A 21-year-old man with a diagnosis of metastatic undifferentiated teratoma was planned to receive 4 cycles of BEP (bleomycin, etoposide and cisplatin) chemotherapy. Cisplatin based chemotherapy plays an important role in the multidisciplinary treatment of urological cancers and is routine for this patient’s disease management.7,8
His past medical history included orchidopexy for an undescended left testis. He also had learning difficulties associated with generalised seizures. Long term medications included sodium valproate (1200 mg twice daily), carbamazepine (400 mg twice daily), and trifluoperazine (1 mg twice daily).
A computed tomography (CT) scan of the brain was performed to exclude brain metastases at diagnosis.
Cycles 1 and 2 of the chemotherapy were relatively uneventful with normal blood parameters. Tumour markers were improving after two cycles of chemotherapy (alpha fetoprotein (AFP) 17 kU/l compared to 506 kU/l at diagnosis (normal range (NR) 0.5–5 ku/l); human chorionic gonadotropin (hCG) 9 iU/l compared to 11118 iU/l at diagnosis (NR 0–2.5 iu/l)). During admission for cycle 3, serum electrolytes showed a low serum sodium (Na) concentration of 126 mmol/l (NR 135–145 mmol/l) with normal serum potassium (K) concentration (4.2 mmol/l, NR 3.5–5.0 mmol/l), normal serum urea (4.5 mmol/l, NR 3.3–6.7 mmol/l), and a low serum creatinine (21 μmol/l, NR 71–133 μmol/l). He was clinically well and normovolaemic on examination. No toxicities were reported with good oral intake and urine output. Serum osmolality was measured at 248 mosm/kg (NR 275–295 mosmol/kg) and urine osmolality was 608 mosm/kg (NR 50–1500 mosmol/kg), hence a diagnosis of SIADH was made in conjunction with endocrinology opinion. Fluid restriction of 1.5 litres/day resulted in his serum Na improving to 132 mmol/l.
Post cycle 3, his repeat blood biochemistry was Na 135 mmol/l, K 3.5 mmol/l, urea 3.7 mmol/l, and creatinine 23 μmol/l, with continued fluid restriction of 1.5 l/day.
Despite fluid restriction, after cycle 4, the patient was admitted with a blood biochemistry of Na 117 mmol/l, K 2.8 mmol/l, magnesium (Mg) 0.30 mmol/l (NR 0.7–1.0 mmol/l), urea 4.6 mmol/l, and creatinine 25 μmol/l. A repeat serum osmolality was 240 mosm/kg and urine osmolality was 475 mosm/kg. Tumour markers had normalised to within normal limits (AFP 4 kU/l and hCG <1 iU/l). He remained clinically well and was normovolaemic on examination. Again, no toxicities from chemotherapy were reported with good oral intake and satisfactory urine output. He was managed with further fluid restriction, K and Mg replacement. At this point, the presence of multiple electrolyte imbalances suggested renal salt wasting rather than SIADH. Urine was therefore sent for Na and K concentration measurements; the results were Na 143 mmol/l (NR 15–30 mmol/1) and K 75 mmol/l (NR 15–30 mmol/l). A biochemistry opinion was consistent with a picture of chemotherapy induced renal salt wasting nephropathy. Fluid restriction was stopped and the patient was given electrolyte supplementation and discharged a few days later.