Acute kidney injury due to glomerular haematuria and obstructive erythrocyte casts associated with thrombocytopaenia and thin basement membrane disease: a case report

BMC Nephrology

John P. Dowling¹  Ian Simpson¹  Susan Brown²  Andy K. H. Lim³ 

[1] Department of Anatomical Pathology, Monash Medical Centre, 246 Clayton Road, Clayton 3168, VIC, Australia;Department of General Medicine, Monash Medical Centre, 246 Clayton Road, Clayton 3168, VIC, Australia;Department of Medicine, Monash University, Monash Health, 246 Clayton Road, Clayton 3168, VIC, Australia

关键词: Chronic kidney disease;    Thin basement membrane disease;    Erythrocyte casts;    Haematuria;    Thrombocytopaenia;    Acute kidney injury;   

Others  :  1231080
DOI  :  10.1186/s12882-015-0176-4

 received in 2015-07-15, accepted in 2015-10-22,  发布年份 2015

【 摘 要 】

Background

Acute kidney injury due to glomerular bleeding has been described with IgA nephropathy and supratherapeutic warfarin anticoagulation. There is usually demonstrable tubular obstruction by erythrocyte casts associated with acute tubular injury. Although severe thrombocytopaenia increases the risk of bleeding, most cases of haematuria have been ascribed to non-glomerular or urological bleeding without a direct link to acute kidney injury. We describe a patient with acute kidney injury due to glomerular bleeding and tubular injury related to severe thrombocytopaenia, who was subsequently found to have thin basement membrane disease.

Case presentation

A 56 year old man presented with macroscopic haematuria, acute kidney injury and a platelet count of 35 × 10 ⁹ /L, in the absence of anticoagulation. Urinalysis demonstrated an active urinary sediment. His kidney biopsy demonstrated extensive intraluminal erythrocyte casts associated with acute tubular injury, along with haemosiderin deposition suggestive of recurrent glomerular bleeding. There was no histological evidence of glomerular pathology but electron microscopy analysis demonstrated thin basement membrane disease and effacement of podocyte foot processes. During long term follow-up, thrombocytopaenia and intermittent haematuria persisted. At 9 months, the patient progressed to Stage 5 chronic kidney disease with the development of gross renal atrophy.

Conclusion

Recurrent macroscopic haematuria may be a risk factor for progressive renal injury in patients with thin basement membrane. The mechanism may be due to recurrent acute kidney injury from glomerular bleeding leading to repeated tubular damage. In the absence of anticoagulation, severe thrombocytopaenia may be a risk factor for heavy glomerular bleeding and acute kidney injury in these patients.

【 授权许可】

   
2015 Lim et al.

【 图 表 】

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