Fanconi syndrome
From Felipedia
Fanconi syndrome is a rare renal disorder of cats in which the proximal renal tubules of the kidney do not properly reabsorb electrolytes and nutrients back into the body, but instead "spill" them in the urine. Symptoms include excessive drinking (polydipsia), excessive urination (polyuria), and glucose in the urine (glucosuria). If Fanconi is left untreated, muscle wasting, acidosis, and poor condition will also occur.
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Causes
Fanconi's syndrome is frequently reported in dogs but not in cats.
The acquired form of Fanconi’s syndrome can be caused by heavy metal poisoning (lead, mercury, cadmium and uranium). Drugs such as a gentamicin, cephalosporins, outdated tetracycline, cisplatin, and streptozotocin can cause proximal renal tubule resorption abnormalities. Chemicals such as Lysol and maleic acid also have been reported to cause the syndrome. Renal cystic disease and neoplasia, including multiple myeloma and monoclonal gammopathies, also have been found to cause acquired Fanconi’s syndrome.
Fanconi’s syndrome is a progressive disease, which, if not treated, ultimately results in transport system failure to the point where solute losses are significant enough to overwhelm other compensatory mechanisms and the animal can no longer maintain homeostasis. The most significant of these is the loss of bicarbonate (HCO3-). Proximal renal tubular acidosis subsequently develops and, if left uncorrected, will ultimately lead to death. In an unaffected dog with a normal acid-base balance, most of bicarbonate ions in the urine are converted to carbonic acid (HCO3- + H2CO3), which is then converted to H2O and CO</sub>2</sub> with the aid of carbonic anhydrase found in the brush border of the renal tubular epithelial cell.
The carbon dioxide formed readily diffuses across the luminal membrane of the renal tubular cell. In this way, bicarbonate is conserved. The hydrogen ion needed to form carbonic acid is supplied by the sodium-hydrogen ion antiporter, which has a high enough Tm to conserve the needed bicarbonate in an unaffected dog. In Fanconi’s syndrome, the Tm is reduced due to either the lack of a sufficient sodium concentration gradient or a defect in the transporter itself. As a result, fewer hydrogen ions are secreted and, thus, less bicarbonate is conserved. The loss of bicarbonate causes an acidemia and the plasma bicarbonate level decreases until it has reached a level which the impaired transport system can handle. Affected dogs can compensate somewhat for the acidemia through respiratory mechanisms (hyperventilation), shifts in intracellular potassium, and secreting hydrogen ions in the distal renal tubule.
Symptoms
Animals suffering from Fanconi’s syndrome typically presents with polyuria and polydypsia, a history of weight loss, a poor hair coat and, sometimes weakness.
Diagnosis
Glucose (sugar), and other nutrients and buffers spill into the animal's urine from the faltering renal tubule system of the kidneys; however, the animal will be found to have a normal to low blood glucose. This condition may be mistaken for diabetes and disastrously mistreated. Blood glucose would be high in diabetes.
Treatment
The outlook is exceptionally good with early detection and treatment. This condition can now be controlled but not cured.
