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Fanconi syndrome in a Bichon Maltese dog: a quantitative approach to acid–base analysis
  1. Ignacio Mesa-Sánchez1,
  2. Katarzyna Purzycka1,
  3. Marcos Isidoro-Ayza2 and
  4. Rafael Ruiz de Gopegui-Fernández1
  1. 1Veterinary Faculty, Department of Animal Medicine and Surgery, Universitat Autònoma de Barcelona, Barcelona 08193, Spain
  2. 2Veterinary Faculty, Servei de Diagnòstic de Patologia Veterinària, Universitat Autònoma de Barcelona, Barcelona 08193, Spain
  1. Correspondence to Dr Ignacio Mesa- Sánchez, e-mail: imesa84{at}


A three-year-old female Bichon Maltese dog presented with inappetence, polyuria, polydipsia, weakness, weight loss, seborrhoea and hypotrichosis. Diagnostic test results were consistent with Fanconi syndrome (euglycaemic glucosuria, hypophosphataemia, hyponatraemia, hypokalaemia, normal anion gap metabolic acidosis, proteinuria, aminoaciduria and increased urinary excretion of electrolytes). The dog died eight months after diagnosis and histopathological findings consisted of diffuse renal tubular necrosis. Fanconi syndrome is a rare disorder in veterinary medicine associated with a reabsorption defect of the proximal renal tubules, resulting in renal tubular acidosis. A quantitative approach to acid–base analysis was applied in this patient. Initial presentation of acidaemia was mainly due to hyponatraemia (increased free water effect) and increased Cl effect. The severe acidaemia observed seven months after initial presentation was primarily associated with hypoperfusion (raised lactate effect), increased unmeasured anions effects and hyponatraemia. A quantitative approach could be more appropriate than a traditional approach in Fanconi syndrome because it considers more of the individual factors affecting the acid–base balance (sodium, chloride, lactate, albumin, phosphate and unmeasured anions), all of which are altered in affected patients.

  • glucosuria
  • metabolic acidosis
  • proximal tubulopathy
  • renal tubular acidosis
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