AKI
Concept of Elimination Acute Kidney Injury (AKI)
- References:
- Giddens, Ch 15
- Lilley, Ch 28
- Lewis, Ch 51, pp. 1204-1230, 1232-1238 (AKI only)
- Wong, pp. 776-783
- Silvestri, pp. 479-481, Ch 55, pp. 784
Student Learning Objectives
- Compare and contrast the pathophysiology and cause of acute renal failure (ARF) with those of chronic renal failure.
- Determine patients at risk for acute renal failure.
- Construct a plan of care for patients with acute renal failure.
Learning Objectives Continued
- Collaborate with the interprofessional team to coordinate high-quality care and promote urinary elimination in patients with acute kidney injury or chronic kidney disease.
- Teach the patient and caregiver(s) about home safety issues affected by impaired elimination and the impairment of fluid and electrolyte balance or acid-base balance resulting from acute kidney injury or chronic kidney disease.
- Prioritize evidence-based nursing care for patients with impaired urinary elimination from either acute kidney injury or chronic renal failure.
- Identify community resources for patients requiring assistance with the management of altered elimination due to acute kidney injury or chronic kidney disease.
- Implement nursing interventions to help patients and families cope with the psychosocial impact caused by acute kidney injury and chronic kidney disease.
- Apply knowledge of anatomy and physiology to assess patients with impaired kidney function from acute kidney injury and chronic kidney disease affecting elimination, fluid and electrolyte balance, or acid-base balance.
- Teach the patient and caregiver(s) about common drugs and other strategies used for acute kidney injury and chronic kidney disease, including pain control and depression management.
- Implement evidence-based nursing interventions to prevent complications in patients undergoing kidney replacement therapy when urinary elimination is not effective in clearing waste or toxins.
Waste Products
Removal of waste products:
- Urea, Creatinine, etc.
- Drugs
- Potassium
Renal Functions:
- Bone structure, Calcium balance, Vitamin D activation
- Blood formation: Renin synthesis, Erythropoietin synthesis
- Water balance: Sodium removal
- Regulation of blood pressure and cardiac activity
- Regulation of blood acidity
Renal Elimination
Excretion of:
- Metabolites
- Drugs
- Toxins
- Waste products (Urea (BUN), Creatinine)
Fluid and Electrolyte Balance: Homeostasis
- Excess water removal; retention during dehydration
- Regulation of Potassium, Calcium, Sodium, Magnesium, Phosphorus
Acid-Base Regulation:
- Excretion of acid or base into blood and urine
Hormone Secretion:
- Endocrine secretion of Erythropoietin (stimulates RBC production)
- Renin (converts angiotensinogen to angiotensin I)
- Prostaglandins
- Converts vitamin D3 to active form (Calcitriol)
Kidney Anatomy
Renal Medulla
Renal Capsule
Renal Column
Minor Calyx
Major Calyx
Renal Pyramids
Renal Cortex
Pelvic space
Renal Pelvis
Renal Vein
Adrenal Gland
Glomerulus:
- Distal Afferent Tubule
- Efferent Arteriole
- Proximal Tubule
- Collecting Duct
- Ureter
Loop of Henle:
- Descending
- Ascending
Diuretics (Classification)
- Osmotic Diuretics
- Carbonic Anhydrase Inhibitors
- Loop Diuretics
- Thiazide Diuretics
- Potassium-Sparing Diuretics
Normal Metabolic Panel (selected components)
- Tests, Expected Ranges, Interpretations:
- Sodium: 135-145 mmol/L
- Major cation (Na+) in extracellular space
- Hypernatremia: increased Na intake, decreased Na loss, excessive loss of body water
- Hyponatremia: decreased Na intake, increased Na loss (diuretics, V/D, increased free body water, third spacing of Na)
- Potassium: 3.5-5.5 mmol/L
- Major cation (K+) in intracellular space
- Hyperkalemia: acute/chronic renal failure, increased intake, K+-sparing diuretics (spironolactone), ACEI, ARBs, hemolysis, acidosis, dehydration
- Hypokalemia: insufficient intake, loss (V/D), insulin/glucose administration, diuretics (loop/thiazide)
- Chloride: 101-111 mmol/L
- Cl has parallel shifts with Na
- Similar hyper/hypo reasons as Na
Normal Metabolic Panel Continued
- Calcium: 8.9-10.3 mg/dL
- Primarily regulated by parathyroids
- Hypercalcemia: hyperparathyroidism, bone tumor, lymphoma
- Hypocalcemia: hypoparathyroidism, renal failure, vitamin D deficiency
- Osmolarity: 275-295 mOsm/L
- Measure of the # of dissolved particles in serum per unit volume
- Increased: hypernatremia, dehydration, hyperglycemia, uremia, ingestion of ETOH, ketosis
- Decreased: hyponatremia, overhydration
- Phosphorous: 3.0-4.5 mg/dL
- Inverse relationship with calcium
- Levels determined by calcium metabolism, PTH secretion, renal excretion, and intestinal absorption
- Hyperphosphatemia: renal failure, increased intake, hypoparathyroidism, bone cancer, hypercalcemia
- Hypophosphatemia: inadequate intake, chronic antacid ingestion, hyperparathyroidism, hypercalcemia, vitamin D deficiency, malnutrition
Normal Metabolic Panel Continued
- BUN: 6-20 mg/dL
- Blood Urea Nitrogen: amount of urea nitrogen in blood (end product of protein metabolism produced by liver and excreted by kidneys)
- Elevated: acute/chronic renal failure, dehydration, hypovolemia, nephrotoxic drugs
- Decreased: overhydration, negative nitrogen balance (malnutrition), nephrotic syndrome
- Creatinine: 0.7-1.2 mg/dL
- Produced by skeletal muscle contraction and excreted by kidneys
- Elevated: acute/chronic renal failure or disease
- Decreased: decreased muscle mass
- eGFR: >60 mL/min/1.73³
- Estimated glomerular filtration rate
- Increased: exercise, pregnancy, high cardiac output syndromes
- Decreased: impaired kidney function, decreased renal perfusion
- BUN/Creat Ratio: 7.0-25
- Increased urea formation = increased ratio: GIB, trauma, dehydration
- Decreased urea formation = decreased ratio: liver disease, low protein intake
Staging of Kidney Function
- Stage 1: GFR 90+, normal kidney function but urine findings or structural abnormalities indicate kidney disease
- Treatment: Observation, control of blood pressure, genetic issues
- Stage 2: GFR 60-89, mildly reduced kidney function
- Treatment: Observation, control of blood pressure and risk factors
- Stage 3:
- 3A: GFR 45-59, moderately reduced kidney function
- Treatment: Observation, control of blood pressure and risk factors
- 3B: GFR 30-44, severely reduced kidney function
- Treatment: Planning for end-stage renal failure
- Stage 4: GFR 15-29, very severe or end-stage kidney failure
- Treatment choices: dialysis or kidney transplant
- Stage 5: GFR <15 or on dialysis, end-stage renal failure
Urinalysis Element
Normal Findings:
- pH: 4.6-8
- Specific Gravity: 1.001-1.035
- Protein: negative or trace
- Glucose: negative
- Ketone: negative
- Nitrates: negative
- Leukocyte Esterase: negative
- Crystals: negative, occasional hyaline crystals
- Casts: negative
- WBC: <5
- RBC: <3
Abnormal Findings:
- pH: Acidic (acidotic state, E. coli infection) or alkaline (UTI, alkalosis, sodium bicarbonate administration)
- Specific Gravity: low (dilute urine/overhydration or inability to concentrate urine); high (concentrated urine/dehydration)
- Protein: positive (glomerular damage)
- Glucose: positive (elevated glucose level)
- Ketone: positive (altered carbohydrate metabolism, dehydration)
- Nitrates: positive (indicates bacteria)
- Leukocyte Esterase: positive (indicates infection)
- Crystals: positive; may indicate infection
- Casts: positive; may indicate renal damage
- WBC: >5 (indicates infection)
- RBC: >3 (indicates infection or injury)
Acute vs. Chronic Renal Failure
Acute Renal Failure
- Onset: Abrupt onset (hours/days)
- Nephron Involvement: 50-95% nephron involvement
- Progression: May not progress, may recover
- Residual Damage: May have some residual renal injury
- Prognosis: Good with maintained or returned renal function
- Potential Progression: Can progress to chronic kidney disease
Chronic Renal Failure
- Onset: Gradual onset (months/years)
- Nephron Loss: Progressive nephron loss
- Symptomatic Threshold: Symptomatic at 75% nephron loss
- Dialysis Requirement: Dialysis at 90-95% nephron loss
- Course: Progressive and permanent
- Management: Lifestyle changes can slow progression
- End Stage Disease: Requires dialysis or transplant
Acute Renal Injury
Associated Conditions:
- Shock
- Heart conditions causing decreased cardiac output
- Surgery
Risk Factors:
- Increased age
- Chronic kidney disease
- Diabetes
Systemic Complications From Acute Kidney Injury
- Metabolic Complications:
- Metabolic acidosis
- Hyperlipidemia
- Hyperkalemia
- Hyponatremia
- Hypocalcemia
- Hypophosphatemia
- Cardiopulmonary Complications:
- Peripheral and pulmonary edema
- Heart failure
- Pulmonary embolism
- Pericarditis
- Pericardial effusion
- Hypertension
- Myocardial infarction
- Neurologic Complications:
- Neuromuscular irritability or weakness
- Asterixis
- Seizures
- Mental status changes
- Immune/Infectious Complications:
- Pneumonia
- Sepsis
- Hematologic Complications:
- Bleeding
- Thrombosis
- Anemia
- Gastrointestinal Complications:
- Nausea
- Vomiting
- Decreased peristalsis
- Enteral nutrition intolerance
- Malnutrition
- Ulcer formation
- Bleeding
- Renal Complications:
- Chronic kidney disease (CKD)
- End-stage kidney disease (ESKD)
- Other Complications:
- Hiccups
- Elevated parathyroid hormone
- Low thyroid hormone level
Frequency of AKI Etiologies
- Acute Tubular Necrosis: 45%
- Prerenal Disease: 21%
- Acute on Chronic Kidney Disease: 13%
- Urinary Tract Obstruction: 10%
- Glomerulonephritis or Vasculitis: 4%
- Acute Interstitial Nephritis: 2%
- Atheroemboli: 1%
Acute Kidney Failure (AKF)
- Definition: Abrupt decline in renal function
- Inability to excrete waste products
- Inability to maintain fluid balance
- Inability to maintain electrolyte balance
- Inability to maintain acid-base balance
Causes of ARF
- Prerenal:
- Perfusion reduction
- Intrinsic/Intrarenal:
- Kidney damage
- Postrenal:
- Urine outflow obstruction
Prerenal Causes
- Description: Sudden/severe drop in blood pressure
- Causes: Blood/fluid loss, sepsis, dehydration, heart disease with decreased perfusion, hypotension due to medications, renal artery stenosis, blockage of blood flow to kidneys
Intrarenal Causes
- Description: Direct kidney damage
- Causes Include:
- Infection (e.g., pyelonephritis)
- Clots in kidney blood vessels (clotting disorders)
- Autoimmune diseases (Glomerulonephritis, Lupus, Scleroderma)
- Acute Tubular Necrosis
- Nephrotoxic drugs
- Contrast media
- NSAIDs & COX-2 Inhibitors
- Antibiotics (e.g., vancomycin)
- Chemotherapeutic agents
Intrarenal (Intrinsic): Peds Exemplars
- Acute Poststreptococcal Glomerulonephritis:
- Antibodies to streptococcal infection form immune complexes
- Immune complexes are trapped in glomerulus causing inflammation and decreased GFR
- Symptoms: edema, oliguria, hypertension
- Diagnosed by elevated ASO titer, UA will show RBC, casts, proteins
- Management: Supportive care, antibiotic therapy, manage fluid overload (low sodium diet)
Postrenal Causes
- Description: Urine outflow obstruction
- Causes Include:
- Plumbing problems (cancer, enlarged prostate, nephrolithiasis, bladder innervation issues, clots in lower urinary tract)
Prevention of AKI
- Strategies:
- Avoid dehydration (oral/IV hydration)
- Avoid hypotension
- Monitor lab values (chemistries, UA)
- Know client’s baseline
- Monitor for reduced urinary elimination
- Maintain a urine output of >30 mL/hour for adults
- Daily weight monitoring (1 kg of weight = 1 L of fluid)
- Decrease nephrotoxic effects of medications
- Avoid nephrotoxic medications, especially in elderly or those with renal insufficiency
- Hydration before/after contrast media administration
- Hold metformin 24-48 hours before/after
Case Study
- Scenario: A patient with renal insufficiency is scheduled for a heart catheterization
- Interventions: To decrease risk of renal damage and AKI.
- Effectiveness Indicators: How to determine if the interventions are successful
Stages of AKI
| Stage | Serum Creatinine | Urine Output |
|---|---|---|
| 1 | 1.5-1.9× baseline or ≥0.3 mg/dL increase over 48 hours | <0.5 mL/kg/hr for 6-12 hours |
| 2 | 2.0-2.9 times baseline | <0.5 mL/kg/hr for ≥12 hours |
| 3 | 3.0 times baseline or ≥4.0 mg/dL or initiation of renal replacement therapy or eGFR <35 mL/min/1.73 m² |
Phases of AKI
- Onset Phase
- Oliguric Phase:
- Inability to excrete fluid/electrolytes/waste
- Possible hyperkalemia: leads to dysrhythmias
- Hyponatremia with fluid overload
- Hypernatremia with excessive sodium intake
- Metabolic acidosis
- Diuretic Phase:
- Diuretic output of 4-5 L/day with loss of electrolytes
- Dehydration, hypokalemia
- Recovery Phase:
- May involve some residual damage
Assessment-History: Recognize Clues
- Past Medical History:
- Risk factors: advanced age, DM, renal insufficiency, PVD, liver disease, HIV, kidney surgery, immune-mediated diseases
- Drug History:
- Particularly nephrotoxic agents
- Diagnostic Testing:
- Contrast agents, surgical procedures, risk factors for hypotension/volume depletion
- Urinary Characteristics:
- Frequency, volume, pattern
Symptoms of AKI
Physical Assessment
- Urine Output: Varies from oliguria to normal levels
- Decreased UOP: red flag
- Signs of Hypervolemia:
- Crackles, S3/S4 heart sounds, JVD, peripheral edema
- Anasarca: generalized edema
- Vital Signs:
- Hypotension, tachypnea, thread pulse, low MAP (<65%)
- Altered mental status
Altered Labs
- Increased BUN/creatinine
- Severe uremia
- Azotemia: nitrogenous waste build-up
- Acidosis, hyperkalemia, muscle weakness, dysrhythmias
- UA: proteinuria, casts, etc.
Diagnostic Assessment
- Ultrasound: Ablations/Obstruction
- CT without contrast or MRI: Kidney perfusion
- KUB X-ray: Kidney size, hydronephrosis/obstruction
- Cystoscopy or Retrograde Pyelography: Identify obstructions in the lower urinary tract
- Kidney Biopsy: Major risk of bleeding
- Labs: Previously discussed
Nursing Interventions-Take Action
- Monitoring and Actions:
- Avoid hypotension
- Maintain euvolemia and normal fluid balance
- Maintain MAP of 80-85 mm Hg
- Reduce exposure to nephrotoxic agents
- Use of contrast agents: Assess renal function before and after
- Adequate hydration before and after
- Desired UOP of 150 mL/hr for the first 6 hours after contrast
- Ongoing assessment for dehydration/overhydration
Nursing Interventions for Low Volume Urine Output
- Monitor and treat fluid volume overload
- Monitor and treat hyperkalemia
- Monitor and treat acidosis
Nursing Interventions for High Volume Urine Output
- Monitor and manage fluid and electrolyte losses
- The onset of polyuria can indicate recovery from AKI
Hyperkalemia Symptoms and Interventions
- Symptoms: Muscle cramps, weakness, paralysis, drowsiness, EKG changes (dysrhythmias), abdominal cramping, diarrhea
- Interventions:
- Hold drugs that raise potassium
- Administer IV glucose and/or IV insulin
- Administer sodium bicarbonate
- Administer sodium polystyrene sulfonate (Kayexalate)
- Renal replacement therapies as necessary
- Cardiac monitoring due to risk of life-threatening dysrhythmias
Hypokalemia Management
- Management: Replace potassium via
- Oral supplementation
- Peripheral line (10-20 mEq/250 mL over 1 hour)
- ICU can administer a higher dose in a central line
- Note: Never administer IV potassium via IV push or rapid infusion
AKI Drug Therapy
- Monitoring: Continually monitor kidney function and drug effects
- Diuretics may not improve kidney function but help eliminate fluid if some kidney function remains
- Fluid Challenge: 500-1000 mL of NS can help improve renal perfusion if not in fluid overload
- Positive Outcomes: Improved BP, MAP, and UOP
AKI Nutrition Therapy
- Nutritional Needs:
- AKI = catabolism (protein breakdown)
- Dietary consultant may be required:
- Protein: 0.8 to 1.0 g protein/kg
- Calories: 30 to 35 kcal/kg
- Sodium, potassium, and fluid; often lower sodium, potassium, phosphorous, and protein
- Higher calories required
- Use of IV fat emulsion infusions (Intralipid)
Continuous Renal Replacement Therapy (CRRT)
- Lines Used in CRRT:
- Access Line: Renal artery
- Return Line: Renal vein
- Filtrate Line: Urether
- Bladder Drainage Bag
Renal Replacement Therapies
- Hemodialysis:
- Temporary access with catheter to central vein (e.g., internal jugular)
- Long term access can be established (fistula, graft)
Intermittent vs. Continuous Renal Replacement Therapy
- Intermittent: Used frequently; takes hours (3-4 hours)
- Continuous: Used in critical patients unable to tolerate rapid fluid shifts; removes fluid over days (24 hours to more than 2 weeks)
Continuous Renal Replacement Therapies: Purpose
- Types:
- CVVH: Continuous venovenous hemofiltration - slow continuous ultrafiltration, removes fluid and solutes, requires replacement fluid
- SCUF: Simplified CVVH, removes just fluid
- CVVHD: Continuous venovenous hemodialysis - requires dialysate and replacement fluid
- CVVHDF: Continuous venovenous hemodiafiltration, same requirements as CVVHD
Pros of CRRT
- Features CRRT offer over hemodialysis:
- Slower blood pump rate (~150 mL/min), improving hemodynamic stability
- Continuous operation with fluid volume removal performed over a longer timeframe
- Flexible solute removal methods including convection (no dialysate needed)
- Reduced hemodynamic instability
- Doesn't require constant specialized monitoring like traditional hemodialysis, but still needs trained ICU nurses
Indications for Renal/Kidney Replacement Therapies
- Indications Include:
- Volume overload causing compromised cardiac and/or pulmonary status
- High serum potassium level
- Metabolic acidosis (serum HCO3− <15 mEq/L)
- BUN >120 mg/dL
- Significant change in mental status
- Pericarditis, pericardial effusion, or cardiac tamponade
Patient Care Protocol for CRRT
- Protocols:
- Change the hemofilter every 24 to 48 hours
- Daily weights and monitoring laboratory values
- Hourly intake and output, vital signs, and hemodynamic status assessment
- Maintain vascular access site to prevent infection
Care During Treatment
- Monitoring:
- High vigilance for hypotension and general condition
- Access site integrity and monitoring
- Alarm for pressure changes
- Filtrate conditions (purity, quality)
Case Studies
Case Study 1
- Patient Background: 65-year-old male, post-surgery for AAA, with history of hyperlipidemia and hypertension.
- Assessment Notes: Lethargic but oriented, normal vital signs detected, bilaterally clear heart and lungs, with soft abdomen.
- Urgent focus: What type of acute kidney injury is this patient most at risk for? (Prerenal, Intrarenal, Postrenal)
Case Study 2
- Patient Background: 43-year-old male presented with right-sided mid back pain diagnosed with nephrolithiasis and hydronephrosis.
- Assessment Notes: Alert but restless, high pain levels, normal heart sounds detected, low peripheral edema.
- Focus questions: What type of AKI is this client at risk for? What changes are anticipated on the chemistry panel? What are priority nursing interventions? What therapeutic management does this patient require?
Summary and Reflections
- Reviewing AKI concepts reinforced the importance of early detection and intervention. Emphasizing the patient’s fluid balance and watching for lab abnormalities are crucial areas for nursing care.