Module 7: Acute Kidney Injury and Chronic Kidney Disease Flashcards
Kidney (Renal) Failure
Partial or complete impairment of kidney function
that results in inability to excrete metabolic waste
products and water
Acute Kidney Injury
Ranges from slight deterioration to severe
impairment
Rapid loss of kidney function with:
Rise in serum creatinine and/or reduction in urine
output
Elevated BUN and K+
Azotemia—accumulation of nitrogenous waste
products
High mortality rate; other life-threatening conditions
Etiology and Pathophysiology of AKI - Prerenal
Prerenal
Causes: factors that reduce systemic circulation
causing reduction in renal blood flow which leads to
oliguria
* Severe dehydration, heart failure, decreased CO
Autoregulatory mechanisms attempt to preserve
blood flow
Prerenal azotemia results in Na+ excretion, increased
Na+ and H2O retention and decreased urine output
Etiology and Pathophysiology of AKI - Intrarenal
Intrarenal
Causes: problems that cause direct damage to kidney
tissue
* Prolonged ischemia
* Nephrotoxins
* Hemoglobin released from hemolyzed RBCs
* Myoglobin released from necrotic muscle cells
* Kidney diseases—acute glomerulonephritis and SLE
Intrarenal
Acute tubular necrosis (ATN)
* Results from ischemia, nephrotoxins, or sepsis
* Severe ischemia causes disruption in basement
membrane and patchy destruction of tubular epithelium
* Nephrotoxic agents cause necrosis of tubular epithelial cells—clog tubules
* Potentially reversible
Etiology and Pathophysiology of AKI - Postrenal
Postrenal
Causes: mechanical obstruction of outflow which
results reflux into renal pelvis, impairing kidney
function
* Benign prostatic hyperplasia, prostate cancer, calculi,
trauma, and extrarenal tumors
Bilateral ureteral obstruction—hydronephrosis; relieve obstruction in 48 hours increased chance of recovery
Acute Kidney Injury
Clinical Manifestations: Oliguric phase
Three phases: oliguric, diuretic, and recovery
RIFLE classification (Table 51.3 in the textbook)
Risk (R)
Injury (I)
Failure (F)
Loss (L)
End-stage renal disease (E)
Oliguric phase
Urinary changes—*oliguria
* Urinary output less than 400 mL/day
* Occurs within 1 to 7 days after injury
* Lasts 10 to 14 days (longer is poor prognosis)
* Urinalysis—casts, RBCs, WBCs, protein
* Specific gravity 1.010
* Osmolality 300 mOsm/kg
50% patients nonoliguric; greater than 400 mL
urine/day
Oliguric phase
Fluid volume
* Hypovolemia may exacerbate AKI
* Decreased urine output leads to fluid retention
Neck veins distended
Bounding pulse
Edema
Hypertension
* Fluid overload can lead to heart failure, pulmonary
edema, and pericardial and pleural effusions
Oliguric phase
Metabolic acidosis
* Impaired kidney cannot excrete hydrogen ions or acid
products of metabolism
* Serum bicarbonate production is decreased
Reabsorption and regeneration defective
* Severe acidosis develops
Kussmaul respirations—increasing exhaled CO2
Oliguric phase
Sodium balance
* Increased excretion of sodium—damaged tubules
* Hyponatremia can lead to cerebral edema
Potassium excess
* Impaired ability of kidneys to excrete K+
* Increased risk with massive tissue trauma
* Usually asymptomatic
* ECG changes—peaked T waves, widened QRS, ST
depression
Oliguric phase
Hematologic disorders
* Leukocytosis—infection may be fatal
Urinary and respiratory infections
Waste product accumulation
* Increased BUN and *serum creatinine levels
Neurologic disorders
* Fatigue and difficulty concentrating
* Seizures, stupor, coma
AKI Diagnostic Studies
Diagnostic studies
Thorough history
Serum creatinine, BUN, electrolytes
Urinalysis
Renal ultrasound
Renal scan
CT scan
Renal biopsy
Diagnostic studies
Contraindications for contrast medium
* MRI or MRA with gadolinium contrast medium—may be fatal
* Contrast-induced nephropathy (CIN)
* Diabetics taking metformin: hold 48 hours before and
after use of contrast medium; risk of lactic acidosis
* If contrast is needed for high-risk patients—use low-
dose and optimal hydration
AKI Care
Ensure adequate intravascular volume and cardiac
output
Loop diuretics (e.g., furosemide [Lasix])
Osmotic diuretics (e.g., mannitol)
Closely monitor fluid intake during oliguric phase
Fluid restriction calculation: All fluid losses for
previous 24 hours + 600 mL
Hyperkalemia therapies
Temporary—move K+ into cells
* Insulin and sodium bicarbonate
dysrhythmias—stabilizes myocardium
* Calcium gluconate
Remove K+ from body
* Sodium polystyrene sulfonate (Kayexalate) or
Patiromer (Veltassa)
* Dialysis
Dietary restriction
Indications for renal replacement therapy (RRT)
Volume overload
Elevated serum potassium level
Metabolic acidosis
BUN level > 120 mg/dL (43 mmol/L)
Significant change in mental status
Pericarditis, pericardial effusion, or cardiac
tamponade
Clinical status of patient
Renal replacement therapy (RRT)
Peritoneal dialysis (PD)
* Not frequently used
Intermittent hemodialysis (HD)
* Emergent therapy
Continuous renal replacement therapy (CRRT)
* Cannulation of artery and vein
* Continuously 24 hours
Nutrition therapy
Maintain adequate caloric intake
* Primarily carbohydrates and fat
* Adequate protein to prevent breakdown
Restrict sodium, K+, phosphate
Calcium supplements or phosphate-binding agents
Enteral/parenteral nutrition
Gerontologic Considerations
Acute Kidney Injury
Decreased GFR with aging
More susceptible to AKI
Dehydration
* Polypharmacy- diuretics, laxatives
* Illness and immobility
Hypotension, diuretic therapy, aminoglycoside
therapy, obstructive disorders, surgery, infection, and
contrast medium
decreased reduced ability to recover
RRT still an option
Chronic Kidney Disease
Progressive, irreversible loss of kidney function
Greater than 26 million American adults have
CKD; more common than AKI
Increased prevalence related to aging population,
increased obesity, increased diabetes and HTN
Over half a million Americans are receiving
treatment for ESRD; high mortality rate
Kidney disease improving global outcomes (KDIGO)
defines CKD as
Kidney damage
* Pathologic abnormalities
* Markers of damage
Blood, urine, imaging tests
Low glomerular filtration rate (GFR)
* <60 mL/min/1.73m2 for longer than 3 months
Leading causes
Diabetes—50%
Hypertension—25%
Other: glomerulonephritis, cystic diseases, urologic
diseases
Persons with CKD are often asymptomatic; ~ 70%
aware
Underdiagnosed and untreated
Course and prognosis are variable
Medicare covers ~80% of the costs
Considered a disability
See Promoting Health Equity Box
Increased incidence with Blacks, Native Americans,
and Hispanics
CKD Clinical Manifestations
Result of retained substances
Urea
Creatinine
Phenols
Hormones
Electrolytes
Water
Uremia
Early stages
No change in urine output
Polyuria may be present related to diabetes.
CKD progression—increasing fluid retention; need
diuretic
After a period on dialysis, patients may become
anuric
Waste product accumulation
As GFR decreases, BUN and serum creatinine levels
increase
BUN level increase
* From kidney failure and protein intake, fever,
corticosteroids, and catabolism
* N/V, lethargy, fatigue, impaired thought processes, and headaches occur
*Serum creatinine clearance—most accurate indicator
Uremia
Uremia
Syndrome in which kidney function declines to the
point that symptoms occur in multiple body systems
Often occurs when GFR is less than or equal to
15 mL/min
Manifestations vary depending on cause, co-
morbidities, age, and adherence to medical regimen
Defective Carb Metabolism
Altered carbohydrate metabolism
Caused by impaired glucose metabolism
* From cellular insensitivity to normal action of insulin
* Mild-moderate hyperglycemia and hyperinsulinemia
Defective carbohydrate metabolism
Patients with diabetes who develop uremia may
require less insulin than before the onset of CKD
Excretion of insulin dependent on kidneys
Insulin dosing must be individualized
May improve after starting dialysis
Elevated Triglycerides
Elevated triglycerides
Hyperinsulinemia stimulates hepatic production of
triglycerides
Altered lipid metabolism
* Decreased levels of enzyme lipoprotein lipase
– Important in breakdown of lipoproteins
Increased VLDLs and LDLs, decreased HDLs
Most patients with CKD die from CV disease
Electrolyte Imbalances
Potassium (K+)
Hyperkalemia
* Most serious electrolyte disorder in kidney disease
* Fatal dysrhythmias
When serum potassium level reaches 7 to 8 mEq/L (7 to 8 mmol/L)
* Decreased excretion, breakdown of cellular protein,
bleeding, and metabolic acidosis leads to increased K+
Other sources: food, dietary supplements, drugs, and IV infusions
Sodium (Na+)
May be high, normal, or low
Impaired excretion causes sodium and water
retention
Dilutional hyponatremia may occur
* Edema
* Hypertension
* HF
Calcium and phosphate
See section on Musculoskeletal System (CKD mineral
and bone disorder)
Magnesium
Hypermagnesemia
* Related to ingestion of magnesium (e.g., milk of
magnesia, magnesium citrate, antacids)
* Can result in absence of reflexes, decreased mental
status, cardiac dysrhythmias, hypotension, respiratory
failure
Metabolic Acidosis
Metabolic acidosis
Results from
* Impaired ability of kidneys to excrete excess acid
* Defective reabsorption and regeneration of bicarbonate
Plasma bicarbonate level usually falls to
approximately 16 to 20 mEq/L (16 to 20 mmol/L)
Anemia
Anemia
Due to decreased production of erythropoietin
* Hormone stimulates bone marrow to make RBCs
Other factors: nutritional deficiencies, decreased RBC
life span, increased hemolysis, blood sampling, GI
bleeding, HD, increased PTH
Also decreased iron stores
Folic acid lost in dialysis
Bleeding tendencies
Defect in platelet function
Infection
Changes in WBC function
Altered immune response and function
Hyperglycemia and external trauma
Cardiovascular Disease closely linked
CV disease and CKD closely linked
Death often related to MI, ischemic heart disease,
PAD, HF, cardiomyopathy, and stroke
Traditional CV risk factors
* Hypertension and elevated lipids
Nontraditional CV risk factors
* Vascular calcification and arterial stiffness
Calcium deposits associated with stiffness of blood
vessels
Vascular smooth muscle cells change
* Chondrocytes or osteoblast-like cells
High calcium and phosphate totals
Impaired renal excretion
Drug therapies to treat bone disease
HTN
Hypertension
Both a cause and a consequence of CKD
* Aggravated by sodium and water retention
* Increased renin production may contribute
HTN, ECF volume overload, and anemia may
develop into left ventricular hypertrophy, which may
lead to cardiomyopathy and HF
* HTN can cause retinopathy, encephalopathy,
nephropathy
*BP control—one of most important goals
Dysrhythmias
Hyperkalemia and decreased coronary artery
perfusion
Uremic pericarditis can progress to effusion and
tamponade
Friction rub, chest pain, and fever
Respiratory
Kussmaul respirations related to acidosis
Dyspnea may occur with
Fluid overload
Pulmonary edema
Uremic pleuritis
Pleural effusions
Respiratory infections
GI
Every part of GI system is affected
Cause: excessive urea
* Stomatitis with exudates and ulcerations
* Uremic fetor (urinous odor of breath)
* Anorexia, nausea, and vomiting
* Diabetic gastroparesis
* GI bleeding
* Constipation
CNS Depression
CNS depression
Lethargy, apathy
Decreased ability to concentrate
Fatigue, irritability
Altered mental ability (late)
Seizures
Coma
Hypertensive encephalopathy
Peripheral neuropathy
Restless legs syndrome
Paresthesias
Motor involvement
Footdrop
Muscle weakness and atrophy
Loss of deep tendon reflexes
Muscle twitching, jerking, asterixis, and nocturnal leg
cramps