Inheritance of Protein-Losing Enteropathy and Nephropathy
of Soft Coated Wheaten Terriers
S Vaden1, U Giger2, K Spaulding1, R Sellon3, M Littman2, T Harris1, M Afrouzian4, J Jennette4, D Williams5, S VanCamp1
1. North Carolina State University, Raleigh NC; 2. University of Pennsylvania, Philadelphia PA; 3. Washington State University, Pullman WA; 4. University of North Carolina, Chapel Hill NC; 5. Texas A&M University, College Station TX Published in the Journal of Veterinary Internal Medicine, 2002, 16:352.

A common syndrome of protein-losing enteropathy (PLE) and/or protein-losing nephropathy (PLN) has been documented in male and female Soft Coated Wheaten Terriers (SCWT). PLE is associated with eosinophilic or lymphocytic/plasmacytic inflammatory bowel disease and is usually diagnosed at an earlier age (mean 4.5 years) than PLN (mean 6 yrs), which is the result of focal mesangioproliferative and sclerosing glomerulonephritis. Although analysis of pedigrees from SCWT at large revealed a common male ancestor, the exact mode of inheritance could not be determined.

The purpose of this study was to further characterize the mode of inheritance of PLE and PLN in SCWT by three types of breedings: Group 1 consists of a litter of 6 SCWT (3 M, 3 F) born to an affected female x affected male SCWT. Group 2 represents a litter of 4 SCWT (1 M, 3 F) born to a brother x sister mating of Group 1 dogs. Group 3 involves an outcross of an affected male SCWT from Group 1 to a healthy Beagle and resulted in 8 (4 M, 4 F) offspring. These dogs were maintained at the North Carolina State University, fed a standard diet, and were serially evaluated through serum biochemical profiles, CBCs, urinalyses, urine protein:creatinine ratios (normal <1) and Fecal Alpha1 Protease Inhibitor (AlphaPI; normal <5.67 ug/g) every 3 months, small intestinal biopsy and renal ultrasound every 6 months and renal biopsy every 12 months. In order to make a diagnosis of PLE and/or PLN, dogs needed to have both laboratory and histopathologic abnormalities that were consistent with the diseases.

In Group 1 SCWT, 6 of 6 developed PLE (n=1), PLN (3) or both (2); the present age of 2 survivors (PLE/PLN, 1; PLN, 1) is 7 yrs. Both of the parents of Group 2 but none of the 4 dogs in Group 2, developed PLN at 4.5 yrs of age, however, 3 of them have PLE (1 dog appears to have no evidence of disease, but has just reached the mean age to develop PLE). Of the 8 outcross dogs in group 3 (present age 5.5 yrs), 1 has PLE/PLN and 1 has PLN.

Although the breeding of affected to affected SCWT in Group 1 and 2 producing primarily affected SCWT is consistent with an autosomal recessive mode of inheritance, the development of PLE and PLN in the SCWT x Beagle outcross suggests an autosomal dominant trait. The risk for SCWT to develop PLE and PLN is clearly inherited, however, further breeding and clinical follow up is needed to reach a definitive conclusion.


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