成功治疗与covid -19相关的塌陷性肾小球病:22个月的随访

Pulkit Gandhi, Caoimhe Sorcha Dowling, Anjali Satoskar, Ankur Shah
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摘要

COVAN (covid -19相关肾病)一词已被用于描述SARS-CoV-2感染个体的局灶节段性肾小球硬化症(FSGS)。这有助于将其与COVID-19患者的大多数急性肾损伤病例区分开来,后者通常由急性肾小管损伤引起。确切的病理生理机制尚不清楚,但可能涉及促炎细胞因子,如1型干扰素,它们被认为可以增加肾小球上皮细胞中APOL1基因的表达。这引发了一系列炎症事件,导致上皮细胞和底层足细胞受损。COVAN的治疗以一般支持措施为中心,包括饮食钠限制、高脂血症和高血压的优化、RAAS阻断和水肿利尿。支持在COVAN中使用糖皮质激素的数据有限;然而,足细胞病的机制与hiv相关肾病相似,APOL1基因突变患者的疾病负担较高。根据以往的经验,在选定的患者中,用糖皮质激素治疗hiv是有益和安全的。在这里,我们报告了一例COVAN,成功地用糖皮质激素治疗,在22个月的随访中,患者仍然完全缓解(蛋白尿)
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Successful treatment of COVID-19-associated collapsing glomerulopathy: 22 months of follow-up.

Successful treatment of COVID-19-associated collapsing glomerulopathy: 22 months of follow-up.

Successful treatment of COVID-19-associated collapsing glomerulopathy: 22 months of follow-up.

The term COVAN (COVID-19-associated nephropathy) has been used to describe collapsing focal segmental glomerulosclerosis (FSGS) in individuals who have been infected with the SARS-CoV-2. This helps differentiate it from the majority of cases of acute kidney injury in COVID-19 patients, which are typically caused by acute tubular injury. The exact pathophysiology is unclear but is proposed to involve pro-inflammatory cytokines such as type 1 interferons, which are thought to increase expression of the APOL1 gene in glomerular epithelial cells. This triggers a cascade of inflammatory events that cause damage to the epithelia and underlying podocytes. The treatment of COVAN is centered on general supportive measures including dietary sodium restriction, optimization of hyperlipidemia and hypertension, RAAS blockade, and diuresis for edema. There is limited data to support the use of glucocorticoids in COVAN; however, the mechanism of podocytopathy is similar to that in HIVAN (HIV-associated nephropathy), with high disease burden in those with APOL1 gene mutation. Based on previous experience, treatment of HIVAN with glucocorticoids is beneficial and safe in selected patients. Here we present a case of COVAN which was successfully treated with glucocorticoids, and at 22-month follow-up patient remained in full remission (proteinuria < 1,000 mg/g) with stable kidney function.

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