Article Text

Ectopic Excretion of Atrial Natriuretic Peptide (ANP) in Acute Lymphoblastic Leukaemia (ALL)
  1. M Gupta1,
  2. D Milford1,
  3. M Velangi2
  1. 1Paediatric Nephrology, Birmingham Children's Hospital NHS Foundation Trust, Birmingham, UK
  2. 2Paediatric Oncology, Birmingham Children's Hospital NHS Foundation Trust, Birmingham, UK


Background Hyponatraemia is an infrequent complication in ALL. It is reported to affect 10% of patients and is usually caused by hypovolaemia following gastrointestinal losses complicating chemotherapy. The syndrome of inappropriate antidiuretic hormone (SIADH) has been reported to complicate malignancy, however hyponatraemia secondary to excessive secretion of ANP in ALL has not been reported. We report a case of ALL in which hyponatraemia is presumed to be caused by ectopic excretion of ANP by leukaemic cells.

Case A 10 year old boy presented with a 10 day history of pain in right lower shin, weight loss and reduced appetite. Examination revealed pallor, bruises on arms and legs, lymphoadenopathy and hepatosplenomegaly. A high white cell count with blast cells was noted. After bone marrow confirmation of ALL, chemotherapy was commenced. Lumber puncture ruled out CNS involvement. Mild hyponatraemia (130-135 mmol/L) was detected at admission and continued for the first two weeks but later declined further to 117 mmol/L in third week. Urinary sodium was noted to be significantly high with fractional excretion of sodium being more than 1%. His sodium requirement was up to 700 mmol/day. ANP was noted to be exceptionally high (106 pg/ml) when severely hyponatraemic. Hyponatraemia resolved over the period of 8 weeks with normalisation of ANP during remission (10 pg/ml).

Discussion and conclusion Our case is an example of severe hyponatraemia in ALL with massive sodium requirement in the presence of a significantly high level of ANP. Common causes of hyponatraemia such as hypovolaemic dehydration were ruled out. SIADH was excluded by the absence of fluid overload and normal urine concentration. Renal function was normal with no evidence of glomerular or tubular damage. Normal echocardiogram ruled out the possibility of cardiotoxicity. Significantly high ANP levels were present with marked hyponatraemia and high urinary sodium losses in the absence of other causes suggesting ectopic excretion of ANP by leukaemic cells; this has not reported in the literature. We suggest considering measuring ANP in unexplained hyponatraemia in ALL.

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