Acute Kidney Injury Overview

Acute Kidney Injury (AKI)

• AKI is a rapid and usually reversible decline in kidney function.
• It's evident by a rapid decline in glomerular filtration rate (GFR) over hours to days.
• AKI can occur in patients with previously normal kidneys or those with chronic kidney disease.

Definition of AKI

• AKI is a clinical syndrome defined by:
  • An abrupt increase in serum creatinine by ≥0.3 mg/dL within 48 hours.
  • A ≥1.5-fold increase in serum creatinine over the prior 7 days.
  • Urine output <0.5 mL/kg/h for 6 hours.
• Only one criterion needs to be met to diagnose AKI (per KDIGO).
• Even small increases in creatinine are associated with increased mortality.

Limitations of Serum Creatinine

• Serum creatinine levels are influenced by various factors:
  • Extracellular volume depletion
  • Decreased kidney blood flow
  • Age
  • Sex
  • Body mass
  • Nutritional status
• Serum creatinine is not specific for AKI and requires differentiation from other causes, such as pre-renal or extra-renal issues.
• Creatinine levels don't accurately reflect early kidney dysfunction; changes are not always sensitive or specific.

Definitions of Terminology

• Azotemia: Accumulation of nitrogenous wastes (high BUN).
• Uremia: Clinical manifestation of symptomatic renal failure.
• Oliguria: Urine output <400 mL/24 hours.
• Anuria: Urine output <100 mL/24 hours.

Incidence and Prevalence of AKI

• Dialysis-dependent AKI incidence: 7200 per million population annually.
• AKI accounts for 5-10% of general hospital admissions.
• AKI accounts for 20-25% of cases in patients with sepsis and ~50% with septic shock.
• Estimated global prevalence of AKI: 72,100 per million population (mostly community-acquired).

Kidney Function Requirements and Categorization

• Kidneys require normal renal blood flow (prerenal).
• Functioning glomeruli, tubules, and interstitium (intrinsic/renal).
• Clear urinary outflow tract (postrenal).
• Distinguishing AKI from chronic renal impairment is essential for patient management.

Staging of AKI

• Staging is based on creatinine (Cr) and urine output (UO) criteria.
• Grade 1 is an increase in Cr by ≥26.5 µmol/l within 48 hours OR 50-99% increase in Cr from baseline.
• UO for grade 1 <0.5 ml/kg/h for 6-12h
• Additional criteria for determining AKI grades:
  • Grade 2 : 100-199% rise in Cr OR >200% rise in Cr OR Cr rising ≥ 354
  • UO for grade 2 : <0.5 ml/kg/h for ≥12h
  • Grade 3: Initiation of RRT OR decrease in eGFR to <35 ml/min/1.73 m²
  • UO for grade 3 : < 0.3 ml/kg/h for ≥ 24h OR Anuria for ≥12h

Risk Factors for AKI

• eGFR <60 ml/min/1.73m2 or a prior history of AKI
• Diabetes
• Heart failure, liver disease
• Neurological or cognitive impairment
• Nephrotoxic drug use
• Iodinated contrast agents (within the past week)
• Symptoms or history of urological obstruction
• Sepsis
• Age 65 years or older

Types of AKI

• Prerenal: Reduced blood flow to the kidneys.
• Intrinsic: Damage to the kidney tissue itself.
  • Glomerular (e.g., GN)
  • Tubular (e.g., ATN)
  • Interstitial (e.g., AIN)
  • Vascular (e.g., vascular occlusions)
• Postrenal: Blockage of urine outflow from the kidneys.

Causes of AKI in Hospitals

• Acute tubular necrosis (most common)
• Acute interstitial nephritis
• Obstruction

Pathogenesis of Prerenal Failure

• Reduced cardiac output or hypovolemia.
• Regional vasoconstriction limits blood flow to non-vital organs.
• Further decrease in blood flow leads to acute kidney injury.

Pathophysiology of Ischemic Acute Renal Failure

• Microvascular and tubular events contribute to ischemic AKI.
• Ischemic events and inflammatory mediators cause renal cell damage leading to obstruction and backleak.

Phases of AKI

• 1. Initiation phase: Normal urine output until kidney damage occurs.
• 2. Oliguria or anuria phase: Reduced urine output (100-400 mL/day or less than 100mL/day).
• 3. Polyuria phase: Increased urine output after a period of oliguria or anuria. Serum creatinine and urea may not immediately improve.
• 4. Recovery phase: Urine output and serum creatinine normalize.

Renal/Intrinsic AKI

• Glomerular : PSGN, SLE, AGN, ANCA-associated, anti-GBM disease, HSP, Cryoglobulinemia, TTP, HUS. (5-15%)
• Tubular : ATN (Ischemia 50%, Toxins 30%) (70-80%)
• Interstitial : AIN (Drug, NSAIDs, Antibiotics, Infiltrative, Granulomatous, Infection) (8-20%)
• Vascular : Vascular occlusions (2%)

Postrenal AKI

• Intrinsic Obstruction : Intra-luminal (Stone, Blood clots, Papillary necrosis), Intra-mural (Urethral stricture, BPH, Ca prostate, bladder tumor, radiation fibrosis).
• Extrinsic Obstruction: Pelvic malignancies, prolapsed uterus, retroperitoneal fibrosis.

Diagnostic Evaluation

• Careful history taking and physical exam.
• Suspect prerenal azotemia in presence of vomiting, diarrhea, glycosuria, or use of diuretics, NSAIDs, ACE inhibitors
• Look for hypotension or tachycardia for signs of hypovolemia or dehydration.
• Evaluate for prostatic disease, nephrolithiasis, or paraaortic malignancy for suspected postrenal AKI.

Management Principals for AKI

• Treat infection aggressively.
• Minimize indwelling lines.
• Remove bladder catheters, if anuric.
• Manage bleeding tendency. (PPI, H2 antagonists, avoid aspirin)
• Transfuse blood if needed.

Optimise Nutritional Support for AKI

• Maintain adequate nutrition for patient survival.
• Maintain protein intake around 1 g/kg/day.
• High protein intake (>1.2 g/kg/day) can worsen azotemia.

RRT (Renal Replacement Therapy)

• Initiate dialysis before complications arise.
• Early RRT improves mortality and recovery rates.
• Specialized treatments are available for critically ill patients.

Additional factors and outcomes of AKI

• AKI is associated with various risk factors, including age, ethnicity, and genetic predisposition.
• AKI can lead to chronic kidney disease and adverse cardiovascular outcomes.
• Early intervention for AKI significantly improves patient outcomes.

This quiz focuses on Acute Kidney Injury (AKI), a rapid decline in kidney function that can be reversible. Learn about the criteria for diagnosing AKI, its limitations, and the factors influencing serum creatinine levels. Understand how AKI impacts patients and the significance of early detection.