Acute Kidney Injury Quiz

Acute Kidney Injury (AKI) Overview

• AKI is the abrupt loss of kidney function
• Effects include waste product retention, electrolyte imbalances, and changes in fluid balance
• Detection involves changes in biomarkers like serum creatinine (SCr), typically lagging 48-72 hours behind the onset of injury

Learning Outcomes

• Distinguish different types of acute kidney injury
• Apply various therapeutic strategies for AKI treatment
• Demonstrate understanding 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 serum creatinine and urine output changes
• Stages include Risk, Injury, Failure, Loss, and End-stage
• Purpose: Standardize definition and severity of AKI

AKIN Criteria

• SCr increase: 0.3 mg/dL over baseline within 48 hours
• Percentage increase: 50% or more increase in SCr within 7 days
• Urine output: Less than 0.5 mL/kg/hour for more than 6 hours

KDIGO Guidelines

• SCr increase: 0.3 mg/dL within 48 hours
• Percentage increase: 50% increase in SCr within the previous 7 days

Risk Factors for AKI

• Age: Increased risk with advanced age
• Comorbidities (HTN, Diabetes): Presence of other health conditions
• Proteinuria: Excess protein in the urine
• Major Surgery: Increased post-operative risk
• Dehydration
• High Blood Pressure
• Infections
• Medications
• Various factors like obstructions etc

Types of AKI

• Pre-renal: Hypo-perfusion to the kidney
• Intrinsic: Damage directly to the kidney
• Post-renal: Obstruction of urinary outflow

Pre-Renal Causes of Decreased Perfusion

• Fluid Loss: Inadequate intake, vomiting, diarrhea, fever
• Blood Loss: Trauma resulting in massive hemorrhage
• Systemic Conditions: Sepsis, heart failure, liver cirrhosis

Medications Affecting Kidney Blood Flow

• Efferent Arteriole: Drugs causing vasodilation (ACEI)
• Prostaglandin Inhibition: Drugs inhibiting vasodilatory prostaglandin synthesis
• Afferent Arteriole: Drugs causing vasoconstriction

Intrinsic AKI Causes:

• Acute tubular injury: Damage to kidney tubules
• Tubulointerstitial injury: Inflammation of kidney tissue
• Glomerulonephritis: Inflammation of kidney filtering units

Glomerular Causes of Intrinsic AKI

• Autoimmune disorders: Immune system attacking kidney tissue
• Oncology drugs: Certain cancer treatments affecting glomeruli
• Specific medications: Interferon, pamidronate, gemcitabine, VEGF inhibitors

Tubular Causes of Intrinsic AKI: Part 1

• Antimicrobials: Certain antibiotics can damage kidney tubules
• Nephrotoxic drugs: Various medications with kidney-damaging effects
• Acute tubular necrosis: Caused by ischemia (lack of blood supply) or exposure to nephrotoxins (toxins)
• Contrast media

Tubular Causes of Intrinsic AKI: Part 2

• Aminoglycoside-associated ATN: Occurs in a significant portion of adults and infants
• Amphotericin B: Can cause AKI in a substantial percentage of cases
• Vancomycin nephrotoxicity: Ongoing debate about its role
• Contrast-induced nephrotoxicity: Occurs in a varying percentage of patients

Vascular/Thrombotic Causes of Intrinsic AKI

• Vasculitis: Inflammation of blood vessels
• Malignant hypertension: Severe high blood pressure
• Thrombotic disorders: Blood clotting issues affecting the kidneys

Interstitial Causes of Intrinsic AKI

• Infections: Pyelonephritis, renal tuberculosis, fungal nephritis
• Medications: Antibiotics, NSAIDs, diuretics
• Immune disorders: Various autoimmune conditions affecting the kidney interstitium

Post-Renal AKI: Obstruction Causes

• Nephrolithiasis: Kidney stones obstructing urine flow
• Benign Prostatic Hypertrophy: Enlarged prostate compressing the urethra
• Surgical Complications: Post-operative issues leading to obstruction

Post-Renal Obstruction Causes

• Kidney stones: Obstruction by calculi
• Prostatic Hypertrophy: Enlarged prostate blocking urine flow
• Retroperitoneal Fibrosis: Scarring around kidneys and ureters

Drug-Induced Crystalluria

• Mechanism: Low solubility drugs crystallize in urine, forming crystals
• Effect: Crystals obstruct the collecting system
• Risk Factors: High drug doses, dehydration, acidic urine

Common Causes of AKI (Summary)

• Pre-renal: Hypovolemia, decreased cardiac output, decreased peripheral vascular resistance
• Intra-renal: Nephrotoxic injury, contrast dye, crush injury, interstitial nephritis, allergies, infections, acute glomerularnephritis, malignant hypertension
• Post-renal: Benign prostatic hypertrophy, bladder cancer, calculi formation, spinal cord disease

Clinical Workup

• Comprehensive evaluation: History, physical examination, and diagnostic tests
• History details: Fluid losses, previous lab results, comorbidities, and medication history
• Physical Exam: Assess vital signs, volume status, and signs of underlying conditions

Laboratory Studies

• Serum Chemistry: Analyze blood samples to assess electrolytes and metabolic status
• Urinalysis: Evaluate urine composition and sediment to identify potential issues
• Complete Blood Count: Measure red and white blood cell counts to detect abnormalities

Radiographic Studies

• Include: Renal ultrasonography, Renal Doppler Ultrasonography, Renal Biopsy
• Renal Ultrasonography: Evaluates kidney size, shape, and structure
• Renal Doppler Ultrasonography: Assesses blood flow to kidneys, helpful in diagnosing renal artery stenosis
• Renal Biopsy: Obtaining a kidney tissue sample for microscopic examination

Therapy for Acute Kidney Injury (AKI)

• Treat the underlying cause
• Discontinue nephrotoxins
• Ensure proper perfusion (monitor fluid status and blood pressure)

Fluid Replacement

• Crystalloids vs. Colloids: Crystalloids are more commonly used for resuscitation in pre-renal AKI
• Colloid solutions: increase intravascular oncotic pressure and shift fluid into the bloodstream

The KDIGO Guideline

• Isotonic crystalloids are the fluid of choice for volume expansion
• Avoid Hydroxyethylstarch due to adverse effects
• Colloids may still play a role in some cases, particularly larger fluid volumes

Diuretics

• Manage fluid overload in AKI
• Facilitates fluid management
• Potential renoprotective effects
• Recommended for treating volume overload and hyperkalemia

Vasopressors

• Maintain adequate mean arterial pressure (MAP) for organ perfusion
• Often necessary when fluid resuscitation alone is insufficient
• Potential risk for further kidney damage

Renal Replacement Therapy (RRT)

• Indications: Anuria, acute fluid overload, severe hyperkalemia, metabolic acidosis, elevated BUN
• Prevalence: Required in a percentage of critically ill patients with AKI
• Optimization: Factors to consider include timing, modality, dose, and clearance
• Timing and initiation: Early initiation is often beneficial
• Modalities: Intermittent hemodialysis (IHD), Continuous therapies, Hybrid therapies

CRRT Advantages (Continuous Renal Replacement Therapy)

• Improved hemodynamic stability
• Reduced downtime for other procedures

Drug Dosing in Dialysis (Important Considerations)

• Molecular weight, protein binding, volume of distribution, dialysis flow rates

Common Dialyzable Drugs

• Important to monitor drug levels for proper dosing
• Important consideration for patient care

Case Study Introduction

• 75-year-old male
• Decreased urine output
• Right hemi-colectomy 4 hours prior
• Vital signs: HR 116 BPM, BP 90/60 mmHg

Patient Medical History

• Hypertension
• Type 2 Diabetes Mellitus
• Gout
• Medications: Lisinopril, Diclofenac, Allopurinol, Spironolactone