Al Zabali Saeed, Alseneidi Sarah, Faqeehi Hassan, Albatati Sawsan, Al Anazi Abdulkarim
Pediatric Nephrology, King Fahad Medical City, Riyadh, SAU.
Cureus. 2024 Sep 23;16(9):e70016. doi: 10.7759/cureus.70016. eCollection 2024 Sep.
Atypical hemolytic uremic syndrome (aHUS) is a life‑threatening condition characterized by microangiopathic hemolytic anemia, thrombocytopenia, as well as acute kidney injury (AKI). It can occur primarily due to complement gene mutations or secondary to another underlying condition. Several cases with Wilms' tumor gene 1 (WT1) mutations that presented with aHUS have been reported. Here, we report four cases of children diagnosed with WT1 mutations and presented initially with aHUS. There are two boys and two girls who presented with thrombotic microangiopathy (TMA), high lactate dehydrogenase, fragmented red blood cell (RBCs), and severe hypertension. All of them were anuric from the first presentation. Therapy with C5 inhibitors was initiated immediately and was associated with hematological remission without renal recovery. Renal replacement therapy (RRT) was started for all of the patients. A renal biopsy was conducted on two patients and showed global glomerulosclerosis. A genetic study identified pathogenic mutations in the WT1 gene. Two of the patients became dialysis dependent, and two patients underwent renal transplantation without the recurrence of aHUS. Our case series emphasizes that a diagnosis of WT1 mutation can be considered in children with aHUS with severe renal manifestations without a response to C5 inhibitors and with global glomerulosclerosis on renal biopsy. To our knowledge, this is the first report of a series of cases of WT1 mutations in pediatric patients presenting with clinical manifestation manifestations of aHUS. This unique finding highlights an association between HUS and WT1 mutation.
非典型溶血性尿毒症综合征(aHUS)是一种危及生命的疾病,其特征为微血管病性溶血性贫血、血小板减少以及急性肾损伤(AKI)。它主要可因补体基因突变而发生,也可继发于另一种潜在疾病。已有数例报告显示,伴有aHUS表现的威尔姆斯瘤基因1(WT1)突变病例。在此,我们报告4例诊断为WT1突变且最初表现为aHUS的儿童病例。有2名男孩和2名女孩,他们均表现为血栓性微血管病(TMA)、高乳酸脱氢酶、破碎红细胞(RBC)以及严重高血压。他们从首次就诊时就无尿。立即开始使用C5抑制剂进行治疗,治疗后血液学缓解但肾功能未恢复。所有患者均开始接受肾脏替代治疗(RRT)。对2例患者进行了肾活检,结果显示为全球肾小球硬化。一项基因研究确定了WT1基因中的致病突变。其中2例患者依赖透析,2例患者接受了肾移植,且aHUS未复发。我们的病例系列强调,对于患有aHUS且有严重肾脏表现、对C5抑制剂无反应且肾活检显示全球肾小球硬化的儿童,可考虑诊断为WT1突变。据我们所知,这是首例关于一系列表现出aHUS临床表现的儿科患者WT1突变病例的报告。这一独特发现凸显了HUS与WT1突变之间的关联。