Acute Kidney Injury

Acute Kidney Injury

1. RIFLE Classification for Staging AKI

   • Risk
     • Serum creatinine increased by x1.5 or GFR decreased by 25% with urine output <0.5ml/kg/hr for 6 hours (Beeman & Emerson, 2013)
   • Injury
     • Serum creatinine increased x2 or GFR decreased by 50% with urine output <0.5 ml/kg/hr for 12 hrs (Beeman & Emerson, 2013)
   • Failure
     • Serum creatinine increased x3 or GFR decreased by 75% or serum creatinine >4mg/dl with acute rise >0.5mg/dl, with urine output <0.3ml/kg/hr or anuria for 12 hrs (Beeman & Emerson, 2013)
   • Loss
     • Persistent acute kidney failure; complete loss of kidney function >4 weeks (Beeman & Emerson, 2013)
   • End Stage Kidney Disease
     • Complete loss of function >3 months (Beeman & Emerson, 2013)

2. Pathology

   • Disruption of blood flow
     • In prerenal AKI, adequate blood supply is unable to reach the kidneys thus reducing the glomerular perfusion pressure
       • Certain drugs may cause vasoconstriction of afferent arterioles such as NSAIDs, or vasodilation of efferent arterioles such as ACE inhibitors and cause a decrease in perfusion pressure (Beeman & Emerson, 2013)
       • If adequate perfusion is restored relatively quickly, then normal renal function will resume in one to two days.
         • Prolonged prerenal injury will result in hypoxic renal cells, which after a few hours will progress to an intrinsic kidney injury of acute tubular necrosis (Beeman & Emerson, 2013).
   • Disruption of outflow
     • Postrenal injury that blocks output of both kidneys is uncommon, but if prolonged may lead to acute tubular necrosis and potentially permanent kidney damage (Beeman & Emerson, 2013).
   • Intrinsic Kidney Injury
     • Of the four types, acute tubular necrosis is most common, and is often associated with intrinsic vascular injury. Many causes and often other types of AKI may lead to ATN.
       • Decrease in GFR
         • Renal blood flow is decreased from 30 to 50 percent, so blood is shunted into the cortex
           • Prostoglandins and leukotrines released as well as sympathetic nervous system stimulation, all contribute to vasoconstriction and further reduced GFR (Beeman & Emerson, 2013).
         • Hypoxia triggers an inflammation response
           • After perfusion is restored, inflammation cells start to help repair nearby cells, however cells further away continue to suffer from hypoxia and die, resulting in further GFR decline (Beeman & Emerson, 2013)
             • Shed cells and inflammatory cells build up in the tubular filtrate and further obstruct urine outflow. This increases pressure, and will force filtrate into the interstitial space and bloodstream.
               • If damage is prolonged and widespread, it is possible for the patient to develop end-stage renal disease (Beeman & Emerson, 2013)
       • Stages of Acute Tubular Necrosis
         • Prodromal Phase
           • Where the injury has occurred, normal or decreasing urine output, and rising levels of serum creatinine and BUN (Beeman & Emerson, 2013)
         • Postoliguric Phase
           • The recovery phase where values gradually return to normal, with tendencies for fluid volume deficiency as urine output is significantly increased. Recovery time may vary from 1 week to 1 year. Patients with a history of ATN may experience progressive loss of kidney function, especially if they had ATN as a child (Beeman & Emerson, 2013)
         • Oliguric Phase
           • Most patients tend to be oliguric, though severe AKI patients may be anuric. Decreased urine output, metabolic acidosis, electrolyte imbalance (particularly hyperkalemia), and hypervolemia (Beeman & Emerson, 2013).

3. Types of Acute Kidney Injury

   • Prerenal
     • Absolute decrease in circulating volume which can be caused by hemorrhage, dehydration, or burns (Beeman & Emerson, 2013)
     • Relative decrease in circulating volume, which can be caused by distributive, third-spacing, deem, and decreased cardiac output.
       • Eventually leading to cardiogenic shock, dysrhythmias, cardiac tamponde, heart failure and myocardial infarction (Beeman & Emerson, 2013)
     • Primary renal hemodynamic abnormalities due to drug-induced impairment of renal auto regulation or occlusion or stenosis or the renal artery (Beeman & Emerson, 2013)
   • Postrenal
     • Caused by kinked or obstructed catheters, benign prostatic hyperplasia, strictures, or intra-abdominal tumours (Beeman & Emerson, 2013)
   • Intrarenal/Intrinsic
     • Tubular (acute tubular necrosis)
       • Ischemic
         • Typically caused by prolonged prerenal failure, transfusion reactions, and rhabdomyolysis (Beeman & Emerson, 2013)
       • Nephrotoxic
         • Certain antimicrobials, prolonged post-renal failure, radiographic contrast media, recreational drugs, environmental agents, and snake/insect venom possess nephrotoxic effects (Beeman & Emerson, 2013)
     • Glomerular
       • Acute glomerulonephritis
     • Interstitial
       • Acute pyleonephritis and/or acute allergic interstitial nephritis affect the interstitial portion of the kidney (Beeman & Emerson, 2013)
     • Vascular
       • Caused by vasculitis or an emboli (Beeman & Emerson, 2013).

4. Etiology

   • Most often nephrotoxic drugs are the cause of an AKI (Meersch et al., 2017)
     • Nonsteroidal antiinflammatory drugs, angiotensin-converting enzyme inhibitors, andangiotensin II receptor blockers
   • Risk factors
     • Comorbidities such as aging population, diabetes, chronic kidney disease, COPD, heart failure (Meersch, Volmering, & Zabock, 2017)/
     • Acute medical conditions such as sepsis, major surgery, hemodynamic instability, and mechanical ventilation (Meersch et al., 2017)
   • Surgical/interventional measures related to AKI development.
     • notropic support, vasopressors, aortic cross-clamping, selective renal ischemia, bleeding complications, and transfusion of blood products (Meersch et al., 2017)

5. Collaborative Care

   • Diagnostic
     • Requires treatment of the precipitating cause, fluid restriction, nutritional therapy, calcium supplements or phosphate-binding agents, initiation of renal replacement therapy, and total parenteral nutrition if indicated (Wood, 2014).
       • Nutritional therapy involves potassium, phosphate, and sodium restrictions with adequate amounts of protein (Wood, 2014)
   • Collaborative Therapy
     • Involves a history and physical exam, identification of precipitating causes, serum creatinine and BUN levels, serum electrolytes, a urinalysis, renal ultrasound, renal scans, CT scans, and retrograde pyelogram if indicated (Wood, 2014).

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