Pathophysiology and Types
This type of AKI is caused by decreased blood flow to the kidneys.
What is prerenal AKI?
Rationale: Prerenal AKI results from reduced renal perfusion due to conditions like hypovolemia, shock, heart failure, or sepsis, leading to decreased GFR.
This urine output measurement, less than 400 mL per day, is a key sign of AKI.
What is oliguria?
Rationale: Oliguria (urine output <400 mL/day) indicates the kidneys are not filtering adequately and is ahallmark clinical sign of AKI.
These two chronic diseases are major risk factors for developing AKI.
What are diabetes mellitus and hypertension?
Rationale: Chronic conditions like diabetes and hypertension damage blood vessels and kidney structures over time, making patients more susceptible to AKI.
These two parameters should be monitored closely for early recognition of AKI.
What are urine output and laboratory values (BUN/creatinine)?
Rationale: Monitoring urine output trends and serial kidney function tests allows nurses to detect AKI early when interventions are most effective.
This is the primary laboratory marker that accumulates when GFR decreases in AKI.
What are BUN and creatinine?
Rationale: When kidney function declines, nitrogenous waste products like blood urea nitrogen (BUN) and creatinine accumulate in the blood because the kidneys cannot filter them effectively.
These lung sounds may be heard in AKI patients due to fluid overload
What are crackles?
Rationale: As kidneys fail to remove excess fluid, pulmonary edema can develop, producing crackles onlung auscultation.
This age group has increased risk for AKI.
Who are individuals over 60 years old?
Rationale: Older adults have decreased renal reserve and are more vulnerable to kidney injury frommedications, dehydration, and other insults.
This intervention is essential for preventing prerenal AKI in at-risk patients.
What is adequate hydration?
Rationale: Maintaining proper fluid balance helps ensure adequate renal perfusion and prevents prerenal AKI from hypovolemia.
This type of AKI involves direct damage to kidney structures such as ATN or glomerulonephritis.
What is intrinsic AKI?
Rationale: Intrinsic AKI occurs when there is direct tissue injury to the kidney itself, including conditions like acute tubular necrosis, glomerulonephritis, or exposure to nephrotoxins.
This dangerous electrolyte imbalance is common in AKI and can cause cardiacarrhythmias.
What is hyperkalemia?
Rationale: The kidneys normally excrete potassium; when they fail, potassium accumulates in the blood, which can lead to life-threatening cardiac dysrhythmias.
These four conditions can cause prerenal AKI by reducing blood flow to the kidneys.
What are dehydration, hemorrhage, heart failure, and sepsis?
Rationale: Any condition that decreases circulating blood volume or cardiac output can reduce renalperfusion and cause prerenal AKI.
These medications should be avoided in AKI patients due to their potential forkidney damage.
What are nephrotoxins (NSAIDs, aminoglycosides, contrast dye)?
Rationale: Nephrotoxic medications can worsen kidney injury and should be avoided or used withextreme caution in AKI patients.
This mechanism causes post-renal AKI by creating back pressure into the kidneys.
What is obstruction of urine flow?
Rationale: Post-renal AKI occurs when an obstruction (such as kidney stones, enlarged prostate, or tumors) blocks urine flow, causing pressure to build up and damage nephrons.
This is the first phase of AKI progression, where the initial injury begins.
What is the initiation phase?
Rationale: The initiation phase is when the kidney injury first occurs, whether from decreased perfusion, toxins, or obstruction.
These chronic conditions—heart disease, obesity, and lupus—increase AKI risk through these mechanisms.
What are decreased cardiac output/perfusion, metabolic stress, and autoimmune inflammation?
Rationale: Heart disease reduces renal blood flow, obesity causes metabolic strain and inflammation, and lupus can cause direct immune-mediated kidney damage, all increasing AKI susceptibility.
This nursing priority involves managing fluids and electrolytes to maintain balance.
What is supportive care/fluid and electrolyte management?
Rationale: Nurses must carefully manage fluid administration, monitor electrolytes, and correctimbalances to prevent complications like hyperkalemia and fluid overload.
Prolonged ischemia in pre-renal AKI can progress to this more serious type of kidneyinjury.
What is intrinsic AKI?
Rationale: If prerenal AKI is not corrected promptly, prolonged decreased blood flow and ischemia can cause direct tissue damage to the kidneys, converting it to intrinsic AKI.
During this phase of AKI, urine output increases and kidney recovery begins.
What is the diuretic phase?
Rationale:
The diuretic phase follows the oliguric phase and is characterized by increasing urine output as the kidneys begin to recover function.
These three causes can lead to post-renal AKI through urinary obstruction.
What are enlarged prostate, kidney stones, and tumors?
Rationale: Physical blockages in the urinary tract from prostatic hypertrophy, calculi, or malignancies can obstruct urine flow and cause post-renal AKI.
This aspect of patient education helps prevent AKI in patients with chronic diseases.
What is chronic disease control and medication safety?
Rationale: Teaching patients to manage diabetes and hypertension, take medications as prescribed, andavoid nephrotoxins reduces AKI risk.
This is the key characteristic that distinguishes AKI from chronic kidney disease.
What is rapid onset (hours to days) and potential reversibility?
Rationale: AKI develops suddenly over hours to days and can often be reversed with prompt treatment,unlike chronic kidney disease, which develops gradually over months to years.
These three acid-base and electrolyte disturbances commonly occur in AKI (2 electrolytes, 1 acid-base condition)
What are hyperkalemia, hyponatremia, and metabolic acidosis?
Rationale: AKI disrupts the kidneys' ability to regulate electrolytes and acid-base balance, leading toelevated potassium, low sodium, and accumulation of acids.
These substances can cause intrinsic AKI through direct nephrotoxicity.
What are nephrotoxins?
Rationale: Certain medications (NSAIDs, aminoglycosides, contrast dye) and toxins can directly damage kidney tubular cells, causing intrinsic AKI.
Managing these risk factors is a key nursing intervention for AKI prevention.
What are modifiable risk factors (hydration status, blood pressure, blood sugar, medication use)?
Rationale: Nurses play a crucial role in identifying and managing risk factors that can be modified toprevent AKI development.
These three main mechanisms can cause AKI.
What are reduced renal perfusion, direct injury, or obstruction?
Rationale: AKI pathophysiology involves either decreased blood flow to kidneys (pre-renal), directdamage to kidney tissue (intrinsic), or blockage of urine flow (post-renal).
These systemic symptoms—fatigue, confusion, nausea, and pruritus—occur due to this accumulation in AKI.
What is the oliguric phase?
Rationale: During the oliguric phase, urine output is significantly decreased, leading to retention offluids, electrolytes, and waste products.
Having this history significantly increases the risk of developing another episode of AKI.
What is previous AKI?
Rationale: Patients who have had AKI before have damaged kidneys with reduced reserve capacity, making them more vulnerable to subsequent episodes.
This nursing assessment finding indicates the recovery phase of AKI has begun.
What is increasing urine output (diuresis)?
Rationale: When urine output begins to increase during the diuretic phase, it signals that kidney function is recovering.
This phase of AKI involves low urine output and retention of fluid and waste products.
What is the oliguric phase?
Rationale: During the oliguric phase, urine output is significantly decreased, leading to retention offluids, electrolytes, and waste products.
This is why early detection of AKI improves patient outcomes.
What is the potential for reversibility with prompt treatment?
Rationale: AKI can often be reversed if identified and treated quickly, preventing progression to chronic kidney disease or the need for dialysis.