Familial glomerulonephropathy, also known as familial renal disease and hereditary nephritis, is associated with abnormalities in the glomeruli, the tiny tufts of capillaries that filter blood in the kidneys by removing fluid and waste products from the blood. When the filters are not working effectively, protein and red blood cells pass into the urine. In the Samoyed breed, glomerulonephropathy is caused by inheritance of abnormal X-linked (sex chromosome) genes resulting in abnormal type IV collagen (major component of glomerular capillary basement membrane). In this case, males are more severely affected and develop chronic kidney failure by 8-16 months of age. Affected females show less severe clinical signs. In the Bull Terrier, Doberman Pinscher, Cocker Spaniel, Soft-Coated Wheaten Terrier, Newfoundland, Shar-Pei and Beagle, familial glomerulonephropathy is associated with inherited autosomal recessive trait and affects males and females similarly. However, unlike Samoyeds, Norwegian Elkhounds may develop kidney failure as early as 3 months of age. Dogs affected with glomerulonephropathy present with weight loss, poor appetite, apathy, vomiting, and increased thirst and urination. Clinical signs eventually lead to chronic kidney failure near 6-10 months of age.
In dogs with hereditary nephritis, treatment is directed toward resolution of clinical signs and improving kidney function. Salt-restricted and protein-restricted diets are also recommended. Despite urine protein loss, dietary protein supplementation is not advisable as proteinuria can worsen. Dogs and cats with fluid buildup (edema) or ascites should be treated with cage rest and dietary sodium restriction. Sometimes, there may be a need for tapping the abdominal cavity with a needle in order to draw off accumulated fluids, if animals experience difficulty breathing and abdominal discomfort. Overzealous use of diuretics (furosemide) may cause dehydration and acute kidney insufficiency. Plasma transfusions provide only temporary benefits.