Acute Kidney Injury: Etiology and Pathophysiology

• Acute Kidney Injury (AKI) can be caused by prerenal, intrarenal, and postrenal factors.

Etiology and Pathophysiology

• Prerenal causes involve factors reducing systemic circulation and renal blood flow, such as severe dehydration and heart failure, which decreases cardiac output.
• Prerenal conditions decrease glomerular filtration rate and cause oliguria.
• Intrarenal causes involve conditions causing direct kidney tissue damage, such as prolonged ischemia and exposure to nephrotoxins.
• Hemoglobin released from hemolyzed RBCs and myoglobin released from necrotic muscle cells also contribute to intrarenal AKI.
• Acute tubular necrosis (ATN) results from ischemia, nephrotoxins, or sepsis, and is potentially reversible. Severe ischemia disrupts the basement membrane, as nephrotoxic agents cause necrosis of tubular epithelial cells.
• Postrenal causes include mechanical obstruction of outflow, such as benign prostatic hyperplasia, prostate cancer, calculi, trauma, extrarenal tumors, and bilateral ureteral obstruction.

AKI Paradigm

• Prerenal AKI can result from dehydration and heart failure, including cardiorenal syndrome, also liver failure, including hepatorenal syndrome.
• Intrarenal AKI can result from intrinsic renovascular disease (hypertensive emergency, and small vessel vasculitis and TTP / HUS), glomerular disease and post-infectious glomerulonephritis.
• Ureteral obstruction, neurogenic bladder, urinary tract infection, medications and benign prostatic hypertrophy (BPH) can cause postrenal AKI.

RIFLE Classification

• The RIFLE classification categorizes AKI into Risk, Injury, Failure, Loss, and End-stage renal disease.
• Risk (R) involves an abrupt decrease (1-7 days) of greater than 25% in GFR or a sustained serum creatinine increase of 1.5 times baseline.
• Injury (I) is defined by a greater than 50% decrease in GFR or a serum creatinine increase of 2 times baseline.
• Failure (F) is marked by a greater than 75% decrease in GFR or a serum creatinine increase of 3 times or greater, or serum creatinine above 4 mg%.
• Loss (L) involves irreversible AKI or persistent AKI lasting more than four weeks.
• End-stage renal disease (E) is present when the condition lasts for more than three months.

Clinical Manifestations

• In the oliguric phase, urinary output is typically less than 400 mL/day, occurring within 1 to 7 days after the initial injury and lasting 10 to 14 days.
• Urinalysis may show casts, RBCs, and WBCs.
• Hypovolemia may worsen AKI; Decreased urine output causes fluid retention, leading to distended neck veins, bounding pulse, edema, and hypertension.
• Fluid volume, if overloaded, can lead to heart failure, pulmonary edema, and pericardial or pleural effusions.
• Metabolic acidosis occurs due to impaired kidney excretion of hydrogen ions, decreasing serum bicarbonate production leading to severe acidosis and Kussmaul respirations.
• There is increased excretion of sodium; hyponatremia can lead to cerebral edema.
• Potassium excess occurs due to impaired kidney's ability to excrete potassium, with increased risk during massive tissue trauma, often asymptomatic, but can cause ECG changes.
• Hematologic disorders such as leukocytosis and accumulation of waste products, leading to elevated BUN and serum creatinine levels are also manifestations.
• Neurologic disorders such as fatigue, difficulty concentrating, seizures, stupor, and coma can also manifest.
• During the diuretic phase, daily urine output increases to 1 to 3 L and may reach 5 L or more, and will need monitoring for hyponatremia, hypokalemia, and dehydration.
• Recovery, kidney function may take up to 12 months to stabilize.

Diagnostics

• Diagnostic studies include thorough history, serum creatinine, urinalysis, kidney ultrasonography, renal scan, CT scan, and renal biopsy.
• MRI with gadolinium contrast medium and MRA with gadolinium contrast medium can be contraindicated for patients with contrast-induced nephropathy (CIN) or nephrogenic systemic fibrosis.

Interprofessional Care

• Management involves ensuring adequate intravascular volume and cardiac output with prescribed fluids.
• Loop diuretics such as furosemide (Lasix), and osmotic such as mannitol, might be prescribed.
• Fluid intake in oliguric patients, as well as hyperkalemia, is typically monitored, and treated with insulin, sodium bicarbonate, calcium carbonate, or sodium polystyrene sulfonate (Kayexalate), if needed.
• Indications for renal replacement therapy (RRT) include volume overload, elevated serum potassium level, metabolic acidosis, BUN level greater than 120 mg/dL (43 mmol/L), significant change in mental status, as well as pericarditis, pericardial effusion, or cardiac tamponade.
• Renal replacement therapy options also include peritoneal dialysis (PD), although it's not frequently used.
• Continuous renal replacement therapy (CRRT) involves cannulation of an artery and vein.
• Nutritional therapy is vital: maintain adequate caloric intake primarily through carbohydrates and fat, limit protein, restrict sodium, increase dietary fat, and consider enteral nutrition.

Nursing Management

• Nursing assessments include measuring vital signs, fluid intake, and output, examining urine, and assessing general appearance.
• Observing dialysis access site, checking mental status, the oral mucosa, lung sounds, heart rhythm, laboratory values, and diagnostic test results, as well.
• Daily weight is measured, electrolyte balance is monitored, and significant fluid losses replaced.
• Aggressive diuretic therapy is provided for fluid volume overload.
• Nephrotoxic drugs are to be used sparingly, and the nurse should assess for hypervolemia or hypovolemia, observing for potassium and sodium disturbances.
• Meticulous aseptic technique practiced, along with skin care and mouth care.

This lesson explores the etiology and pathophysiology of Acute Kidney Injury (AKI), including prerenal, intrarenal, and postrenal factors. It covers conditions reducing renal blood flow, direct kidney tissue damage, and mechanical obstruction of urinary outflow. Acute tubular necrosis (ATN) is also discussed.