Acute Kidney Injury

Med/Surg II exam 3

What defines Acute Kidney Injury (AKI), and what core functional change occurs in the kidneys?

A sudden, usually reversible decline in overall kidney function characterized by a rapid reduction in the Glomerular Filtration Rate (GFR), impairing waste excretion and fluid/electrolyte balance.

What defines prerenal AKI, and what percentage of hospitalized AKI cases does it account for?

Reduced renal blood flow (hypoperfusion) without structural tissue damage to the kidneys; accounts for 65% to 75% of all hospitalized AKI cases.

What defines intrarenal AKI, and what is the #1 cause of intrarenal tissue damage?

Direct structural damage to the renal parenchyma (cortex and medulla). Acute Tubular Necrosis (ATN) is the #1 cause, driven by ischemia or nephrotoxic agents. Accounts for 35% of AKI cases.

What defines postrenal AKI, and what mechanical factors cause it?

Mechanical obstruction of urine outflow below the kidneys, increasing intra-tubular pressure; caused by BPH, pelvic masses, blood clots, calculi/stones, or neurogenic bladder. Accounts for 5% of AKI cases.

What criteria define Stage 1 AKI under KDIGO guidelines?

Serum creatinine 1.5 to 1.9 times baseline OR urine output < 0.5 mL/kg/hr for 6 to 12 hours.

What criteria define Stage 2 AKI under KDIGO guidelines?

Serum creatinine 2.0 to 2.9 times baseline (or an increase >= 0.3 mg/dL) OR urine output < 0.5 mL/kg/hr for >= 12 hours.

What criteria define Stage 3 AKI under KDIGO guidelines?

Serum creatinine 3.0 times baseline (or >= 4.0 mg/dL), initiation of renal replacement therapy (dialysis), urine output < 0.3 mL/kg/hr for >= 24 hours, or anuria for >= 12 hours.

What is cardiorenal syndrome, and why does it occur in AKI?

An acute, reciprocal dysfunction where acute renal failure accelerates acute heart failure or myocardial infarction due to fluid retention and vascular congestion.

How does rhabdomyolysis cause intrarenal AKI?

Massive muscle breakdown releases myoglobin into the bloodstream, which precipitates and obstructs renal tubules (accounting for 7–15% of AKI cases).

What is the global annual incidence of AKI, and what percentage of ICU admissions develop AKI?

AKI affects 209 million people worldwide annually and develops in 37% of intensive care unit (ICU) admissions.

Why are adults ages 75 and older at significantly elevated risk for AKI?

Due to age-related physiological declines in baseline GFR combined with a higher prevalence of chronic multi-system comorbidities.

What chronic comorbidities increase a client's susceptibility to AKI by causing renal vascular compromise?

Diabetes mellitus (types 1 and 2), hypertension, and hyperlipidemia.

How does severe COVID-19 infection precipitate AKI?

Via systemic cytokine-driven inflammation, direct viral renal tissue invasion, and hemodynamic instability/hypotension.

What occupational and environmental exposures serve as key etiological risk factors for AKI?

Exposure to agricultural pesticides and performing heavy physical labor in extreme heat leading to severe dehydration.

What common over-the-counter and prescription pain medications impair renal autoregulation?

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs), such as ibuprofen, naproxen, and ketorolac.

What anti-hypertensive medication classes can reduce GFR and precipitate prerenal/intrarenal AKI?

ACE inhibitors (e.g., lisinopril) and Angiotensin Receptor Blockers (ARBs) (e.g., losartan).

What antimicrobials are well-known nephrotoxic agents requiring close blood level monitoring?

Aminoglycosides (e.g., gentamicin) and Vancomycin.

What diagnostic imaging agent is a major cause of hospital-acquired intrarenal AKI?

Iodinated contrast media (contrast dye).

What gastrointestinal and psychiatric medications are identified as potential nephrotoxic drivers of AKI?

Proton pump inhibitors (PPIs) (omeprazole, pantoprazole) and Lithium.

NCLEX CRITICAL NURSING ACTION: What must the nurse immediately do upon confirming an AKI diagnosis regarding medications?

Audit the MAR and collaborate with the provider/pharmacist to discontinue all nephrotoxic medications and adjust renally excreted drug dosages.

What clinical signs distinguish early prerenal hypovolemic AKI?

Oliguria, hypotension, tachycardia, dizziness, dry mucous membranes, and skin tenting.

What physical assessment findings indicate fluid volume overload in intrarenal AKI?

Rapid weight gain, hypertension, peripheral edema, lung crackles, an S3 gallop, and jugular vein distention (JVD).

What physical sign on cardiac auscultation indicates uremic pericarditis?

A pericardial friction rub, caused by uremic waste inflammation of the pericardial sac.

What is uremic frost, and what causes it in severe kidney failure?

White crystalline urea deposits left on the skin after sweat evaporates, caused by severe uremic waste accumulation.

NEURO RED FLAGS: What neurological manifestations signal uremic encephalopathy in AKI?

Progressive lethargy, severe confusion/disorientation, asterixis (flapping hand tremor), and seizures.

Which symptoms commonly seen in Chronic Kidney Disease (CKD) are uncommon in acute AKI presentation?

Polyuria, nocturia, and pruritus.

What GFR threshold indicates an emergency need for renal replacement therapy (dialysis)?

A GFR < 15 mL/min/1.73 m².

What diagnostic test helps differentiate prerenal hypoperfusion from intrarenal Acute Tubular Necrosis (ATN)?

A fluid challenge (infusing IV fluids); if urine output and kidney function improve, the injury is confirmed as prerenal.

What laboratory test evaluates acid-base imbalance resulting from the kidneys' inability to excrete hydrogen ions?

Arterial Blood Gases (ABGs), which show metabolic acidosis.

What initial non-invasive imaging study is performed to rule out postrenal urinary obstruction?

A renal ultrasound or KUB (kidneys, ureters, bladder) radiograph.

Why is hyperkalemia the most life-threatening electrolyte emergency in AKI?

High serum potassium disrupts cardiac conduction, triggering lethal arrhythmias or cardiac arrest.

What is the physiological purpose of IV Calcium Gluconate in acute hyperkalemia emergency treatment?

It stabilizes the cardiac cell membrane to protect the heart against fatal arrhythmias (does NOT lower potassium levels).

How does administering IV Regular Insulin paired with IV Dextrose lower serum potassium?

Insulin shifts potassium out of the bloodstream and into cells; dextrose prevents hypoglycemia.

How does inhaled Albuterol assist in treating acute hyperkalemia?

As a beta-2 agonist, albuterol acts synergistically with insulin to drive potassium into cells.

How does Sodium Polystyrene Sulfonate (Kayexalate) lower serum potassium?

It exchanges sodium ions for potassium ions in the intestine, allowing potassium to be excreted in stool.

CONTRAINDICATION: When is Sodium Polystyrene Sulfonate (Kayexalate) strictly contraindicated?

In clients with bowel obstruction, paralytic ileus, or impaction, due to the risk of intestinal necrosis.

How do loop diuretics (furosemide/Lasix) assist in managing hyperkalemia and fluid overload?

They inhibit sodium and potassium reabsorption in the loop of Henle, increasing urinary excretion of fluid and potassium.

CONTRAINDICATION: When is furosemide (Lasix) contraindicated in AKI?

In clients with anuria (zero urine production).

DAILY WEIGHT SAFETY: What daily weight increase must a nurse report to the provider immediately?

A weight gain of 3 lb (1.36 kg) or more in 1 day (indicating acute fluid retention).

What non-pharmacological positioning intervention helps relieve dyspnea in an AKI client with pulmonary edema?

Elevating the head of the bed (HOB) to maximize diaphragm movement and lung expansion.

What daily dietary potassium restriction is enforced for a client with AKI?

Restricted to 40 mEq/day.

What daily dietary phosphorus restriction is enforced for a client with AKI?

Restricted to 800 mg/day.

What daily caloric intake recommendation is required for AKI clients, and why?

35 to 50 kcal/kg/day, to provide adequate energy and prevent catabolism of body muscle protein.

What patient teaching safety measure prevents injury in a client receiving loop diuretics for AKI?

Instruct the client to change positions slowly to prevent orthostatic hypotension and falls.

NCLEX Recognize Cues: What physical exam cues indicate deteriorating fluid volume overload in AKI?

Rapid weight gain, worsening peripheral edema, new lung crackles, JVD, S3 gallop, and hypertension.

NCLEX Analyze Cues: What laboratory cluster signals an acute uremic emergency?

Elevated BUN/creatinine, GFR < 15, serum potassium > 5.0 mEq/L, and metabolic acidosis on ABGs.

NCLEX Prioritize Hypotheses: What is the #1 nursing priority when managing a client in acute AKI?

Correcting fluid volume overload and life-threatening hyperkalemia.

NCLEX Take Action: What emergency drug combination is administered first for hyperkalemia with ECG changes?

IV Calcium Gluconate (for cardiac membrane stabilization) followed by IV Regular Insulin + IV Dextrose.

NCLEX Take Action: What nursing interventions prevent skin breakdown in a client with uremic frost?

Provide frequent skin hygiene with lukewarm water (avoid harsh soaps), trim fingernails to prevent scratching, apply emollients, and turn/reposition q2h.

NCLEX Evaluate Outcomes: What clinical findings indicate effective treatment of Acute Kidney Injury?

Declining serum creatinine/BUN toward baseline, normal serum potassium (3.5–5.0 mEq/L), urine output > 0.5 mL/kg/hr, clear lung sounds, and stable daily weights.