Mahlum Lisa M, Rollings Christopher, Basseches Jessica, Bracker Kiko
Emergency and Critical Care Department, Angell Animal Medical Center (AAMC), Boston, MA 02130, USA.
J Vet Emerg Crit Care (San Antonio). 2010 Dec;20(6):601-10. doi: 10.1111/j.1476-4431.2010.00596.x.
To describe a case of presumptive secondary pseudohypoaldosteronism (PHA) in a cat with urinary tract infection and chronic urethral obstruction. The obstruction was believed to have resulted from sloughed urinary bladder mucosa secondary to pressure necrosis.
A 5-year-old, 4 kg, castrated male Siamese cat presented for vomiting and stranguria. Medical history included a perineal urethrostomy for urethral obstruction. Physical examination revealed a large, painful, nonexpressible urinary bladder. Point-of-care testing demonstrated electrolyte derangements consistent with a postrenal azotemia and metabolic acidosis. Results of urine culture was positive for bacterial growth. Diagnostic imaging revealed presence of retroperitoneal fluid, marked urinary bladder wall thickening, bilateral hydroureter, mild bilateral pyelectasia, and small nephroliths. The patient was treated for a urinary tract obstruction and infection. In the 3 weeks following initial discharge, the patient was evaluated on multiple occasions for lethargy, intermittent vomiting, inappropriate urination, and progressive polyuria and polydipsia. Although the urinary bladder was easily expressed during repeat examinations, it was persistently distended and subjectively thickened upon palpation. Repeat ultrasound of the urinary tract showed evidence of sloughed tissue in the bladder lumen, likely secondary to chronic urethral obstruction and pressure necrosis. A cystotomy was performed to remove the necrotic tissue, and a revised perineal urethrostomy was done due to a partial urethral stricture. Bladder biopsies were obtained at this time. Postoperatively, the cat was reported by the owners to be urinating normally but continued to be polyuric and polydipsic in the week following discharge. One week after surgery, the cat presented in hypovolemic shock with laboratory findings consistent with a presumptive diagnosis of secondary PHA.
PHA has not been reported previously in a cat. This case report suggests that aldosterone resistance should be considered in cats with consistent laboratory findings and a history of documented obstructive uropathy and urinary tract infection.
描述一例患有尿路感染和慢性尿道梗阻的猫疑似继发性假性醛固酮减少症（PHA）的病例。据信，梗阻是由压力性坏死继发的膀胱黏膜脱落所致。
一只5岁、体重4千克的去势雄性暹罗猫因呕吐和排尿困难就诊。病史包括因尿道梗阻行会阴尿道造口术。体格检查发现膀胱肿大、疼痛且无法排空。即时检测显示电解质紊乱，符合肾后性氮质血症和代谢性酸中毒。尿培养结果显示有细菌生长。诊断性影像学检查发现腹膜后有积液、膀胱壁明显增厚、双侧输尿管积水、双侧轻度肾盂积水以及小肾结石。该患者接受了尿路梗阻和感染的治疗。在首次出院后的3周内，该患者因嗜睡、间歇性呕吐、排尿不当以及进行性多尿和烦渴多次接受评估。尽管在重复检查时膀胱很容易排空，但它持续膨胀，触诊时感觉质地增厚。尿路的重复超声检查显示膀胱腔内有脱落组织的迹象，可能继发于慢性尿道梗阻和压力性坏死。进行了膀胱切开术以清除坏死组织，并因部分尿道狭窄进行了改良会阴尿道造口术。此时获取了膀胱活检组织。术后，主人报告猫排尿正常，但出院后一周仍持续多尿和烦渴。术后一周，这只猫出现低血容量性休克，实验室检查结果符合继发性PHA的疑似诊断。
此前尚未有猫发生PHA的报道。本病例报告提示，对于实验室检查结果一致且有记录的梗阻性尿路病和尿路感染病史的猫，应考虑醛固酮抵抗。
