Acute Kidney Injury (AKI) Definition

Definition of AKI

• Acute Kidney Injury (AKI) is a rapid loss of renal function due to damage to the kidneys, causing a wide range of life-threatening metabolic and fluid & electrolyte imbalances.
• Accepted criterion for AKI: 50% or greater increase in serum creatinine above baseline (normal= less than 1 mg/dL) or oliguria (less than 0.5 mL/kg/h).

Pathophysiology of AKI

• Impaired blood flow → hypoperfusion to kidney, resulting in decreased GFR.
• Actual damage to kidney tissue, including acute tubular necrosis (ATN) and intratubular obstruction.
• Obstruction distal to the kidney by renal calculi, strictures, blood clots, etc.

Categories of AKI

• Prerenal (hypoperfusion of kidney): results from hypovolemia, hypotension, and reduced cardiac output.
• Intrarenal (actual damage to kidney tissue): results from acute tubular necrosis, intratubular obstruction, and changes in glomerular permeability.
• Postrenal (obstruction to urine flow): results from obstruction distal to the kidney.

Causes of AKI

• Prerenal Failure: hemorrhage, gastrointestinal losses, renal losses, cardiogenic shock, myocardial infarction, anaphylaxis, and vasodilation.
• Intrarenal Failure: aminoglycoside antibiotics, angiotensin-converting enzyme inhibitors, heavy metals, nonsteroidal anti-inflammatory drugs, radiopaque contrast agents, solvents and chemicals, acute glomerulonephritis, and infectious processes.
• Postrenal Failure: urinary tract obstruction, including benign prostatic hyperplasia, blood clots, calculi, and tumors.

Phases of AKI

• Initiation: begins with the initial insult and ends when oliguria develops, lasting around 10-14 days.
• Oliguria: characterized by a decrease in urine output, increased serum urea, creatinine, uric acid, organic acids, potassium, and magnesium.
• Diuresis: a gradual increase in urine output, signaling the start of glomerular filtration recovery.
• Recovery: laboratory values stabilize and eventually decrease, indicating improved renal function, which may take 3-12 months.

Laboratory Values

• Prerenal azotemia: decreased amount of sodium in the urine (less than 20 mEq/L).
• Intrarenal azotemia: urinary sodium levels greater than 40 mEq/L with urinary casts.

Evaluation and Diagnosis

• Evaluation for changes in urine output, including hematuria and low specific gravity.
• Ultrasonography, CT or MRI scan, and serum KFT to diagnose AKI.### Assessment and Diagnosis
• Decreased GFR, oliguria, and anuria can lead to hyperkalemia, which can cause dysrhythmias
• Metabolic acidosis and increased blood phosphate concentrations can occur
• Low calcium levels can result from decreased absorption from the intestine and as a compensatory mechanism for elevated blood phosphate levels

Treatment Objectives

• Prevent complications
• Restore normal chemical balance
• Eliminate the underlying cause
• Maintain fluid balance
• Provide renal replacement therapy

Medical Management

• Monitor CVP and hourly urine output in ICU patients
• Treat hypotension promptly
• Continually assess renal function
• Prevent and treat infections
• Treat wounds, burns, and sepsis
• Prevent infections from ascending in the urinary tract
• Relieve obstruction in postrenal AKI
• Provide supportive therapy in intrarenal AKI

Pharmacologic Therapy

• Diuretics such as Mannitol and Furosemide (Lasix) may be used
• Dialysis may be initiated to prevent complications
• Administer cation-exchange resins (Sodium Polystyrene Sulfonate, Kayexalate) orally or by retention enema for hyperkalemia
• IV dextrose 50%, insulin, and calcium may be used for hemodynamically unstable patients
• Sodium bicarbonate therapy or dialysis may be used for metabolic acidosis

Monitoring Fluid and Electrolyte Balance

• Monitor serum electrolyte levels and physical indicators of complications
• Monitor cardiac function and musculoskeletal status closely for signs of hyperkalemia
• IV solutions must be carefully selected based on the patient's fluid and electrolyte status
• Monitor cardiac function and musculoskeletal status closely for signs of hyperkalemia

Nutritional Therapy

• Weigh daily
• Provide a high-carbohydrate diet to spare protein for tissue healing
• Restrict foods and fluids containing potassium or phosphorus
• Provide a high-protein, high-calorie diet in the diuretic phase
• Resume activities gradually following the diuretic phase

Nursing Management

• Assess for urine output, edema, distention of the jugular veins, alterations in heart sounds and breath sounds, and difficulty in breathing
• Report immediately to the physician and prepare for emergency treatment if severe fluid and electrolyte disturbances occur
• Provide physical and emotional support to the patient and family
• Monitor pulmonary function and promote it through deep breathing and coughing exercises
• Prevent infection through asepsis and careful skin care
• Provide skin care through frequent turning, bathing with cool water, and keeping the skin clean and moisturized