Vol 2-2 Case Report

Clinicopathological Description of a Urinary Bladder Leiomyosarcoma in a Dog

Derick S Alves1, Fabiana Elias2, Helvécio L S Junior3, Guilherme Thizen3, Rômulo S A Eloi4, Carlos E Fonseca-Alves1*

1Institute of Health Science, Paulista University – UNIP, Bauru – SP, Brazil.

2Universidade Federal da Fronteira Sul (UFFS), Realeza, PR, Brazil.

3Departamento de Medicina Veterinária, Faculdade UPIS, Brasília, DF - Brazil.

4HistoPato-Análise Anatomopatológica Veterinária, Brasília, DF, Brazil.

Urinary bladder cancer is uncommon in dogs, corresponding to 1% of all reported canine malignancies. Smooth muscle neoplasms can be benign (leiomyomas) or malignant (leiomyosarcoma) and are rare in humans and animals. As the incidence of urinary bladder leiomyosarcoma in dogs is low, our report presents the clinical and pathological aspects of primary urinary bladder leiomyosarcoma in a dog. A 10-year-old boxer breed dog was referred to the veterinary hospital presenting with dysuria for a month, appetite loss for seven days, abdominal distension for two weeks, and anuria for the last three days. After a physical examination and laboratory tests, an abdominal mass was diagnosed, and a laparotomy was performed. During the surgery, it was found that the urinary bladder neoplasm occupied the bladder trigone region, involving the ureters, and causing obstruction. The urinary bladder was reconstructed successfully, and the patient was kept under post-operative evaluation. In the post-operative recovery, an acute kidney disease was observed, which was irresponsive to the clinical treatment. Due to the advanced stage of the disease and the non-response to treatment, euthanasia was performed after surgery, and the animal was sent for necropsy. In this case, leiomyosarcoma was manifested as an expansive, low infiltration, and non-metastatic disease, causing obstruction of the ureters and consequent hydronephrosis.

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Vol 2-2 Original Research Article

Lysophosphatidic Acid Prevents Ischemia Reperfusion Injury but does not Prevent Tubular Dysfunction

Sabrina R. Gonsalez1, Aline L. Cortes1, Mayara A. Romanelli1, Paula Mattos-Silva2, Andrew C. Curnow3, Minolfa C. Prieto3,4, Marcelo Einicker-Lamas2, Lucienne S. Lara1

1Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

2Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

3Department of Physiology, School of Medicine, Tulane University School of Medicine, New Orleans, LA, USA

4Tulane Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA, USA

Lysophosphatidic acid (LPA) protects the kidneys from tissue ischemic reperfusion injury (IRI), but its impact on renal function is primarily limited to glomerular function. We estimated the status of renal function by a complete glomerular and tubular functional analysis to test the hypothesis that LPA treatment during ischemia-reperfusion (I/R) protects renal function by attenuating IRI. Male Wistar rats were subjected to bilateral kidney I/R. Along with ischemia, LPA was administered. LPA increased levels of plasma LPA, downregulated LPA2R, prevented interstitial fibronectin and TGF-β1 accumulation, and prevented a decrease in glomerular filtration rate (GFR). I/R increased urine volume and proteinuria and decreased fractional Na+ excretion (FENa) and urine osmolality. These effects were not prevented by LPA. The reduction in FENa was attributed to disruption in tubular Na+ transport and downregulation of protein kinase C (PKC) activity. LPA treatment maintained (Na++K+)ATPase activity to the control level, due to a sustained sensitivity to PLC/PKC pathway. Na+-ATPase activity was insensitivity to LPA treatment. This ineffectiveness was associated with downregulation of LPA2R, resulting in low FENa. Altogether, LPA treatment maintained normal kidney structure and prevented the reduction of glomerular function. However, even in the setting of preserved GFR, impaired tubular function may present a high risk for silent progression of kidney disease.

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