Acute Kidney Injury Overview

Acute Kidney Injury (AKI) Overview

• AKI is defined as an abrupt loss of kidney function.
• Effects include waste product retention, electrolyte imbalances, and changes in fluid balance.
• Detection relies on biomarker changes, particularly serum creatinine (SCr), which often lags 48-72 hours behind the onset of injury.

Learning Outcomes

• Differentiate various types of AKI.
• Understand and apply different treatments for AKI.
• Demonstrate knowledge of renal replacement therapy (RRT).

AKI Classification Systems

• RIFLE: Risk, Injury, Failure, Loss, End-stage
• AKIN: Acute Kidney Injury Network
• KDIGO: Kidney Disease Improving Global Outcomes

RIFLE Classification

• Criteria are based on changes in serum creatinine and urine output.
• Stages include risk, injury, failure, loss, and end-stage.
• Purpose is to standardize the definition and severity of AKI.

AKIN Criteria

• SCr increase of 0.3 mg/dL or more within 48 hours.
• 50% or greater increase in SCr within 7 days.
• Less than 0.5 mL/kg/hour urine output for more than 6 hours.

KDIGO Guidelines

• SCr increase of 0.3 mg/dL or more within 48 hours.
• 50% or greater increase in SCr within 7 days.

Types of AKI

• Pre-renal: Hypoperfusion (e.g., shock, dehydration).
• Intrinsic (or Intrarenal): Damage to kidney tissues (e.g., acute tubular necrosis, glomerulonephritis).
• Post-renal: Obstruction to urine outflow (e.g., kidney stones, enlarged prostate).

Risk Factors for AKI

• Age (increased risk with advanced age).
• Comorbidities (e.g., hypertension, diabetes).
• Major surgery.
• Proteinuria.
• Dehydration.
• High blood pressure.
• Infections.

Medications Affecting Kidney Function

• Certain drugs may cause vasoconstriction (e.g., afferent arteriole) or vasodilation (efferent arteriole).
• Prostaglandin inhibition
• Use of nephrotoxic drugs.

Tubular Causes of Intrinsic AKI

• Acute tubular injury.
• Tubulointerstitial injury.
• Glomerulonephritis.

Glomerular Causes of Intrinsic AKI

• Autoimmune disorders.
• Oncology Drugs.
• Specific Medications

Tubular Causes of Intrinsic AKI (Part 1)

• Antimicrobials
• Nephrotoxic Drugs
• Acute Tubular Necrosis

Tubular Causes of Intrinsic AKI (Part 2)

• Aminoglycoside-associated ATN
• Amphotericin B
• Vancomycin Nephrotoxicity
• Contrast-induced Nephrotoxicity

Vascular/Thrombotic Causes of Intrinsic AKI

• Vasculitis
• Malignant hypertension
• Thrombotic disorders

Interstitial Causes of Intrinsic AKI

• Infections (e.g., pyelonephritis, renal tuberculosis, fungal nephritis).
• Medications (e.g., antibiotics, NSAIDs, diuretics).
• Immune disorders.

Post-Renal AKI Obstruction Causes

• Nephrolithiasis (kidney stones).
• Benign prostatic hypertrophy.
• Surgical complications.

Drug-Induced Crystalluria

• Mechanism: Low solubility drugs crystallize in urine.
• Effects: Crystals block the collecting system.
• Risk Factors: High drug doses, dehydration, and acidic urine.

Common Causes of AKI

• Pre-renal: Hypovolemia, dehydration, decreased cardiac output, decreased peripheral vascular resistance.
• Intrarenal: Nephrotoxic injury, contrast dye, crush injury, interstitial nephritis, allergies, infections, acute glomerulonephritis, malignant hypertension, thrombotic disorders, vasculitis.
• Post-renal: Benign prostatic hypertrophy, bladder cancer, calculi formation.

Clinical Workup

• Comprehensive evaluation of the patient's medical condition, including history, physical examination, and diagnostic tests.

Medical History and Physical Examination

• Gathering information on fluid loss, prior lab results, comorbidities, and medication history.
• Identifying risk factors (e.g., heart/liver disease, infections, prior urinary tract issues).
• Assessing vital signs, volume status, and underlying conditions during a physical examination.

Labs Work

• Comprehensive lab testing (electrolytes, kidney biomarkers).

Laboratory Studies

• Serum Chemistry: Analyzing blood samples for electrolytes and metabolic status.
• Urinalysis: Evaluating urine composition and sediment.
• Complete blood count: Measuring RBC and WBC to detect abnormalities.

Radiographic Studies

• Imaging tests provide valuable insights into underlying causes of acute kidney injury.
• Renal Ultrasonography: Evaluating kidney size, shape, and structure.
• Renal Doppler Ultrasonography: Assessing blood flow to the kidneys, helpful in diagnosing renal artery stenosis.
• Renal Biopsy: Obtaining a small sample of kidney tissue for microscopic examination.

Therapy for Acute Kidney Injury (AKI)

• Treat underlying cause.
• Discontinue nephrotoxins.
• Ensure proper perfusion (monitor fluid status and BP).

Fluid Replacement

• Crystalloids are more commonly used than colloids for resuscitation in pre-renal AKI.
• Colloids increase intravascular oncotic pressure (e.g., using albumin, gelatins, etc.).

KDIGO Guideline

• Isotonic crystalloids are the preferred fluid for volume expansion.
• Avoid Hydroxyethylstarch (HES).
• Colloids may still be used in patients requiring larger fluid volumes (e.g., albumin).

Diuretics

• Diuretics are used to manage fluid overload in AKI.
• Loop diuretics (e.g., furosemide) are commonly used to reduce fluid overload and hyperkalemia.

Vasopressors

• Used to maintain adequate mean arterial pressure (MAP).
• Fluid resuscitation may not be enough.
• Norepinephrine and dopamine common vasopressors.

Renal Replacement Therapy (RRT)

• Indications include anuria, acute fluid overload, severe hyperkalemia, metabolic acidosis, and a BUN level above 100 mg/dL.
• Early initiation of RRT has shown reduced mortality.
• Modalities include intermittent and continuous therapies.

Timing of RRT

• Early initiation of RRT can improve mortality.
• Volume overload and solute imbalances suggest RRT.
• Consideration of risk and benefits of early versus late RRT.

CRRT Advantages

• Maintaining hemodynamic stability.
• Reduced downtime for procedures.

Drug Dosing in Dialysis

• Smaller molecular weight drugs are more easily removed.
• Highly protein-bound drugs have less unbound drug for dialysis.
• Drugs with larger volumes of distribution are poorly dialyzable.

Common Dialyzable Drugs

• List of drugs effectively removed by dialysis.
• Monitoring drug levels crucial in dialysis patients.

Case Study Introduction

• A 75-year-old man with a right hemi-colectomy.
• Decreased urine output.
• Vital signs: HR 116 BPM, BP 90/60 mmHg.

Patient Medical History

• Hypertension, type 2 diabetes mellitus, gout.
• Medications: Lisinopril, diclofenac, allopurinol, spironolactone.

Case Study: 75-year-old Man (continued)

• The patient had right hemi-colectomy.
• History of hypertension, type 2 diabetes, and gout.
• Current medications.

Question 1

• Classify the patient's renal failure.
  • Pre-renal (due to hypovolemia).

Question 2

• Immediate action for decreased urine output.
  • Fluid challenge with saline (0.9% normal saline).

This quiz explores the fundamentals of Acute Kidney Injury (AKI), including its definition, effects, and classification systems such as RIFLE and AKIN. Participants will learn to differentiate types of AKI, apply treatments, and understand renal replacement therapy. Improve your knowledge of this critical renal condition!