18.104.22.168 Acute pyelonephritis and/or acute allergic
interstitial nephritis affect the interstitial portion
of the kidney (Beeman & Emerson, 2013).
22.214.171.124 Caused by vasculitis or an emboli
(Beeman & Emerson, 2013).
3.1.1 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).
3.1.2 Asfar and colleagues discovered that
patients with chronic hypertension,
prevented the development of severe AKI
during sepsis (Ostermann & Liu, 2017).
3.1.3 Many studies found that within the perioperative
setting, there is a link between intraoperative
hypotension and the development of
postoperative AKI (Ostermann & Liu, 2017).
3.2.1 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).
3.2.2 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).
126.96.36.199 Basically all immune
cells are involved in
processes of AKI
(Ostermann & Liu, 2017).
3.2.3 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).
3.3 Tubular Cell
3.3.1 Microcirculatory dysfunction results in tubular cell injury as well as
direct exposure to substances in the filtrate (Ostermann & Liu, 2017).
3.3.2 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).
188.8.131.52 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).
4.1.1 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).
184.108.40.206 Nutritional therapy involves potassium, phosphate,
and sodium restrictions with adequate amounts of
protein (Wood, 2014).
4.2.1 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).