Acute Kidney Injury (AKI)

Continuing Education Activity

• AKI Definition: Previously known as acute renal failure, AKI is a sudden and often reversible reduction in kidney function, indicated by increased creatinine or decreased urine volume.
• Etiologies: Prerenal, intrarenal, and postrenal, which can overlap.
• Treatment Importance: Identifying causes is crucial for effective treatment and improved patient outcomes.

Objectives

• Identify risk factors and clinical indicators for early AKI recognition and intervention.
• Differentiate AKI causes to guide treatment strategies.
• Implement evidence-based guidelines for AKI prevention and management.
• Effectively communicate with patients about AKI and treatment plans.

Introduction

• AKI Prevalence: Common in hospitalized patients, up to 7% in admissions and 30% in ICU admissions.
• Identification Criteria: RIFLE, AKIN, and KDIGO, with KDIGO being the most recent and used.
  • Increase in serum creatinine by ≥0.3mg/dL within 48 hours.
  • Increase in serum creatinine to 1.5 times the baseline within 7 days.
  • Urine volume <0.5mL/kg/h for 6 hours.

Etiology

• Pressure Gradient: Influenced by renal blood flow, which affects glomerular filtration rate (GFR).
• Prerenal AKI Causes: Reduced blood flow due to hypovolemia, systemic hypoperfusion, renal vasoconstriction, etc.
• Intrinsic Renal Causes: Conditions affecting glomerulus or tubule, e.g., acute tubular necrosis, glomerulonephritis.
• Postrenal Causes: Obstructions causing urinary backflow, e.g., bladder outlet obstruction, renal calculi.

Epidemiology

• Hospital Prevalence: Seen in 1% of hospital admissions and 2-5% during hospitalization. Up to 67% in ICU.

Pathophysiology

• Cellular Insult: Etiology-driven, often due to ischemia or toxins causing cell death and tubular dysfunction.

Histopathology

• Renal Biopsy: Used when significant management impact is expected. Differentiates intrinsic renal patterns.

History and Physical

• Evaluating Etiology: History and physical exams focus on hypovolemia, hypotension, or drug use causes.
• Common Hospital Causes: ATN (45%), prerenal disease (21%), CKD (13%), urinary obstruction (10%).

Evaluation

• Thorough Search: For prerenal, intrarenal, and postrenal disease causes. Includes comprehensive metabolic panels, urine studies, and imaging.
• Biomarkers: Newer ones like NGAL and KIM-1 are more sensitive than creatinine but not widely used.

Treatment / Management

• Fluid Challenge: To determine prerenal cause; fluid improvement indicates prerenal AKI.
• Managing Complications: Hyperkalemia and volume overload need management with dietary changes, diuretics, or dialysis.

Differential Diagnosis

• Consider Other Conditions: Renal calculi, chronic kidney disease, hypovolemia, cardiac issues, etc.

Prognosis

• Recovery: Often complete if underlying issues are corrected early. Persistent AKI can result in long-term damage.
• Mortality Rates: In-hospital mortality is 40-50%, higher in ICU patients.

Complications

• Metabolic Issues: Hyperkalemia, acidosis, and volume overload are common.
• Organ-related Complications: Cardiovascular, gastrointestinal, and neurological issues.

Deterrence and Patient Education

• Preserving Renal Function: Avoid nephrotoxic agents, ensure hydration, and proper medication management.

Enhancing Healthcare Team Outcomes

• Interprofessional Approach: Education on AKI, monitoring for nephrotoxic medications, patient education to reduce AKI morbidity.