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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-
3
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