Clinical signs of vitamin B6 deficiency in cats include growth depression, a mild microcytic, hypochromic anemia with elevated serum iron, convulsive seizures and irreversible kidney lesions consisting of areas of tubular atrophy and dilatation, fibrosis and calcium oxalate nephrosis (Gershoff et al., 1959b).
Vitamin B6-induced renal damage due to the deposition of large amounts of calcium-oxalate throughout the kidneys has been reported by a number of researchers (Gershoff et al., 1959b; Carvalho Da Silva et al., 1959a; Blanchard et al., 1991; Kirk et al., 1995). With a vitamin B6 repletion diet there is a decline in urinary oxalates and improvement of hematocrits and weight gains (Bai et al., 1989; Blanchard et al., 1991).
Histologically, the kidneys of vitamin B6-deficient cats resemble those seen in humans suffering from idiopathic oxalosis. Abnormal amounts of hemosiderin are deposited in the spleen and liver, giving the liver a bright orange color. Thus, as in the dog, it is clear that the anemia is not related to an inability to absorb iron (Ralston Purina, 1987).
Vitamin B6 deficiency has been reported to produce behavioral, neurophysiological and neuropathological abnormalities in a variety of species including cats. Buckmaster et al. (1993) used BAEP and determined that vitamin B6 deficiency in cats affected peripheral and brainstem auditory pathways. The finding of prolonged interwave intervals in vitamin B6-deficient cats was consistent with slowed axonal conduction velocity secondary to defective myelination.
