Page 956 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
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Urinary system                                      931



  VetBooks.ir  RENAL DISEASES

          ACUTE KIDNEY INJURY
                                                         common toxins encountered. These drugs can cause
                                                         AKI by directly damaging tubular cells with con-
          Definition/overview                            sequent tubular cell necrosis. NSAID-related AKI,
          AKI is defined as a sustained decrease in GFR lead-  and drug-related AKI in general, is more likely to
          ing  to azotaemia  and  fluid  and  acid–base  distur-  cause permanent damage compared with other
          bances. It is caused by decreased renal perfusion   causes of AKI.
          (pre-renal or haemodynamic failure), primary renal   Glomerulonephritis is mostly associated with
          dysfunction (intrinsic renal failure) or obstruction of   CKD but can also be associated  with subacute or
          urine flow (post-renal failure). Pre-renal failure and   acute kidney injury. It is characterised by intraglo-
          renal failure are the most common.             merular inflammation and cellular proliferation.

          Aetiology/pathophysiology                      Clinical presentation
          Any cause of renal hypoperfusion such as dehydra-  The most common clinical complaints are anorexia,
          tion from GI disease, heavy exercise or blood loss   abdominal  discomfort,  dehydration, dullness,  pig-
          may lead to pre-renal AKI. This is more likely if   menturia and PU/PD. Concurrent disease may result
          the  hypoperfusion  is  prolonged.  Nephrotoxins   in additional clinical abnormalities. Alterations
          such us aminoglycoside antimicrobials, oxytetra-  in vital parameters depend on the underlying dis-
          cycline, non-steroidal anti-inflammatory drugs   ease that caused the AKI. These may be normal,
          (NSAIDs), endogenous pigments (myoglobin or    increased or, rarely, decreased. In addition to depres-
          haemoglobin), heavy metals, vitamins D or K  and   sion and anorexia, uraemia can cause encephalopa-
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          plant toxins (onions, red maple leaves and, rarely,   thy, although this is uncommon. Urine production
          acorn  poisoning) are often associated with intrinsic   in horses with AKI is variable. Horses may be anuric
          renal failure, especially in horses with concurrent   (no urine production), oliguric (decreased urine pro-
          renal hypoperfusion. Glomerulonephritis, intersti-  duction), normouric or polyuric (increased urine
          tial nephritis and renal microvascular thrombosis   production). Oedema may be present with anuric or
          are more complex entities of intrinsic renal  failure.   oliguric renal failure. Mucous membranes are usually
          Post-renal failure may occur from functional or   injected or hyperaemic. Laminitis may be present as
          mechanical urinary tract obstruction or urinary   a result of AKI or the underlying disease process.
          tract rupture. Other,  less  frequent, post-renal
          causes of AKI can be intraluminal (e.g. bilateral  Differential diagnosis
          renal calculi, papillary necrosis, coagulated blood,   Differential diagnoses include shock, urinary
          bladder carcinoma and fungus) or extraluminal   tract  calculi, sabulous urolithiasis, cystitis, bladder
          (e.g. retroperitoneal fibrosis, colorectal malignancy   paralysis, peritonitis, visceral pain and cantharidin
          and trauma/haematoma).                         toxicosis.
            Structural and biochemical changes that result
          in vasoconstriction, desquamation of tubular cells,  Diagnosis
          intraluminal tubular obstruction and transtubular   Diagnosis  is  based  on  history,  clinical  signs,  serum
          backflow of the glomerular filtrate are pathophysi-  biochemical analysis and urinalysis. Palpation p/r
          ological mechanisms that characterise AKI. Several   should be  performed  where  possible to  assess renal
          clinical conditions can lead to kidney ischaemia as a   size, the presence of peri-renal oedema and renal pain
          result of either extrarenal or intrarenal factors that   or the presence of obstruction in the ureters, blad-
          compromise renal blood flow. In addition, toxins   der or urethra. Typically, kidneys will be increased in
          that lead to tubular necrosis share many pathophysi-  size in AKI (Fig. 7.14) and decreased in CKD.
          ological features with ischaemic AKI. Amino-     Increases in blood urea and creatinine are invari-
          glycoside antimicrobials and NSAIDs are the most   ably present. Hypocalcaemia can also be associated
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