| Fanconi syndrome is a generalized proximal tubular reabsorptive defect resulting in excessive loss of many solutes in the urine. It has been reported as an acquired condition in dogs (gentamicin nephrotoxicosis and an idiopathic form) and in a heritable form in a variety of breeds (most notably Basenjis), in which it develops gradually in adults of both sexes. There is excessive urinary loss of glucose, sodium, potassium, phosphorus, uric acid, bicarbonate, and amino acids. Blood
glucose concentrations are normal. Serum electrolytes are normal early in the disease, but hypophosphatemia, hypokalemia, and metabolic acidosis are seen in the later stages. |
| Clinical signs include polydipsia, polyuria, and weight loss. Signs of uremia may be present if the animal is in Stage III chronic kidney disease. Diagnosis is based on documentation of increased urinary fractional excretion of glucose, sodium, potassium, phosphorus, and bicarbonate in the presence of normal plasma concentrations. Differential diagnoses include simple renal glucosuria and chronic kidney disease from other causes. The microscopic renal changes in the heritable form
are not remarkable in the early stages but progress to nonspecific findings characteristic of chronic kidney disease. A genetic marker has been developed. A treatment regimen to reverse the tubular defect has not been described. The histologic appearance of the acquired forms of Fanconi syndrome vary, depending on the cause. |
| Oral supplementation of sodium chloride, potassium, phosphate, and bicarbonate is indicated if the corresponding serum concentration is low. Dogs with acute or chronic kidney disease should be treated symptomatically as appropriate. The heritable disease is slowly progressive despite therapy and usually results in death from uremia. |
