In the surrounding of the pancreatic tail has been observed band-like thicknesses in the direction of the spleen, peritoneum, fundus, prerenal
and adrenal fascia, segmental narrowing of the splenic artery as well as obstruction and fibrosis of the splenic vein with numerous collateral vessels.
In our case, the sequence of events was probably development of prerenal
failure due to the natriuretic effect of trimethoprim, resulting in further accumulation of trimethoprim and increasing the risk of hyperkalaemia.
The etiologies of AKI are categorized as prerenal
(decreased renal perfusion), intrinsic renal (pathology affecting vessels, glomeruli, tubules, or interstitium), and post-renal (obstruction of urinary flow).
The ratio is usually elevated (> 20: 1) in prerenal
conditions and in some patients with obstructive uropathy, also in patients with significant upper gastrointestinal bleeding.
In addition, the patients were compared in terms of the presence of polymorphism according to the factors considered important for the severity of inflammation, which were >1 attack, presence of pseudocyst, increasing prerenal
fascia thickness on CT, and fluid collection in two or more areas.
The patient's acute kidney injury was attributed to dehydration with a fractional excretion of sodium (FENa) less than 1% suggestive of prerenal
. His kidney function was expected to improve with volume replacement and DKA treatment.
We suggest that dogs with leishmaniosis and moderate to high increases in SDMA concentrations without proteinuria should be carefully evaluated for other diseases or pathogenic mechanisms which could lead to prerenal
impairment of renal perfusion.
AKI is usually due to decrease in effective circulation, which if not corrected leads to acute tubular necrosis.
The patient's initial AKI appeared prerenal
with a urinary FeNa of 0.5% and FeUrea of 37%.
Urinary biochemistry has been utilized since the 1970s, mainly to help differentiate two conditions, namely, reversible (prerenal
) or transient AKI (T-AKI), from an established AKI, acute tubular necrosis (ATN), or persistent AKI (P-AKI) .
Laboratory results revealed leukocytosis, prerenal
azotemia, elevated liver enzymes, and mildly elevated lipase (Table 1).
The clinical picture was suggestive of prerenal
AKI (FeNa < 1%) and renal tubular acidosis (RTA).