Acute Kidney Injury (AKI) Lecture Flashcards

Physiological Functions of Healthy Kidneys

  • Water Regulation: Maintains total body water balance and intravascular volume homeostasis.
  • Blood Pressure Regulation: Controls systemic blood pressure through fluid volume regulation and enzymatic pathways.
  • Waste Excretion: Filters and excretes metabolic waste products from the bloodstream, including:
    • Urea
    • Uric acid
    • Exogenous drugs
    • Toxins
  • Bone Health Maintenance: Healthy kidneys convert Vitamin D into its active hormonal form, calcitriol, which promotes and increases calcium (CaCa) absorption from the intestinal tract into the blood.
  • Acid-Base Balance: Regulates systemic hydrogen ion and bicarbonate levels to maintain systemic pH balance.
  • Electrolyte Balance: Maintains homeostasis of key systemic electrolytes.
  • Hematopoiesis Support: Synthesizes and releases erythropoietin, an endocrine hormone that signals the bone marrow to produce red blood cells (RBCs).

Pathophysiology and Diagnostics of Acute Kidney Injury (AKI)

  • Definition: An abrupt, acute disruption in renal/kidney function that severely impairs the body's capability to maintain fluid, electrolyte, and acid-base homeostasis.
  • Clinical Progression & Reversibility:
    • Represents a rapid loss of renal function.
    • May be fully reversible if identified and treated promptly.
    • Can progress to chronic kidney disease if damage is permanent.
  • Primary Treatment Goals: Replace renal function artificially/supportively while minimizing potential clinical complications.
  • Diagnostic Serum Criteria: Characterized by an acute increase in serum creatinine levels of 50%50\% or greater above baseline.
  • Urine Output Classifications:
    • Normal Output: Normal urinary volume maintained.
    • Nonoliguria: Urine output volume greater than >800 mL/day>800\,mL/day.
    • Oliguria: Urine output volume reduced to less than <0.5 mL/kg/hr<0.5\,mL/kg/hr.
    • Anuria: Severe urine output reduction to less than <50 mL/day<50\,mL/day.

Etiology and Etiological Classifications of AKI

  • Prerenal AKI:
    • Overview: Represents the most common cause of acute kidney injury in acute care settings.
    • Pathophysiology: Results from reduced blood perfusion reaching the kidneys ("before kidney" physiological defect).
    • Etiological Factors:
      • Volume Depletion: Caused by severe vomiting, excessive diarrhea, active hemorrhage/bleeding, or extensive burn injuries.
      • Cardiac Dysfunction: Conditions precipitating a significant decline in cardiac output (C.O.).
      • Systemic Vasodilation: Severe vasodilation induced by anaphylaxis, antihypertensive medications, other vasodilating pharmacological agents, or severe sepsis.
      • Vascular Obstruction: Narrowing of the main renal arterial vessels (renal artery stenosis).
  • Intrarenal (Intrinsic) AKI:
    • Overview: Caused by direct structural or cellular tissue damage located inside the kidneys.
    • Etiological Factors:
      • Prolonged Renal Ischemia: Severe tissue ischemia secondary to extensive muscle trauma/injury, massive burn injuries, or severe blood transfusion reactions.
      • Nephrotoxic Agents: Direct structural damage from nephrotoxic agents and toxic medications.
      • Infectious/Inflammatory Processes: Parenchymal inflammation caused by acute glomerulonephritis or acute pyelonephritis.
  • Postrenal AKI:
    • Overview: Occurs due to physical obstruction of urine outflow distal to the renal parenchyma.
    • Etiological Factors:
      • Benign Prostatic Hyperplasia (BPH).
      • Malignancies: Compression from prostate cancer, cervical cancer, or colon cancer.
      • Calculi: Nephrolithiasis or urolithiasis (kidney stones).
      • Neoplasms: Renal tumors.
      • Trauma: Direct physical renal trauma.
      • Vascular Occlusion: Intraluminal blood clots within the urinary tract structure.

Systemic Clinical Manifestations in High-Risk AKI Patients

  • Cardiac System Dysfunction: Secondary to fluid overload, hyperkalemia, and electrolyte disturbances.
  • Respiratory System Compromise: Secondary to fluid overload and compensatory mechanisms for metabolic derangements.
  • Fluid and Electrolyte Disturbances: Imbalances in systemic volume, sodium, potassium, and phosphate.
  • Immune System Impairment: Elevated vulnerability to secondary infections and systemic physiological stress.

Sequential Stages and Clinical Phases of AKI

  • Initiation Phase:
    • Commences with the initial cellular or ischemic kidney injury.
    • Concludes at the onset of the oliguric phase.
  • Oliguric Phase:
    • Clinical Definition: Marked reduction in total urine output volume to less than <400 mL/day<400\,mL/day (note: this phase is not present in all cases of AKI).
    • Duration: Typically lasts approximately 1−2 weeks1-2\,\text{weeks}; clinical efforts aim to minimize the duration of this phase as much as possible.
    • Clinical Observations & Diagnostic Findings:
      • Azotemia & Neurological Signs: Elevated Blood Urea Nitrogen (BUN) and serum creatinine levels result in central nervous system signs including confusion, fatigue, and sluggishness.
      • Cutaneous Signs: Severe generalized itching (pruritus) caused by metabolic waste accumulation in the tissue.
      • Fluid & Electrolyte Alterations: Mild hyponatremia due to hemodilution from excess fluid retention; peripheral and systemic edema.
      • Hyperkalemia: Serum potassium levels rising above >5 mEq/L>5\,\text{mEq/L}, precipitating dangerous EKG changes including tall peaked T waves, widened QRS complexes, and prolonged PR intervals.
      • Acid-Base Disturbances: Arterial Blood Gas (ABG) analysis demonstrates metabolic acidosis.
      • Urinalysis Findings: Highly concentrated urine presenting with a elevated specific gravity greater than >1.020>1.020.
    • Phase-Specific Nursing Interventions:
      • Dietary Modification: Administer a low-protein diet because hepatic protein catabolism yields urea, which exacerbates hyperazotemia.
      • Patient Safety: Implement protective safety protocols to safeguard patients from falling or injury secondary to metabolic confusion.
      • Fluid Management: Restrict fluid intake strictly; perform rigorous intake and output (I&O) tracking; collect daily weight measurements to assess systemic fluid retention.
      • Respiratory Monitoring: Frequently assess respiratory status and patterns for signs of metabolic acidosis compensation.
      • Renal Replacement: Initiate renal dialysis therapy as the definitive treatment for severe oliguric renal failure.
  • Diuretic Phase:
    • Pathophysiology: Renal nephrons begin recovering cellular function and resume blood filtration. BUN and serum creatinine levels start to decline, Glomerular Filtration Rate (GFR) improves, and cognitive/mental status subsequently improves.
    • Duration: Typically lasts approximately 1−3 weeks1-3\,\text{weeks}.
    • Clinical Characteristics: Recovering nephrons lack the physical ability to concentrate urine, leading to massive osmotic diuresis producing 3−6 L/day3-6\,L/day of highly dilute urine.
    • Primary Clinical Risks: Severe hypovolemia, dehydration, and rapid electrolyte depletion.
    • Phase-Specific Nursing Interventions:
      • Maintain meticulous intake and output (I&O) recording.
      • Obtain accurate daily weights.
      • Administer intravenous (IV) fluids to prevent hypovolemic shock.
      • Provide targeted electrolyte supplements to replace urinary fluid and electrolyte losses.
      • Monitor continuously for signs and symptoms of severe dehydration.
      • Maintain active patient safety measures.
  • Recovery Phase (End Phase):
    • Pathophysiology: Characterized by the gradual return of normal physiological renal functions while structural tissue healing occurs.
    • Clinical Indicators: Glomerular Filtration Rate (GFR) normalizes, urine output returns to normal baseline levels, and laboratory serum markers (BUN, creatinine, and electrolytes) stabilize.
    • Duration: Can take up to 1 year1\,\text{year} or longer to achieve complete recovery.
    • Prognostic Factors: Total recovery duration and success depend on the extent of tissue damage sustained (particularly during the oliguric phase) and patient age. Certain individuals sustain permanent renal damage and never achieve complete functional recovery, progressing to end-stage renal failure.

Pharmacological and Dietary Interventions in AKI

  • Pharmacological Therapies:
    • Kayexalate: Administered to bind potassium in the gastrointestinal tract to treat hyperkalemia.
    • Intravenous (IV) Insulin: Administered to facilitate the rapid intracellular shift of serum potassium.
    • Diuretics: Utilized cautiously during the oliguric phase to attempt renal stimulation.
    • Fluid and Electrolyte Replacements: Administered during the diuretic phase to match massive urinary losses.
    • Sodium Bicarbonate Therapy: Administered to correct severe systemic metabolic acidosis.
    • Calcium-Based Phosphate-Binding Agents: Administered orally to decrease intestinal absorption of dietary phosphate, preventing continued toxic rises in serum phosphate levels.
  • Nutritional Management Interventions:
    • Caloric Composition: High-carbohydrate diet to meet daily metabolic demands and prevent catabolic protein breakdown.
    • Dietary Restrictions: Complete avoidance of food items containing high concentrations of potassium or phosphorus.
    • Specific Excluded Foods & Beverages:
      • Bananas
      • Citrus fruits
      • Citrus juices
      • Coffee