Regulatory: Acute Kidney Injury (AKI)

Pro-inflammatory cytokines are released in response to cell injury, leukocytes and macrophages drawn to the kidneys.

Pathophysiology/Etiology

Symptoms

Labs/Diagnostics

Risk Factors

Complications

Collaborative Treatment

Dizziness, lightheaded, orthostatic hypotension

Dry skin & mucous membranes

Decreased UO

Edema, swelling

SOB

AMS -- Confusion

Nausea

Tachycardia, irregular HR

Etiology: Fluid volume depletion leading to renal hypoperfusion

Hyperkalemia, cardiac disturbances

Blood test measuring Creatinine & BUN

Cr increased >0.3 mg/dL from baseline

Urine specific gravity >1.020

UO <0.5 mL/kg per hr

High ratio, 20:1

Reduced Na excretion <20 mEq/L

HTN

Diabetes

CKD

Sepsis, hypovolemia

Acid-base changes, metabolic acidosis

Fluid volume overload, pulmonary edema

Careful fluid resuscitation to increase circulating volume & restore renal perfusion

Monitor UO and fluid overload

Address underlying cause interfering with renal perfusion

Pharmacological

Vasopressors (Norepinephrine) - increase BP to restore GFR

Reduced GFR

Inotropes (Dobutamine) - improve heart contractility

Dialysis to remove waste from blood

Monitor electrolytes, especially potassium & calcium

Balance electrolytes - polystyrene sulfonate, calcium infusion

Trauma or illness causes systemic hypotension, vasodilation and decreased renal perfusion (onset)

Pressure gradient necessary to filter fluids and maintain GFR unable to occur. Accumulation of nitrogenous wastes, retention of fluid and sodium to promote fluid balance (oliguric).

Lack of blood flow damages microvascular endothelial cells, smooth muscle. Also causes tubular obstruction and injury. Cell death and necrosis in the kidney occurs.

Pro-inflammatory cytokines are released in response to cell injury, leukocytes and macrophages drawn to the kidneys.

With blood flow restoration, gradual return of UO and stabilization of Cr, BUN, and electrolytes (diuretic phase). Over time kidneys kidneys are able to regenerate endothelial cells and repair microvascular damage to restore GFR (recovery).

Prolonged fluid restoration leads to sustained cell destruction and permanently decreased renal function. Microvascular atrophy, tubule loss, and fibroblast deposits. Can lead to CKD.