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首页> 外文期刊>Medicine. >Description of a transient proximal tubulopathy induced by amino acids perfusion in peptide receptor radionuclide therapy: A case report
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Description of a transient proximal tubulopathy induced by amino acids perfusion in peptide receptor radionuclide therapy: A case report

机译：氨基酸灌注在肽受体放射性核素治疗中诱导的瞬时近端微管疗法：案例报告

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Rationale: Peptide receptor radionuclide therapy (PRRT) with radiolabeled somatostatin analogs is a targeted internal radiotherapy method used to treat tumors expressing somatostatin receptors. Concomitant amino acids perfusion is systematically performed in order to inhibit the proximal tubular uptake of the radionuclide and thus prevent nephrotoxicity. Patient concerns: a 67-year-old woman with an intestinal neuroendocrine tumor with multiple lymphadenopathies and liver metastases. The patient displayed a carcinoid syndrome with flushes including facial erythrosis and paresthesia. During the treatment, the patient exhibited emesis and severe cramps. Diagnosis: We describe incomplete proximal tubulopathy induced by an amino acid therapy with [177Lu]-DOTA0-Tyr3-octreotate, which was reversible after treatment discontinuation. This diagnosis relies on metabolic acidosis, hypophosphatemia due to renal loss, tubular proteinuria and generalized aminoaciduria. Serum creatinine remained stable during and after the procedure. Interventions: PRRT with radiolabeled somatostatin analog ([177Lu]-DOTA0-Tyr3-octreotate). In order to prevent PRRT induced nephrotoxicity, we used a solution of 20 amino acids including 22 g/L Lysine and 16.8 g/L Arginine. Metoclopramide was successfully used to control vomiting. During the treatment and at the time of cramps, the blood sample showed hypophosphatemia at 0.3 mmol/L justifying intravenous phosphate supplementation. The cramps disappeared after this infusion. Outcomes: Hypophosphatemia with low TmPO4/GFR was observed as well as an increase in β2-microglobulinuria, urinary polyclonal light chains, and amino aciduria involving all amino acids . All these disturbances disappeared the day after the treatment and there was no acute kidney injury after 5 PRRT sessions. Six months after PRRT discontinuation, the patient had neither renal failure nor proximal tubulopathy . Aminoacid induced tubulopathy involves the main ligands of the megalin receptor. It has recently been demonstrated that cilastatin is a megalin inhibitor in the proximal tubule and therefore could represent an attractive alternative to amino acids for this purpose. Lessons: This case report is a description of a nephroprotective strategy in which partial, and transient tubulopathy is induced, in order to decrease proximal absorption of a tubulotoxic molecule. This little known strategy could be used to prevent proximal tubular injury caused by others megalin-mediated nephrotoxicity medication.
机译：基本原理：肽受体放射性核素治疗（PRRT）具有放射性标记的生长抑制素类似物是用于治疗表达生长抑素受体的肿瘤的靶内放射疗法方法。伴随氨基酸灌注以抑制放射性核素的近端管吸收，从而防止肾毒性。患者担忧：一名67岁女性，肠道神经内分泌肿瘤，具有多种淋巴结病和肝转移。患者展示了一种霉菌综合征，含有面部赤膜病和痛苦。在治疗过程中，患者表现出呕吐和严重的痉挛。诊断：通过用[177LU] -DOTA0-TYR3- octreotate描述由氨基酸治疗诱导的不完全近端微管疗法，在处理停止后可逆。这种诊断依赖于代谢酸中毒，由于肾脏损失，管状蛋白尿和广义氨基遗传症而缺血症。在程序期间和之后血清肌酐保持稳定。干预：PRRT与放射性标记的生长抑制菌素类似物（[177LU] -DOTA0-TYR3- octreetate）。为了防止PRRT诱导的肾毒性，我们使用了20个氨基酸的溶液，包括22g / L赖氨酸和16.8g / L精氨酸。甲氧氯丙酰胺成功用于控制呕吐。在治疗期间和在痉挛时，血液样品在0.3mmol / L标准的静脉内磷酸盐补充剂中显示出次磷血症。这种输液后痉挛消失了。结果：观察到低TMPO4 / GFR的次磷血症以及β2-微球蛋白尿，泌尿多克隆光链和涉及所有氨基酸的氨基酸尿的增加。所有这些干扰都在治疗后的一天消失，5个PRRT会话后没有急性肾脏损伤。 PRRT停止后六个月，患者既不肾衰竭也不近端微管病。氨基酸诱导的微管疗法涉及肿瘤受体的主要配体。最近已经证明，西兰拉汀是近端小管中的巨蛋白抑制剂，因此可以为此目的代表氨基酸的有吸引力的替代品。课程：本病例报告是对促进肾功能亢进症的肾红外药物疗法的描述，以降低管霉菌毒素的近端吸收。这种鲜为人知的策略可用于防止由其他巨大介导的肾毒性药物引起的近端管状损伤。

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