AKI

Chapter 51: Acute Kidney Injury and Chronic Kidney Disease

Kidney (Renal) Failure

  • Definition: Partial or complete impairment of kidney function that results in the inability to excrete metabolic waste products and water.

  • Affects every body system; Examples of systemic impacts include:

    • Metabolic imbalances

    • Hypertension

    • Cardiovascular dysfunction

  • Treatments and dietary changes can be complex and challenging.

  • Impacts various life aspects:

    • Lifestyle

    • Occupation

    • Family relationships

    • Self-image

Comparison of Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD)

  • Criteria for comparison:

    • Onset:

    • AKI: Sudden onset.

    • CKD: Gradual onset over years.

    • Common Causes:

    • AKI: Acute tubular necrosis.

    • CKD: Diabetic nephropathy.

    • Diagnostic Criteria:

    • AKI: Acute reduction in urine output and/or elevated serum creatinine levels.

    • CKD: GFR < 60 mL/min/1.73m² for > 3 months and/or kidney damage for > 3 months.

    • Reversibility:

    • AKI: Potentially reversible.

    • CKD: Progressive and irreversible.

    • Cause of Death:

    • AKI: Infection.

    • CKD: Cardiovascular disease.

Acute Kidney Injury

Spectrum of Injury

  • Characterized by the rapid loss of kidney function presenting as:

    • Rise in serum creatinine.

    • Elevated blood urea nitrogen (BUN).

    • Increased potassium levels (K+).

    • Reduction in urine output.

  • Azotemia: accumulation of nitrogenous waste products in the blood.

  • Mortality Rate: Approximately 1 in 5 patients with AKI.

  • Often follows severe prolonged hypotension, hypovolemia, or exposure to toxic agents.

Causes of Acute Kidney Injury

  • Prerenal Causes: Factors that reduce systemic circulation causing reduced renal blood flow and glomerular perfusion leading to oliguria. Common factors include:

    • Severe dehydration

    • Heart failure

    • Decreased cardiac output (CO)

    • Autoregulatory mechanisms to maintain blood flow include:

    • Renin-angiotensin-aldosterone system (RAAS)

    • Antidiuretic hormone (ADH)

    • Adrenal cortex hormones.

    • Prerenal azotemia results in:

    • Sodium (Na+) excretion.

    • Increased Na+ and H₂O retention impacting urine output. Extended prerenal causes may transition to intrarenal AKI, that compromises kidney tissue.

  • Intrarenal Causes: Conditions that directly damage kidney tissue affecting nephrons, such as:

    • Prolonged ischemia.

    • Nephrotoxins: Aminoglycosides (antibiotics), contrast agents.

    • Release of hemoglobin from hemolyzed RBCs.

    • Release of myoglobin from necrotic muscle cells.

    • Kidney diseases—acute glomerulonephritis, systemic lupus erythematosus (SLE, Lupus).

  • Postrenal Causes: Mechanical obstruction of outflow leading to backflow and kidney dysfunction. Examples include:

    • Benign prostatic hyperplasia

    • Prostate cancer

    • Calculi (kidney stones)

    • Trauma

    • Extrarenal tumors.

    • Bilateral ureteral obstruction can result in hydronephrosis or kidney dilation, increasing hydrostatic pressure, promoting tubular blockage.

    • If obstruction is relieved within 48 hours, recovery likelihood increases; otherwise leads to tubular atrophy or irreversible fibrosis.

Clinical Manifestations of Acute Kidney Injury

  • Three phases:

    • Oliguric Phase:

    • Reduced urine output (< 400 mL/day).

    • Occurs 1-7 days post-injury and lasts 10-14 days.

    • Urinalysis may show casts, RBCs, WBCs, protein.

    • Specific gravity at 1.010, similar to serum.

    • Osmolality at approximately 300 mOsm/kg.

    • 50% of patients may be nonoliguric (> 400 mL urine/day).

    • Fluid Volume:

      • Hypovolemia exacerbates AKI.

      • Decreased urine out leads to anuria, distended neck veins, bounding pulse, edema, hypertension, and potential heart failure.

    • Metabolic Acidosis:

      • Impaired excretion of hydrogen ions leading to decreased serum bicarbonate production.

      • Results in severe acidosis, seen with Kussmaul's respirations (increased exhalation of CO₂).

    • Sodium Balance:

      • Increased sodium excretion due to damaged tubules, risk of hyponatremia leading to cerebral edema.

    • Potassium Excess:

      • Elevated K+ levels from impaired excretion, especially with tissue damage, asymptomatic until significant.

      • ECG changes (e.g., peaked T waves, widened QRS, ST depression).

      • Importance of monitoring sodium intake to avoid further complications.

    • Hematologic Disorders:

      • Increased risk of leukocytosis, urinary and respiratory infections.

      • Elevated BUN and serum creatinine.

      • Neurologic symptoms include fatigue, difficulty concentrating, seizures, stupor, or coma.

  • Diuretic Phase (1 to 3 weeks):

    • Daily urine output ranging from 1 to 3 L or even up to 5 L due to osmotic diuresis from high urea levels.

    • Need monitoring for:

    • Hypovolemia

    • Hypotension

    • Hypo/hypernatremia

    • Hypokalemia

    • Dehydration.

    • Duration may be up to 3 weeks, during which acid-base balance, electrolytes, and waste levels stabilize.

    • Recovery Phase:

    • Major healing noted by week 2, though complete recovery may take up to 12 months.

    • Begins with an increase in GFR and a decrease in BUN and creatinine, influenced by the severity of injury and any complications.

Diagnostic Studies for Acute Kidney Injury

  • Comprehensive history to consider prerenal, intrarenal, and postrenal stages.

  • Diagnostic markers include:

    • Serum creatinine (not elevated until 50% of kidney function lost).

    • BUN and electrolytes.

    • Urinalysis revealing larger particles (indicative of intrarenal issues).

    • Imaging studies: renal ultrasound, CT scans, renal scans, and renal biopsy.

Interprofessional Care

  • Objectives:

    • Ensure adequate intravascular volume and cardiac output.

    • Administer diuretics such as:

    • Loop diuretics (e.g., furosemide [Lasix]).

    • Osmotic diuretics (e.g., mannitol).

    • Fluid intake must be closely monitored during the oliguric phase with a calculated restriction based on fluid losses from the prior 24 hours + 600 mL for insensible loss.

  • Hyperkalemia Therapies:

    • Insulin and sodium bicarbonate: helps temporarily move K+ into cells; stabilizes myocardium against dysrhythmias.

    • Calcium gluconate: raises the threshold for dysrhythmias.

    • Sodium polystyrene sulfonate (Kayexalate) or Patiromer (Veltassa): help in potassium removal.

    • Dialysis: for effective K+ removal from the body.

  • Nutritional Therapy:

    • Focus on maintaining adequate caloric intake, primarily from carbohydrates and fats.

    • Sufficient protein intake to prevent breakdown and promote energy utilization.

    • Sodium, K+, phosphate limits established.

    • Use of calcium supplements or phosphate-binding agents as necessary.

    • Enteral or parenteral nutrition may be applied, particularly if used in conjunction with hemodialysis (HD).

  • Indications for Renal Replacement Therapy (RRT):

    • Volume overload.

    • Elevated serum potassium levels.

    • Metabolic acidosis.

    • BUN levels > 120 mg/dL (43 mmol/L).

    • Significant mental status changes.

    • Pericarditis, pericardial effusion, or cardiac tamponade.

    • Patient's clinical status needs continuous evaluation without a consensus on the optimal timing to commence treatment.

Nursing Management of Acute Kidney Injury

  • Assessment Parameters:

    • Monitoring vital signs.

    • Daily weight measurements.

    • Strict intake/output tracking.

    • Detailed examination of urine.

    • General health appearance evaluation.

    • Observation of dialysis access sites.

  • Further Assessment Considerations:

    • Level of consciousness and mental status.

    • Oral mucosa condition.

    • Lung sounds.

    • Cardiac rhythm.

    • Results of laboratory values and diagnostic tests.

Gerontologic Considerations in Acute Kidney Injury

  • Aging leads to:

    • Decreased GFR.

    • Reduced ability to adapt to changes in fluid volume, solute load, and cardiac output.

    • Increased vulnerability to AKI due to factors such as:

    • Dehydration.

    • Polypharmacy (diuretics, laxatives).

    • Illness and immobility.

    • Determining factors include:

    • Hypotension.

    • Treatment with diuretics and aminoglycosides.

    • Obstructive disorders, surgical interventions, infections, and use of contrast media.

    • RRT options remain applicable even in elderly patients.

Chronic Kidney Disease (CKD)

  • Definition: Progressive, irreversible loss of kidney function.

  • Prevalence: Over 26 million American adults are affected (1 in 9); CKD is more prevalent than AKI.

  • Factors contributing to increased prevalence include:

    • Aging population.

    • Higher obesity rates.

    • Increase in diabetes and hypertension incidence.

  • Over half a million Americans are receiving treatment for end-stage renal disease (ESRD), which has a high mortality rate.

  • CKD may go unrecognized until late, as the kidneys adapt, allowing substantial nephron loss without symptoms; approximately 70% live with CKD unknowingly.

  • Leading Causes:

    • Diabetes (50%).

    • Hypertension (25%).

    • Additional causes include glomerulonephritis, cystic kidney diseases, and urologic diseases.

Diagnostic Criteria for Chronic Kidney Disease

  • According to Kidney Disease Improving Global Outcomes (KDIGO): CKD is defined by:

    • Kidney damage or a low glomerular filtration rate (GFR) < 60 mL/min/1.73m² for more than 3 months.

    • ESRD is classified as GFR < 15 mL/min, where dialysis or transplant is necessary for life sustainability.

Stages of Chronic Kidney Disease

Stage

GFR (mL/min/1.73m²)

Clinical Action Plan

1

≥ 90

Diagnosis and treatment; cardiovascular disease (CVD) risk reduction; slow progression.

2

60–89

Estimation of progression.

3a

45–59

Evaluation and treatment of complications.

3b

30–44

More aggressive treatment of complications.

4

15–29

Preparation for renal replacement therapy (RRT) such as dialysis or transplant.

5

< 15

RRT if uremia is present and patient desires treatment; necessary for survival.

Course and Prognosis of Chronic Kidney Disease

  • Course and prognosis of CKD can be variable and depend on:

    • Underlying causes.

    • Patient's condition and age.

    • Healthcare quality and support.

  • Medicare typically covers ~80% of costs associated with CKD.

  • It is classified as a disability; the remaining cost could be covered by states, insurers, or patients themselves.

  • Health Equity Considerations: Increased incidence is noted among:

    • African American populations.

    • Native Americans.

    • Hispanics.

Clinical Manifestations of Uremia

  • Uremia occurs when kidney function declines sufficiently, and symptoms manifest across multiple body systems;

    • Typically noted when GFR ≤ 15 mL/min.

  • Manifestations vary based on:

    • Underlying cause

    • Co-morbid conditions

    • Patient age

    • Adherence to medical protocols.

  • Patient adaptation to functional decline is gradual, allowing tolerance to changes.

Psychological Symptoms

  • Anxiety

  • Depression

Neurologic Symptoms

  • Fatigue

  • Headache

  • Sleep disturbances

  • Encephalopathy

Cardiovascular Symptoms

  • Hypertension

  • Heart failure

  • Coronary artery disease

  • Pericarditis

  • Peripheral artery disease

Ocular Symptoms

  • Hypertensive retinopathy

Gastrointestinal Symptoms

  • Anorexia

  • Nausea

  • Vomiting

  • Gastrointestinal bleeding

  • Gastritis

Endocrine/Reproductive Symptoms

  • Hyperparathyroidism

  • Thyroid abnormalities

  • Amenorrhea

  • Erectile dysfunction

Pulmonary Symptoms

  • Pulmonary edema

  • Uremic pleuritis

  • Pneumonia

Integumentary Symptoms

  • Pruritus

  • Ecchymosis

  • Dry, scaly skin

Metabolic Symptoms

  • Carbohydrate intolerance

  • Hyperlipidemia

Hematologic Symptoms

  • Anemia

  • Increased bleeding and infection risk

Musculoskeletal Symptoms

  • Vascular and soft tissue calcifications

  • Osteomalacia

  • Osteitis fibrosa

  • Peripheral neuropathy (including paresthesias and restless leg syndrome)

Early Stages of Chronic Kidney Disease

  • In early CKD stages, urine output may remain unchanged.

  • Polyuria may be present, particularly in cases related to diabetes.

  • As CKD progresses, increased fluid retention is noted, often requiring diuretics.

  • Post-dialysis, patients might experience anuria.

Electrolyte and Metabolic Disturbances

  • Hyperkalemia: Most serious electrolyte disorder when potassium levels reach 7 to 8 mEq/L (7 to 8 mmol/L).

    • Increased due to a mix of inadequate excretion, cellular breakdown, gastrointestinal bleeding, and metabolic acidosis—leading to fatal dysrhythmias.

  • Sodium (Na+): Levels may fluctuate; impaired excretion results in sodium retention, potentially causing dilutional hyponatremia, edema, and hypertension. Sodium intake typically restricted to 2 g/day.

  • Hypercalcemia: Results in decreased muscle and nerve excitability presenting as fatigue, weakness, and confusion, potentially leading to severe conditions such as hallucinations and seizures.

  • Hyperphosphatemia: Asymptomatic unless calcium binds with phosphorus leading to hypocalcemia symptoms, associated with calcified deposits.

  • Hypermagnesemia: Elevated magnesium levels may lead to absent reflexes, decreased mental status, cardiac dysrhythmias, hypotension, and respiratory failure.

Additional Clinical Manifestations

  • Pruritus: Resulting from calcium-phosphate deposits and sensory neuropathy, leading to intense itching.

  • Uremic Frost: Extremely rare, characterized by crystallization of urea on the skin when BUN exceeds 200 mg/dL.

  • Anemia: Caused by decreased erythropoietin production due to kidney damage, hemolysis, low calcium affecting erythropoiesis in bone marrow, nutritional deficiencies, or loss of blood during dialysis.

  • Infection Risk: Immunologic responses are hampered, leading to increased susceptibility.

  • Infertility and Decreased Libido: Experienced in both sexes with low sperm counts and amenorrhea; significant risks presented to pregnancy during dialysis.