ArticleCEN case reports2025
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.
Article in CEN case reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Erythrocytes as immunomodulators in trauma: orchestrating clearance pathways, inflammation, and organ injury.Frontiers in immunology · 2026Review
- Article
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9 authors.
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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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