Macroscopic hematuria-associated severe acute kidney injury triggered by kidney stone formation in a patient with thin basement membrane and no history of microscopic hematuria.

IF 1 Q4 UROLOGY & NEPHROLOGY CEN Case Reports Pub Date : 2024-10-17 DOI:10.1007/s13730-024-00942-7
Shuzo Kaneko, Ririko Murata, Ainori Hoshimoto, Rina Hisada, Makiko Harano, Emi Anno, So Hagiwara, Eri Imai, Michio Nagata
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Abstract

Macroscopic hematuria (MH)-associated acute kidney injury (AKI) is a rare condition that causes acute tubular damage due to severe glomerular bleeding with MH. A 66-year-old Japanese woman with no significant past medical history was referred for severe kidney injury with oliguric MH. Her prior medical checkup results showed no occult blood in her urine. Seven days earlier, she had experienced transient severe acute right lumbar back pain. On admission, her serum urea nitrogen was 147 mg/dL, serum creatinine (sCr) 18.3 mg/dL, urinary red blood cells (RBCs) > 100/hpf, urinary protein 28.8 g/gCr, with no hydronephrosis in either kidney, but two stones were found in the right kidney and right ureteropelvic junction. At the start of her hemodialysis, the patient was treated with high-dose steroids because of suspected rapidly progressive glomerulonephritis. A renal biopsy of the left kidney showed acute tubular injury with massive RBC casts filling the tubular lumen. Glomerulitis was not detected, but electron microscopy revealed diffuse glomerular thin basement membrane (TBM). Despite immediate steroid discontinuation, the patient's renal function and MH improved, and she was weaned from hemodialysis. The stones resolved 2 months after onset, but microscopic hematuria persisted for 7 months post-onset. The sCr level was fixed at 1.1 mg/dL 20 months post-onset. This is the first report of MH-AKI in a TBM without the risk of MH-AKI development, such as bleeding tendency or iron overload. In this TBM, a colic attack of the renal urinary tract induced glomerular bleeding, and intolerance to hematuria may have caused severe tubular damage.

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一名基底膜较薄且无镜下血尿病史的患者因肾结石形成引发的镜下血尿相关性重度急性肾损伤。
镜下血尿(MH)相关性急性肾损伤(AKI)是一种罕见的疾病,由于 MH 引起严重的肾小球出血而导致急性肾小管损伤。一名 66 岁的日本女性因严重肾损伤伴少尿血尿转诊,既往无明显病史。她之前的体检结果显示尿液中没有隐血。七天前,她出现了一过性急性右腰背痛。入院时,她的血清尿素氮为 147 mg/dL,血清肌酐(sCr)为 18.3 mg/dL,尿红细胞(RBC)> 100/hpf,尿蛋白为 28.8 g/gCr,两个肾脏均无肾积水,但在右肾和右输尿管盆腔交界处发现了两颗结石。在开始进行血液透析时,患者被怀疑患有快速进展性肾小球肾炎,因此接受了大剂量类固醇治疗。左肾的肾活检显示急性肾小管损伤,大量红细胞铸型充斥肾小管管腔。虽然没有发现肾小球炎,但电子显微镜检查发现了弥漫性肾小球薄基底膜(TBM)。尽管立即停用了类固醇,但患者的肾功能和MH均有所改善,并脱离了血液透析。结石在发病 2 个月后消退,但显微镜下血尿持续了 7 个月。发病后 20 个月,sCr 水平稳定在 1.1 mg/dL。这是第一例在没有出血倾向或铁超载等 MH-AKI 发病风险的 TBM 中发生 MH-AKI 的报告。在该 TBM 中,肾泌尿道绞痛发作诱发了肾小球出血,对血尿的不耐受可能造成了严重的肾小管损伤。
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来源期刊
CEN Case Reports
CEN Case Reports UROLOGY & NEPHROLOGY-
CiteScore
1.90
自引率
0.00%
发文量
80
期刊介绍: Clinical and Experimental Nephrology (CEN) Case Reports is a peer-reviewed online-only journal, officially published biannually by the Japanese Society of Nephrology (JSN).  The journal publishes original case reports in nephrology and related areas.  The purpose of CEN Case Reports is to provide clinicians and researchers with a forum in which to disseminate their personal experience to a wide readership and to review interesting cases encountered by colleagues all over the world, from whom contributions are welcomed.
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