Kidney Week

Abstract: PUB220

AKI Associated with Anticoagulant-Related Nephropathy in a Newly Diagnosed IgA Nephropathy

Session Information

• Publication Only

Category: Glomerular Diseases

• 1203 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

• Chalkia, Aglaia, Nephrology Department, Hippokration General Hospital, Athens, Greece

Aglaia Chalkia,

• Kapota, Athanasia, Nephrology Department, Hippokration General Hospital, Athens, Greece

Athanasia Kapota,

• Agelis, Georgios, Nephrology Department, Hippokration General Hospital, Athens, Greece

Georgios Agelis,

• Mpora, Margarita, Nephrology Department, Hippokration General Hospital, Athens, Greece

Margarita Mpora,

• Kourniotis, Dimitris, Nephrology Department, Hippokration General Hospital, Athens, Greece

Dimitris Kourniotis,

• Alexakou, Zoe, Nephrology Department, Hippokration General Hospital, Athens, Greece

Zoe Alexakou,

• Damianaki, Katerina, Nephrology Department, Hippokration General Hospital, Athens, Greece

Katerina Damianaki,

• Petras, Dimitrios I., Nephrology Department, Hippokration General Hospital, Athens, Greece

Dimitrios I. Petras,

Introduction

Anticoagulant-related nephropathy (ARN) is a type of acute kidney injury (AKI) that may be caused by anticoagulation with warfarin and other anticoagulants. It is an underestimated cause of AKI with poor renal prognosis. AKI is probably resulting from glomerular hemorrhage and the characteristic pathologic findings consist of obstruction of renal tubules by red blood cell casts, which do not contain Tamm-Horsfall protein.

Case Description

A 58-year-old Caucasian man presented with AKI stage 3 (serum creatinine 5.9mg/dL) complaining of macroscopic hematuria. Two months ago, he underwent aortic valve replacement with a mechanical valve and he began taking acenocoumarol as an anticoagulant agent (serum creatinine 0.9mg/dL). He also presented INR 2.2, several dysmorphic erythrocytes in urinary sediment and 24-h urinary protein excretion 5g/day. The renal biopsy revealed mild mesangial hypercellularity, acute tubular necrosis with occlusive red blood cell casts and interstitial inflammation. The immunofluorescence presented mild mesangial deposits of IgA (2+) and C3 (1+). We consider that the cause of AKI was anticoagulant-related nephropathy rather than IgA nephropathy because there was no history of prior infection and the presence of numerous RBC tubular casts could not be explained just by these glomerular findings (mild mesangial proliferation, as well as mild deposits of IgA by immunofluorescence). Due to the severe interstitial nephritis, pos prednisolone 1mg/Kg/daily was added to his treatment, with a gradual reduction in 4 months and acenocoumarol was replaced by tinzaparin. After 1year renal function remains stable at creatinine level 2.5mg/dL, proteinuria <1gr/24h, without microscopic hematuria.

Discussion

This case report highlights an unusual severe cause of AKI “anticoagulant-related nephropathy”, in which the majority of patients remains hemodialysis dependent. Patients with underlying glomerulopathies, associated with hematuria are predisposed to be risk factors. Considering the poor renal prognosis, it highlights the necessity for close vigilance of renal function, as well as, urine sediment in patients, who begin on anticoagulation, especially with pre-existing renal diseases, including glomerulopathies and those with glomerular hyperfiltration.