Acute Kidney Injury (AKI)

RIFLE Classification for Staging AKI
1. Risk
  1. Serum creatinine increased x1.5 or GFR decreased by 25%, with urine output <0.5ml/kg/hr for 6hrs (Beeman & Emerson, 2013).
2. Injury
  1. Serum creatinine increased x2 or GFR decreased by 50%, with urine output <0.5ml/kg/hr for 12hrs (Beeman & Emerson, 2013).
3. Failure
  1. 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 12hrs (Beeman & Emerson, 2013).
4. Loss
  1. Persistent acute kidney failure; complete loss of kidney function>4 weeks (Beeman & Emerson, 2013).
5. End-stage kidney disease
  1. Complete loss of kidney function >3 months (Beeman & Emerson, 2013).
Types of Acute Kidney Injury
1. Prerenal
  1. Absolute decrease in circulating volume, which can be causes by hemorrhage, dehydration or burns (Beeman & Emerson, 2013).
  2. Relative decrease in circulating volume, which can be caused by distributive shock, third-spacing, deem, and decreased cardiac output.
    1. Eventually leading to cariogenic shock, dysrhythmias, cardiac tamponde, heart failure and myocardial infarction (Beeman & Emerson, 2013).
  3. Primary renal hemodynamic abnormalities due to drug-induced impairment of renal auto regulation or occlusion or stenosis of the renal artery (Beeman & Emerson, 2013).
2. Postrenal
  1. Caused by kinked or obstructed catheters, benign prostatic hyperplasia, strictures, or intraabdominal tumours (Beeman & Emerson, 2013).
3. Intrarenal/Intrinsic
  1. Tubular (acute tubular necrosis)
    1. Ischemic
      1. Typically caused by prolonged prerenal failure, transfusion reactions, and rhabdomyolysis (Beeman & Emerson, 2013).
    2. Nephrotoxic
      1. Certain antimicrobials, prolonged post-renal failure, radiographic contrast media, recreational drugs, environmental agents, and snake/insect venom possess neprotoxic affects (Beeman & Emerson, 2013).
  2. Glomerular
    1. Acute glomerulonephritis
  3. Interstitial
    1. Acute pyelonephritis and/or acute allergic interstitial nephritis affect the interstitial portion of the kidney (Beeman & Emerson, 2013).
  4. Vascular
    1. Caused by vasculitis or an emboli (Beeman & Emerson, 2013).
Pathophysiology
1. Haemodynamic Instability
  1. Association between the time spent in relative hypotension and the development of AKI in patients with sepsis was shown in the FINNAKI study (Ostermann & Liu, 2017).
  2. Asfar and colleagues discovered that patients with chronic hypertension, prevented the development of severe AKI during sepsis (Ostermann & Liu, 2017).
  3. Many studies found that within the perioperative setting, there is a link between intraoperative hypotension and the development of postoperative AKI (Ostermann & Liu, 2017).
2. Inflammation
  1. Inflammation and the need for leukocytes are key mediators of all phases of endothelial and tubular cell injury within the invitation and maintenance phase of AKI (Ostermann & Liu, 2017).
  2. As soon as a endothelial or tubular epithelial cell injury occurs, an immune response is triggered. It consists of activation of inflammatory cells and recruitment and invasion of WBCs (Ostermann & Liu, 2017).
    1. Basically all immune cells are involved in these pathophysiological processes of AKI (Ostermann & Liu, 2017).
  3. Systematic inflammation can contribute to the pathogenesis of AKI - for example, elevated levels of interleukin 6 have been linked to the development of AKI, cardiac surgery, and severely ill patients with acute respiratory distress (Ostermann & Liu, 2017).
3. Tubular Cell Injury
  1. Microcirculatory dysfunction results in tubular cell injury as well as direct exposure to substances in the filtrate (Ostermann & Liu, 2017).
  2. Structural changes such as: apical membrane blabbing, opening of tight junctions, loss of polarity, cell detachment from the basement membrane and cell swelling are all manifestations of tubular cell injury (Ostermann & Liu, 2017).
    1. Damage to the mitochondria may also occur, an increase in mitochondrial fragmentation encourages the excess production of ROS, release of cytokines and cellular death. All contributing to the further progression of AKI, therefore, tubular cells have a diverse role in AKI (Ostermann & Liu, 2017).
4. Renal Venous Congestion
5. Tubular Obstruction
6. Auto-Immune Processes
7. Hypersensitivity Immune Reaction
Collaborative Care
1. Diagnostic
  1. 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).
    1. Nutritional therapy involves potassium, phosphate, and sodium restrictions with adequate amounts of protein (Wood, 2014).
2. Collaborative Therapy
  1. 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).
Etiology
1. Risk factors
  1. Comorbidities such as, aging population, diabetes, chronic kidney disease, COPD, heart failure (Meersch, Volmering, & Zarbock, (2017).
  2. Acute medical conditions such as, sepsis, major surgery, hemodynamic instability, and mechanical ventilation (Meersch et al., 2017).
2. Most often nephrotoxic drugs are the cause of AKI (Meersch et al., 2017).
3. Surgical/interventional measures related to AKI development
  1. Inotropic support, vasopressors, aortic cross-clamping, selective renal ischemia, bleeding complications, and transfusion of blood products (Meersch et al., 2017).
By Natasha Sharp

Próximo

Acute Kidney Injury (AKI)

Descrição

Resumo de Recurso

Anexos de mídia

Semelhante

	Criado por Natasha Sharp quase 7 anos atrás