Refractory Hyperkalemia With Type 4 Renal Tubular Acidosis Associated With Tubulointerstitial Nephritis and Renal Papillary Necrosis Following Intravenous Lipid Emulsion Therapy in a Cat.

Carlos Torrente, Patricia Bou, Marta Riba, Dania Fernández, Luis Bosch
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Abstract

Objective: To describe type 4 renal tubular acidosis (RTA) and acquired pseudohypoaldosteronism in a cat with acute kidney injury (AKI) presumably associated with lipid infusion therapy for permethrin toxicosis.

Case summary: A 1-year-old neutered male cat presented with acute weakness, ataxia, fasciculations, tremors, hyperthermia, and seizures resulting from permethrin toxicosis. Upon admission, IV diazepam and 20% IV lipid emulsion were administered. Forty-eight hours after discharge, the patient was readmitted for lethargy, anorexia, polyuria, and vomiting. Upon admission, the patient exhibited signs of depression, dehydration, and moderate hypoperfusion. Initial assessments included CBC, serum biochemistry profile, and urinalysis. Further diagnostic workup and abdominal point-of-care ultrasound revealed clinical findings compatible with AKI. Laboratory analysis confirmed severe hyperkalemia, hyperchloremic normal anion gap metabolic acidosis, decreased fractional excretion of potassium, and decreased transtubular potassium gradient in the urine, all consistent with a diagnosis of secondary or acquired pseudohypoaldosteronism and type 4 RTA. Emergency medical treatment for hyperkalemia was initiated, but control of serum potassium concentration was unsuccessful. Peritoneal dialysis (PD) and general supportive care were initiated 24 h after admission. Mineralocorticoid support (continuous rate infusion of hydrocortisone) was initiated 4 days after admission due to suspected deficiency/resistance to aldosterone at the distal nephron. Unfortunately, despite PD, refractory hyperkalemia persisted, and the cat died 16 days after admission. Histopathological examination confirmed an acute and severe renal papillary necrosis.

New or unique information: To the authors' knowledge, this is the first description of type 4 RTA in a cat. Furthermore, we hypothesize that, according to the histopathological findings, this presentation of AKI may be secondary to the use of IV lipid emulsion for permethrin toxicosis, a complication not previously reported in the veterinary literature.

猫静脉脂质乳治疗后顽固性高钾血症伴4型肾小管酸中毒伴小管间质性肾炎和肾乳头状坏死
目的:研究猫急性肾损伤(AKI)与氯菊酯中毒脂质输注治疗相关的4型肾小管酸中毒(RTA)和获得性假性醛固酮减少症。病例总结:一只1岁的绝育公猫因氯菊酯中毒出现急性虚弱、共济失调、抽搐、震颤、高热和癫痫发作。入院时给予静脉滴注安定和20%静脉滴注脂乳。出院后48小时,患者因嗜睡、厌食、多尿和呕吐再次入院。入院时,患者表现出抑郁、脱水和中度灌注不足的症状。初步评估包括全血细胞计数、血清生化特征和尿液分析。进一步的诊断检查和腹部护理点超声显示临床表现符合AKI。实验室分析证实严重的高钾血症、高氯血症、正常阴离子间隙代谢性酸中毒、少量钾排泄减少、尿中经短突钾梯度降低,所有这些都符合继发性或获得性假性醛固酮增多症和4型RTA的诊断。对高钾血症进行紧急医疗治疗,但未能成功控制血清钾浓度。入院后24小时开始腹膜透析(PD)和一般支持治疗。由于怀疑远端肾元醛固酮缺乏/抵抗,入院后4天开始矿化皮质激素支持(持续输注氢化可的松)。不幸的是,尽管PD,难治性高钾血症持续存在,猫在入院后16天死亡。组织病理学检查证实急性严重肾乳头状坏死。新的或独特的信息:据作者所知,这是第一次描述猫的4型RTA。此外,根据组织病理学结果,我们假设AKI的出现可能是继发于使用IV脂质乳剂治疗氯菊酯中毒,这是一种兽医文献中未报道的并发症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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