images in haematology
Acute kidney injury from tumour lysis syndrome and urate crystalluria
A 74-year-old man with B-cell chronic lymphocytic leukaemia and anaemia due to stage C disease, commenced treatment with intravenous bendamustine 100 mg/m2 on days 1 and 2. A full blood count (FBC) at the time of treatment showed Hb 90 g/l, white blood cells (WBC) 714 9 109/l and platelets 158 9 109/l with impaired renal function [urea 32 mmol/l, creatinine 118 lmol/l, estimated glomerular filtration rate (eGFR) 52 ml/min]. A recent computerized tomography (CT) scan had shown no significant lymphadenopathy, organomegaly or renal abnormality. He had a long history of gout treated intermittently with analgesics. He was not given allopurinol because of the perceived high incidence of rashes when this drug is used together with bendamustine. The patient was admitted 1 week later with profound fatigue, vomiting and oliguria. The FBC now showed pancytopenia (WBC 13 9 109/l, Hb 67 g/l, platelets 115 9 109/l) with serum creatinine 846 lmol/l, potassium 59 mmol/l, calcium 214 mmol/l, phosphate 291 mmol/l, urate 124 mmol/l and eGFR 5 ml/min. The acute kidney injury was deemed secondary to tumour lysis syndrome. Non-contrast CT imaging showed dilatation of the collecting systems of both kidneys (long arrows)
First published online 26 May 2015 doi: 10.1111/bjh.13510
and significant perinephric stranding bilaterally. There were foci of high density in the bladder (short arrows) and distal ureters suggestive of uric acid crystallization. He was treated with intravenous fluids, insulin, dextrose and rasburicase. Within hours his urine output recovered, following which there was a polyuric phase with progressive recovery of renal function (creatinine 93 lmol/l, potassium 36 mmol/l, urate < 006 mmol/l and eGFR > 60 ml/min by day 5 of admission). This patient illustrates the potential danger of administering chemotherapy in the absence of allopurinol or rasburicase prophylaxis. The case is unusual in that, in addition to direct renal damage from hyperuricaemia, there was also an element of post-renal obstructive uropathy from urate crystalluria, which was visible on imaging. The patient was very close to requiring renal dialysis, but with the recovery of urine output following rasburicase treatment, this was not ultimately required. Ben Pearson-Stuttard1, Richard Soutar2 and Mike Leach2 1
Department of Medicine, University of Glasgow, and 2Department of
Haematology, Gartnavel Hospital, Glasgow, UK. E-mail: [email protected]
ª 2015 John Wiley & Sons Ltd British Journal of Haematology, 2015, 170, 444
Acute kidney injury from tumour lysis syndrome and urate crystalluria
A 74-year-old man with B-cell chronic lymphocytic leukaemia and anaemia due to stage C disease, commenced treatment with intravenous bendamustine 100 mg/m2 on days 1 and 2. A full blood count (FBC) at the time of treatment showed Hb 90 g/l, white blood cells (WBC) 714 9 109/l and platelets 158 9 109/l with impaired renal function [urea 32 mmol/l, creatinine 118 lmol/l, estimated glomerular filtration rate (eGFR) 52 ml/min]. A recent computerized tomography (CT) scan had shown no significant lymphadenopathy, organomegaly or renal abnormality. He had a long history of gout treated intermittently with analgesics. He was not given allopurinol because of the perceived high incidence of rashes when this drug is used together with bendamustine. The patient was admitted 1 week later with profound fatigue, vomiting and oliguria. The FBC now showed pancytopenia (WBC 13 9 109/l, Hb 67 g/l, platelets 115 9 109/l) with serum creatinine 846 lmol/l, potassium 59 mmol/l, calcium 214 mmol/l, phosphate 291 mmol/l, urate 124 mmol/l and eGFR 5 ml/min. The acute kidney injury was deemed secondary to tumour lysis syndrome. Non-contrast CT imaging showed dilatation of the collecting systems of both kidneys (long arrows)
First published online 26 May 2015 doi: 10.1111/bjh.13510
and significant perinephric stranding bilaterally. There were foci of high density in the bladder (short arrows) and distal ureters suggestive of uric acid crystallization. He was treated with intravenous fluids, insulin, dextrose and rasburicase. Within hours his urine output recovered, following which there was a polyuric phase with progressive recovery of renal function (creatinine 93 lmol/l, potassium 36 mmol/l, urate < 006 mmol/l and eGFR > 60 ml/min by day 5 of admission). This patient illustrates the potential danger of administering chemotherapy in the absence of allopurinol or rasburicase prophylaxis. The case is unusual in that, in addition to direct renal damage from hyperuricaemia, there was also an element of post-renal obstructive uropathy from urate crystalluria, which was visible on imaging. The patient was very close to requiring renal dialysis, but with the recovery of urine output following rasburicase treatment, this was not ultimately required. Ben Pearson-Stuttard1, Richard Soutar2 and Mike Leach2 1
Department of Medicine, University of Glasgow, and 2Department of
Haematology, Gartnavel Hospital, Glasgow, UK. E-mail: [email protected]
ª 2015 John Wiley & Sons Ltd British Journal of Haematology, 2015, 170, 444
