Every Cat Logo

Familial amyloidosis in Abyssinian cats

Paltrinieri S, Sironi G, et al. Changes in serum and urine SAA concentrations and qualitative and quantitative proteinuria in Abyssinian cats with Familial Amyloidosis: A five-year longitudinal study (2009-2014). J Vet Intern Med. 2015 Mar; 29(2):505-512.

One inherited disease affecting Abyssinians cats is familial amyloidosis (FA). While amyloid can be found in several different tissues, the kidneys are the primary target organ in the Abyssinian. Kidney lesions are primarily found in the renal medulla and glomeruli where secondary inflammation and fibrosis induce chronic kidney disease (CKD). 

By special staining, this type of familial amyloidosis is composed of amyloid A (AA). Serum amyloid A is a major acute phase protein that increases in several inflammatory conditions. Amyloid sequences similar to amyloid proteins of other species have been found in the SAA genes of Abyssinian cats. The sequences though are different from those found with Siamese cats, a breed mostly affected with hepatic amyloidosis. In spite of having information on the genetic variability of the problem in cats, studies have failed to specifically identify the mutations involved in over-production of amyloid. No tests therefore have been developed to identify affected cats and the only manner to prevent the disease is through the exclusion of cats with a familial history of FA from mating.

The disease course of FA is variable in the conditions of appearance, severity and progression. The deposition of amyloid may deposit within one year and cause kidney disease or slowly and kidney function may stay relatively stable for years.

Since FA in Abyssinian cats is often a diagnosis made postmortem, this study evaluated whether sequential analysis of serum SAA, urinary SAA, urinary protein:creatinine (UPC) ratio or sodium-dodecylsulfate agarose gel electrophoresis might help early identify FA in cats. They took blood and urine samples every 4 months over a 4 year period between 23 Abyssinian cats in two catteries, one of low prevalence for FA and the other of high prevalence.

Evaluation of the cattery with low prevalence, Cattery A, did not identify the presence of FA. But Cattery B, the high prevalence cattery, had 7 of 14 cats with FA. Overall, serum amyloid A concentrations were not different significantly between catteries or between cats with FA. On the other hand, urine SAA was significantly higher in Cattery B, especially in cats in the terminal phases of amyloidosis. Proteinuria was found periodically from cats in both catteries, more so in those with FA. Urine protein electrophoresis only noted mixed proteinuria in cats with FA. Therefore, the results suggest that serum amyloid A and UPC ratio are not useful in locating cats in an early phase of FA, but increases in urine SAA with or without proteinuria may be noted before onset of clinical signs in cats with the disease. (VT)

See also:
Niewold TA, van der Linde-Sipman JS, et al. Familial amyloidosis in cats: Siames and Abyssinian AA proteins differ in primary sequence and pattern of deposition. Amyloid. 1999 Sep; 6(3):205-209.