Decitabine-induced kidney thrombotic microangiopathy with glomerular crescents formation and tubular necrosis: A case report.

INTRODUCTION

Chemotherapeutic agents of direct cell damage play a role in initiating thrombotic microangiopathy (TMA), however still being underdiagnosed. Decitabine (DAC) is a pyrimidine analogue of the nucleoside cytidine, which can lead to injury to endothelium. Biopsy-proven DAC-induced kidney injury is rare.

PATIENT CONCERNS

A 47-year-old Chinese man with membranous nephropathy presented recurrent edema and acute kidney injury after a 3-day course of low dose DAC infusion because of cyclophosphamide-relating thrombocytopenia.

DIAGNOSIS

Laboratory data revealed nephrotic syndrome, hematuria, renal glycosuria and hypokalemia with hyperchloridemia. Renal pathological findings revealed TMA with secondary glomerular crescents formation (28%), partial foot process effacement and acute tubular necrosis. A diagnosis of DAC-induced renal TMA was considered.

INTERVENTIONS

As DAC had been timely discontinued before admission, the patient only received supportive treatment.

OUTCOMES

The patient achieved rapid remission of acute kidney injury after DAC withdrawal, and his serum creatinine further decreased to normal level after 6 months.

CONCLUSION

Careful monitoring of renal function especially serum creatinine should be emphasized during DAC treatment.