Dr RIVINDU WIJAYARATNE1, Dr BRYONY BEAL1, Dr LUCY BIRTWISTLE1, Dr NEHA CHANDRASEKAR1, Dr AKSHAY ATHAVALE1,2,3
1Department Of Renal Medicine, Gosford Hospital, New South Wales Health, Gosford, Australia, 2School of Medicine and Public Health, University of Newcastle, New South Wales, Australia, Newcastle, Australia, 3Faculty of Medicine and Health, Macquarie University, New South Wales, Australia, Macquarie Park, Australia
Biography:
Rivindu Wijayaratne is a resident medical officer at Central Coast LHD with a strong interest in nephrology stemming from his time in medical school. He had undertaken a renal rotation at Gosford Hospital where he had expanded his knowledge base. Rivindu had worked in association with the quality improvement committee within the central coast aiming to improve quality standards locally. Rivindu plans to train towards basic physician training post his residency training.
Background:
Gemcitabine is a known cause of drug induced thrombotic microangiopathy (DITMA), often associated with severe acute kidney injury (AKI). Drug discontinuation and supportive care is the mainstay of treatment. Treatments including plasma exchange, fresh frozen plasma, corticosteroids and eculizumab demonstrate varying success rates.
We report a case of gemcitabine induced thrombotic microangiopathy (TMA) in a patient with bladder cancer occurring two months after commencement of therapy. Clinical care was complicated by severe AKI requiring dialysis and septic shock.
Case Report:
A 51-year-old female with metastatic bladder cancer receiving gemcitabine and cisplatin, radical cystectomy with ileal conduit presented to hospital with right-sided flank pain. Initial investigations showed creatinine 107 umol/L, estimated glomerular filtration rate (eGFR) of 52 ml/min/1.73m², haemoglobin of 88g/L and platelet count 90×10⁹/L. Renal imaging demonstrated an 8mm obstructive right-sided ureteric calculus and atrophic left kidney.
Post treatment of initial poly-microbial septic shock, she developed progressive DITMA with worsening oligoanuric kidney injury with creatinine 335 umol/L and eGFR 12 ml/min/1.73m². Thrombocytopaenia with platelets 14×10⁹/L and schistocytes on blood film were noted. Antiglobulin test was weakly positive, ADAMTS13 was 42% and Shiga toxin was negative.
Treatment included frequent red cell and platelet transfusion, hemodialysis and broad-spectrum antibiotics. Although eculizumab was considered, heamatologic parameters spontaneously improved following gemcitabine discontinuation. Kidney function improved and dialysis was ceased. Three months post discharge, creatinine was 106 umol/L, eGFR 52 ml/min/1.73m², haemoglobin 105 g/L and platelet count 259×10⁹/L.
Conclusion:
This case highlights gemcitabine associated TMA post septic shock causing severe dialysis requiring AKI. While underlying mechanisms of DITMA are not well understood, clinicians should be aware of the self-limiting nature of the condition and available therapies in refractory cases.