Felipedia

Familial renal amyloidosis occurs in Abyssinians, Siamese and Oriental Shorthaired cats. Affected Abyssinian cats are usually young when diagnosed, around 4 - 6 months, also some are not diagnosed until later. Amyloid deposits are usually diffuse and affect organs such as the thyroid glands, adrenals, spleen, gastrointestinal tract, liver, heart and pancreas.

Symptoms of amyloidosis in cats is usually related to renal deposits of amyloid plaques.

Siamese and Oriental Shorthaired cats have been reported to develop fatal liver haemorrhage from amyloid deposition in the liver. Amyloid deposition can be rapid and severe resulting in signs of renal failure or deposition can be mild and only identified at necropsy. The mode of inheritance is not yet known. Serum amyloid A protein has been identified suggesting amyloid in the Abyssinian is reactive (secondary). Amyloid deposition occurs primarily in the renal medulla leading to signs of renal failure including poor coat, weight loss, polyuria/polydipsia, and anorexia. Physical examination findings are also those of CRF including dehydration, stomatitis, pale membranes and small, irregular kidneys. Affected Abyssinian cats usually are presented for poor hair-coat, weight loss, polydipsia, polyuria, lethargy, and anorexia. Physical examination findings include dehydration; pallor of mucous membranes, gingivitis and oral ulceration; and kidneys that are small, firm, and irregular on palpation. Laboratory evaluation reveals evidence of chronic renal failure including azotemia, hyperphosphatemia, metabolic acidosis, non-regenerative anaemia, and isosthenuria. Proteinuria is a variable finding and reflects the severity of glomerular involvement.

Figs. 1&2. Amyloid (brown yellow colour) in the gromerulus of the kidney

The cause(s) of amyloidosis is thought to be genetic. This disorder often results in kidney failure and the cat's prognosis is often poor. Amyloidosis is a disease characterized by the extracellular deposition of protein fibrils which have a specific configuration called the beta-pleated sheet. This configuration leads to the staining properties and insolubility of amyloid. The animal does not mount an inflammatory response to amyloid. Amyloid can be deposited in any organ. Organ malfunction develops as normal tissue is encroached upon by amyloid deposition.

The diagnosis of amyloidosis requires proper pathologic evaluation of an adequate renal biopsy specimen. A wedge of kidney containing both cortical and medullary tissue obtained at laparotomy is more likely to yield a definitive diagnosis than a percutaneous needle biopsy specimen, because of the prominent medullary distribution of renal amyloidosis in the cat.

There is no proven specific treatment for amyloidosis. The disease is invariably fatal.

Treatment of amyloidosis is largely limited to symptomatic therapy of chronic renal failure. Underlying inflammatory disease is uncommonly detected but any concomitant infections should be treated appropriately. Systemic reactive amyloidosis also has been observed in Siamese and Oriental shorthaired cats. Severe liver involvement in these breeds can lead to liver rupture and acute abdominal haemorrhage. Treatment of the underlying disease may result in regression of amyloid and associated signs. Corticosteroids are contraindicated as they enhance the experimental production of amyloid in lab animals. Melphalan (L-phenylalanine mustard - a chemotherapy agent) may decrease the synthesis of amyloid in patients with myeloma. Other drugs which may mobilize amyloid or slow the rate of deposition include: D-Penicillamine, colchicine, DMSO, and thymosin (see Drug dosages) although the response to treatment is usually poor. Supportive treatment as for chronic renal disease is probably the best method.