), or crystals (oxalate, uric acid). Pigmented casts suggest rhabdomyolysis or hemolysis.
4.2 Systemic Manifestations¶
Hyperkalemia, metabolic acidosis, and uremic toxins cause fatigue, confusion, and cardiac arrhythmias. Severe cases may present with pericarditis, pulmonary edema, or encephalopathy.
5. DIFFERENTIAL DIAGNOSIS¶
Differential diagnoses include prerenal azotemia, chronic kidney disease (CKD), and postrenal obstruction. Conditions like sepsis, heart failure, and drug toxicity must be considered. Urine sediment and imaging help distinguish etiologies.
5.1 Prerenal vs. Intrinsic AKI¶
Prerenal azotemia shows low FeNa (<1%), while intrinsic AKI has FeNa >1%. Urine output and response to fluids differentiate prerenal from intrinsic causes.
6. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis relies on SCr, urine output, and urine analysis. Imaging (ultrasound, CT) identifies postrenal obstruction. Biomarkers like NGAL and KIM-1 improve early detection. KDIGO criteria guide staging and management.
6.1 Laboratory Tests¶
Serum creatinine, BUN, electrolytes, and urine electrolytes (Na, K, urea) are critical. Urine sediment analysis reveals casts, RBCs, or crystals. FeNa helps differentiate prerenal vs. intrinsic AKI.
6.2 Imaging¶
Renal ultrasound or CT identifies obstruction. Doppler ultrasound assesses renal perfusion. Contrast-enhanced CT may detect parenchymal disease or stones.
7. MANAGEMENT & TREATMENT¶
Management includes fluid resuscitation, discontinuation of nephrotoxins, and dialysis for severe cases. Supportive care addresses electrolyte imbalances and complications. Renal replacement therapy (RRT) is indicated for hyperkalemia, uremia, or volume overload.
Table 321-3: Management of Acute Kidney Injury¶
| GENERAL ISSUES | SPECIFIC ISSUES |
|---|---|
| Optimize hemodynamics, discontinue nephrotoxins | Nephrotoxin-specific (e.g., fluids for rhabdomyolysis) |
| Maintain MAP >65 mmHg | Volume overload (salt/water restriction, diuretics) |
| Ensure adequate nutrition (20–30 kcal/kg/day) | Hyponatremia (restrict free water, hypertonic saline) |
| Initiate RRT when indicated | Hyperkalemia (loop diuretics, potassium binders) |
7.1 Fluid and Electrolyte Management¶
Fluid resuscitation with isotonic saline or lactated Ringer’s. Diuretics (furosemide) for oliguria. Monitor for hyperkalemia, acidosis, and volume overload.
7.2 Dialysis Indications¶
Indicated for severe hyperkalemia, uremic symptoms, fluid overload, or when medical management fails. Continuous renal replacement therapy (CRRT) is preferred in hemodynamically unstable patients.
8. PROGNOSIS & COMPLICATIONS¶
AKI is associated with high mortality, especially in patients with preexisting CKD or sepsis. Complications include CKD progression, cardiovascular disease, and uremic syndrome. Long-term outcomes depend on severity and underlying causes.
8.1 Long-Term Risks¶
AKI increases risk of CKD, cardiovascular events, and mortality. Survivors may develop chronic kidney disease or require long-term dialysis.
8.2 Uremic Complications¶
Uremic toxins cause neurological symptoms (confusion, seizures), cardiovascular instability, and bleeding. Dialysis is critical to remove toxins and correct electrolyte imbalances.
9. SPECIAL CONSIDERATIONS¶
Pregnancy (preeclampsia), elderly (decreased renal reserve), and pediatric patients (drug toxicity) require tailored management. AKI in CKD patients is more severe and less responsive to treatment.
9.1 Pregnancy¶
Preeclampsia is a leading cause of AKI in pregnancy. Monitoring for hypertension, proteinuria, and fetal well-being is critical. Dialysis may be required for severe cases.
9.2 Pediatrics¶
Children are at higher risk for AKI due to drug toxicity (contrast, aminoglycosides) and infections. Early recognition and fluid resuscitation are vital.
10. KEY POINTS & CLINICAL PEARLS¶
AKI is a clinical diagnosis with KDIGO criteria. Prerenal azotemia responds to fluids, while intrinsic AKI requires addressing underlying causes. Dialysis is indicated for severe complications. Early recognition and management improve outcomes. Biomarkers like NGAL and KIM-1 aid in early detection.