Acute Kidney Injury Overview

Acute Kidney Injury

• Kidney function involves maintaining fluid and electrolyte balance, removing water-soluble waste products, regulating urine composition, and performing key endocrine functions.
• Electrolyte levels are crucial:
  • Potassium: 3.5-5.0 mEq/L
  • Sodium: 135-145 mEq/L
  • Calcium: 8.5-10.5 mg/dL
  • Phosphorus: 3.0-4.5 mg/dL
• Hormonal regulation is essential, including:
  • Erythropoietin, stimulating red blood cell development and production.
  • Vitamin D, important for calcium regulation.
• Osteodystrophy happens when vitamin D is impaired, causing poor calcium absorption and decreased calcium, stimulating parathyroid hormone release.
• Clinical problems include:
  • Anemia due to reduced red blood cell production.
  • Reduced blood flow.
  • Renin-Angiotensin-Aldosterone System activation leading to hypertension, damaging glomerulus capillaries.
• Types of Azotemia (renal failure):
  • Prerenal: Reduced blood flow to the kidneys (e.g., hemorrhage, dehydration). Key lab findings include elevated BUN-to-creatinine ratio (>20:1) and low urine sodium concentration.
  • Intrinsic (Renal): Damage to the kidney itself (e.g., acute tubular necrosis, ATN). Key lab findings include normal or lower BUN-to-creatinine ratio and high urine sodium concentration.
  • Postrenal: Blockage of urine outflow (e.g., kidney stones, enlarged prostate). Key lab findings include BUN-to-creatinine ratio that initially elevates then normalizes and high urine sodium concentration.
• Treatment Approaches
  • Prerenal Azotemia: Identifying and treating the underlying cause (e.g., dehydration, heart failure) is key along with providing fluids during recovery. Also monitoring kidney function frequently and avoiding nephrotoxic drugs during recovery.
  • Intrinsic Renal Azotemia: Identifying and treating the underlying cause (e.g., ATN). Removing nephrotoxic drugs, managing electrolytes, and supporting care such as hydration are essential.
  • Postrenal Azotemia: Relieving the obstruction, use of catheters or surgery if needed, supporting kidney function with frequent monitoring, and managing resulting electrolyte imbalances are crucial.
• Pathophysiology:
  • Prerenal Azotemia (Initiation): Blood overfills the ventricle due to damaged heart tissue. Can result from hemorrhage, dehydration, burns, heart failure, and myocardial infarction.
• Prerenal AKI: NSAIDS, Ace inhibitors, ARBs (reduce glomerular perfusion). Medications that can cause kidney damage.
  • Intrarenal (Intrinsic) Azotemia: Acute tubular necrosis is the most common cause, caused by radiographic contrast media. The most common antibiotics that cause damage include certain aminoglycoside antibiotics.
  • Acute Tubular Necrosis (AKI): Three phases (Initiation, Maintenance, Recovery) differing in symptoms. Initiation phase is characterized by decreased urine output, mild increase in BUN, and creatinine levels. The maintenance phase exhibits oliguria (<30 cc/hr) and fluid overload. Recovery phase shows increasing urine output (>400 cc/hr) and normalization of BUN and Creatinine levels.
• Postrenal AKI: Benign prostatic hyperplasia, kinked or obstructed catheters, intra-abdominal tumors, and calculi are common causes.
• Clinical Manifestations: Elevated blood pressure, S3 heart sound (indicating problems with left ventricular function), pulmonary crackles, jugular venous distention, and anemia are possible signs.
• Diagnostic Tests: Urinalysis, serum electrolytes, elevated serum creatinine, blood urea nitrogen, complete blood count are essential.
• Treatments:Renal Ultrasonography can help identify obstructive causes. Medications include loop diuretics (bumetanide, ethacrynic acid, furosemide, torsemide) and osmotic diuretics(mannitol, urea).
• Electrolyte Modifiers: Calcium chloride, calcium gluconate, sodium bicarbonate, sodium polystyrene sulfonate can be used to adjust electrolyte imbalances.
• Dialysis: Three main types (hemodialysis, peritoneal dialysis, continuous renal replacement therapy) to remove toxins and lower elevated drug levels.
• Hemodialysis Access: Arteriovenous fistula, arteriovenous graft, central venous catheter.
• Peritoneal Dialysis: waste products are moved into a dialysate solution and drained. Peritoneal catheter used.
• Implementation of Care: Crucial monitoring of intake and output, daily weights, assessing vital signs, and monitoring electrolytes and fluid restriction.