Renal effects of potassium niobate

Abstract

The renal effects of a single intravenous dose of 30 mg/kg of niobium as potassium niobate were observed in female mongrel dogs and in female albino rats for various time intervals up to 30 days. In dogs, niobium produced marked decreases in glomerular filtration rate, the maximal rate of tubular secretion of p-aminohippurate, and the maximal rate of tubular reabsorption of glucose. Histologic studies of the kidneys revealed injuries in both the proximal and the distal tubules. Some tubular lumina were filled with granular pigment throughout all levels of cortex and medulla, while others contained casts. The epithelial cells were flattened in some areas and necrotic in others. Niobium-poisoned rats showed marked increases in water intake and urine volume, and decreases in urinary density and osmolality. Urinary sodium execretion increased for the first 2 days but decreased on day 7. Rats lost their urine-concentrating ability, failed to respond to injection of antidiuretic hormone, and peak urine excretion rate after a water load was delayed. Increases in kidney weight and kidney weight to body weight ratios were noted. The renal histologic changes, like those in dogs, involved both proximal and distal tubules, and consisted of tubular dilation and the presence of scattered hyaline casts and deposits of granular pigment. Tubules occasionally showed necrosis, regeneration, and early fibrosis.