Back to Search Start Over

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.

Authors :
Kaneko S
Murata R
Hoshimoto A
Hisada R
Harano M
Anno E
Hagiwara S
Imai E
Nagata M
Source :
CEN case reports [CEN Case Rep] 2024 Oct 17. Date of Electronic Publication: 2024 Oct 17.
Publication Year :
2024
Publisher :
Ahead of Print

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.<br /> (© 2024. The Author(s), under exclusive licence to Japanese Society of Nephrology.)

Details

Language :
English
ISSN :
2192-4449
Database :
MEDLINE
Journal :
CEN case reports
Publication Type :
Academic Journal
Accession number :
39417987
Full Text :
https://doi.org/10.1007/s13730-024-00942-7