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Acute kidney injury
/content/chapter/10.22233/9781910443354.chap21
Acute kidney injury
- Authors: Sarah Crilly Guess and Gregory F. Grauer
- From: BSAVA Manual of Canine and Feline Nephrology and Urology
- Item: Chapter 21, pp 246 - 253
- DOI: 10.22233/9781910443354.21
- Copyright: © 2017 British Small Animal Veterinary Association
- Publication Date: January 2017
Abstract
Acute kidney injury is most often caused by an ischaemic, toxic or infectious insult and may result in acute renal failure, which is usually defined as an acute onset of azotaemia superimposed on an inability to concentrate urine. This chapter looks at pathophysiology; aetiology; risk factors; early detection of AKI; evaluation of patients with suspected AKI; and therapy.
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Figures
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21.1
In this schematic representation of the four phases of acute kidney injury (AKI), normal proximal tubular epithelial cells are represented in the first row. In phase 1, the infectious/ischaemic/toxic insult causes increased presence of inflammatory mediators, and decreased intracellular adenosine triphosphate (ATP), leading to phase 2, when increased intracellular sodium (Na+) and calcium (Ca2+) concentrations and further destruction of the brush border occur. The basement membrane may also become exposed as cells are desquamated. Leucocytes migrate to the site of damage in phase 2. Phase 3 shows ongoing damage (apoptosis) and early repair. Phase 4 is when epithelial cells are further repaired and proliferate to cover the exposed basement membrane. This figure demonstrates the continuum of AKI that occurs over these four phases. K+ = potassium. (Courtesy of Mal Rooks Hoover, CMI, Kansas State University) © 2017 British Small Animal Veterinary Association
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21.1
In this schematic representation of the four phases of acute kidney injury (AKI), normal proximal tubular epithelial cells are represented in the first row. In phase 1, the infectious/ischaemic/toxic insult causes increased presence of inflammatory mediators, and decreased intracellular adenosine triphosphate (ATP), leading to phase 2, when increased intracellular sodium (Na+) and calcium (Ca2+) concentrations and further destruction of the brush border occur. The basement membrane may also become exposed as cells are desquamated. Leucocytes migrate to the site of damage in phase 2. Phase 3 shows ongoing damage (apoptosis) and early repair. Phase 4 is when epithelial cells are further repaired and proliferate to cover the exposed basement membrane. This figure demonstrates the continuum of AKI that occurs over these four phases. K+ = potassium. (Courtesy of Mal Rooks Hoover, CMI, Kansas State University)
/content/figure/10.22233/9781910443354.chap21.ch21fig2
21.2
Photomicrograph of the renal cortex of a cat with ethylene glycol toxicosis. The proximal renal tubules frequently contain semi-transparent, refractile calcium oxalate crystals associated with renal tubular epithelial attenuation and loss (arrowed) with regeneration (*) and infiltrates of lymphocytes and plasma cells in the interstitial spaces. (Courtesy of Chanran K. Ganta BVSc PhD DACVP, Kansas State University Veterinary Diagnostic Laboratory) © 2017 British Small Animal Veterinary Association
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21.2
Photomicrograph of the renal cortex of a cat with ethylene glycol toxicosis. The proximal renal tubules frequently contain semi-transparent, refractile calcium oxalate crystals associated with renal tubular epithelial attenuation and loss (arrowed) with regeneration (*) and infiltrates of lymphocytes and plasma cells in the interstitial spaces. (Courtesy of Chanran K. Ganta BVSc PhD DACVP, Kansas State University Veterinary Diagnostic Laboratory)
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21.5
Electrocardiogram (ECG) showing absent P waves, bradycardia and tall T waves, suggestive of hyperkalaemia. (Paper speed: 25 mm/s; heart rate: 40 beats/min; 1 cm = 1 mV). (Courtesy of Dr Justin Thomason, Kansas State University) © 2017 British Small Animal Veterinary Association
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21.5
Electrocardiogram (ECG) showing absent P waves, bradycardia and tall T waves, suggestive of hyperkalaemia. (Paper speed: 25 mm/s; heart rate: 40 beats/min; 1 cm = 1 mV). (Courtesy of Dr Justin Thomason, Kansas State University)