AKI

Acute Kidney Injury (AKI)

Overview

  • Definition: Acute Kidney Injury (AKI) is characterized by a rapid loss of kidney function, which can range from slight deterioration to severe impairment.

  • Key Terms:

    • AZOTEMIA: Accumulation of nitrogenous waste products in the blood.

    • RIFLE classification: A framework for categorizing AKI.

Key Functions of the Kidneys

  • Maintaining fluid & electrolyte balance: Regulates the levels of different ions and fluids in the body.

  • Regulating blood pressure: Through the renin-angiotensin-aldosterone system (RAAS).

  • Detoxifying blood & eliminating wastes: Filters out toxins from the bloodstream.

  • Maintaining acid/base balance: Regulates pH levels by excreting hydrogen ions and reabsorbing bicarbonate.

  • Aiding red blood cell production: Through the secretion of erythropoietin, which stimulates red blood cell formation in the bone marrow.

Factors Affecting Kidney Function

  • Past Health History: Conditions such as diabetes, hypertension, lupus, metabolic disorders, cancer, infections, benign prostatic hyperplasia (BPH).

  • Medications: Certain drugs can adversely affect kidney function.

  • Surgeries: Previous surgical interventions may influence kidney health.

  • Chemotherapy or Radiation: Potentially nephrotoxic agents from cancer treatments can lead to AKI.

Diagnostic Studies for Kidney Function

  • Blood Urea Nitrogen (BUN): Used to identify the presence of renal problems.

    • Normal Range: 6-20 mg/dL

  • Creatinine: More reliable than BUN for renal function assessment.

    • Normal Range: 0.6-1.3 mg/dL

  • Creatinine Clearance: Approximately indicates glomerular filtration rate (GFR).

  • Glomerular Filtration Rate (GFR): Normal GFR is approximately 125 mL/min.

Kidney (Renal) Failure

  • Definition: Partial or complete impairment of kidney function, leading to an inability to excrete metabolic wastes and water.

  • Impact: Affects all body systems, complicating treatment and dietary changes, and influences lifestyle, occupation, family relationships, and self-image.

Acute Kidney Injury - Causes

  • Categories:

    • Prerenal causes: Factors that reduce systemic circulation, leading to decreased renal blood flow.

    • Intrarenal causes: Direct damage to kidney tissue.

    • Postrenal causes: Mechanical obstruction of urinary outflow.

Etiology and Pathophysiology

Prerenal Causes

  • Factors such as severe dehydration, heart failure, and decreased cardiac output lead to oliguria (low urine output). Autoregulatory mechanisms attempt to preserve blood flow.

Intrarenal Causes

  • Issues causing direct damage to kidney tissue, including:

    • Prolonged ischemia

    • Nephrotoxins: Substances that harm renal cells.

    • Hemoglobin from hemolyzed RBCs and myoglobin from necrotic muscle cells.

    • Kidney diseases such as acute glomerulonephritis and systemic lupus erythematosus.

Acute Tubular Necrosis (ATN)

  • Resulting from ischemia, nephrotoxins, or sepsis.

  • Severe ischemia disrupts the basement membrane, causing extensive tubular epithelial damage.

  • Nephrotoxic agents may lead to necrosis of tubular epithelial cells, clogging the tubular structures; the condition can be potentially reversible.

Postrenal Causes

  • Mechanical obstruction causes reflux into renal pelvis, impairing kidney function.

  • Examples include benign prostatic hyperplasia, prostate cancer, kidney stones (calculi), trauma, and extrarenal tumors.

  • Bilateral ureteral obstruction can lead to hydronephrosis, and relieving the obstruction within 48 hours increases the chance of recovery.

Clinical Manifestations of Acute Kidney Injury

  • Phases of AKI: 1. Oliguric 2. Diuretic 3. Recovery

  • RIFLE Classification:

    • Risk (R)

    • Injury (I)

    • Failure (F)

    • Loss (L)

    • End-stage renal disease (E)

Oliguric Phase

  • Urinary Changes: Oliguria defined as less than 400 mL/day, occurring 1 to 7 days post-injury and lasting 10 to 14 days.

  • Urinalysis Findings: May show casts, RBCs, WBCs, and protein. Specific gravity approximately 1.010, osmolality at about 300 mOsm/kg.

  • Fluid Volume Impact: Hypovolemia may exacerbate AKI, leading to fluid retention, distended neck veins, bounding pulse, and edema. Potential complications include heart failure and pulmonary edema.

  • Metabolic Acidosis: Impaired kidneys cannot excrete hydrogen ions; serum bicarbonate production decreases.

  • Electrolyte Disruption:

    • Sodium balance becomes impaired, leading to hyponatremia and risk of cerebral edema.

    • Increased potassium levels due to failure to excrete K+ may cause cardiac changes such as peaked T waves, widened QRS, and ST segment depression.

  • Hematologic Disorders: Increased risk of infections. Elevated BUN and creatinine levels result from waste accumulation. Neurological impacts may include fatigue, seizures, stupor, and coma.

Diuretic Phase

  • Lasts from 1 to 3 weeks, with daily urine output ranging from 1 to 3 L, sometimes up to 5 L.

  • Caused by osmotic diuresis due to elevated urea and inability to concentrate urine. Monitoring for hypovolemia and electrolyte imbalances is critical.

  • Recovery Phase: May take up to 12 months; characterized by increased GFR and decreased BUN and creatinine, influenced by the severity of the injury and any complications.

Diagnostic Studies for AKI

  • Thorough History: Collecting a complete medical and medication history to assess risk.

  • Required Tests:

    • Serum creatinine, BUN, electrolytes.

    • Urinalysis, renal ultrasound, renal scans, CT scans, renal biopsy.

Interprofessional Care Goals for AKI

  • Main Objectives:

    • Eliminate the underlying cause of AKI.

    • Manage signs and symptoms effectively.

    • Prevent complications associated with renal impairment.

Management Strategies

  • Fluid Management: Ensure adequate intravascular volume and cardiac output. Use loop diuretics (e.g., furosemide) and osmotic diuretics (e.g., mannitol).

  • Controlling Hyperkalemia:

    • Temporary measures to shift potassium into cells using insulin and sodium bicarbonate;

    • Stabilizing myocardium with calcium gluconate;

    • Removing potassium from the body through agents like sodium polystyrene sulfonate or dialysis. Dietary restriction of potassium is also essential.

Renal Replacement Therapy (RRT)

  • Indications:

    • Volume overload

    • Elevated serum potassium levels

    • Severe metabolic acidosis

    • BUN level > 120 mg/dL

    • Significant changes in mental status

    • Symptoms indicating pericarditis or cardiac tamponade.

Types of Dialysis

  • In-Center Hemodialysis: Common method, typically performed three times a week for three to four hours.

  • Peritoneal Dialysis (PD): Not frequently used; involves dialysis within the peritoneal cavity.

  • Continuous Renal Replacement Therapy (CRRT): Utilizes continuous strategy over 24 hours, typically for critically ill patients.

Nutrition Therapy for AKI

  • Dietary Recommendations: Focus on maintaining adequate caloric intake primarily through carbohydrates and fats.

  • Protein Restrictions: Adequate protein intake should be maintained to prevent muscle breakdown, along with careful restrictions on sodium, potassium, and phosphate.

  • Supplementation: Use calcium supplements or phosphate-binding agents as needed. Consider both enteral and parenteral nutrition.

Nursing Management of AKI

  • Assessment Focus Areas:

    • Vital signs

    • Daily weights

    • Strict intake and output monitoring

    • Manual examination of urine, general patient appearance, and dialysis access points.

  • Mental and Neurological Assessment: Including consciousness level, oral mucosa inspection, lung sounds, heart rhythm, and laboratory findings altitude consciousness level, mental state, and laboratory results.

Gerontologic Considerations

  • Aging Factors:

    • Decreased renal function with age results in higher AKI susceptibility.

    • Increased risk factors include dehydration, polypharmacy, and underlying health issues such as hypotension or infections.

    • Renal replacement therapy remains an option, though recovery may be more challenging.

Nephrotoxic Drugs

  • Includes several drug classes, notably:

    • Aminoglycosides: Such as gentamicin, vancomycin, tobramycin.

    • Cephalosporins: Including cephalexin, cefoxitin.

    • Other classes: NSAIDs, ACE inhibitors, salicylates, IV contrast agents, lithium, and certain chemotherapeutics (e.g., cisplatin).

Contrast-Induced Nephropathy

  • Definition: Nephrotoxic injury resulting from contrast media used in diagnostic imaging studies.

  • Management:

    • Ensure to withhold metformin 48 hours before and after contrast use to prevent lactic acidosis.

    • Hydration strategies and possible use of bicarbonate and N-acetylcysteine for prevention and treatment.