Acute renal failure (ARF) was induced in rat following a single injection of
sodium chromate. A transient
polyuria and a 10-fold decrease in glomerular filtration rate was immediately observed after
sodium chromate administration. Urinary
sodium and
potassium excretion were reduced within 24 h and remained decreased for 8 to 10 days. Progressive recovery of normal renal functions, mainly
electrolyte excretion and filtration rate was observed 12 days after
sodium chromate administration.
Urinary kallikrein excretion (UKE) was decreased only 48 h after
sodium chromate administration. However the proportion of the active and inactive form excreted was unchanged. UKE remained also at a reduced level for 8 to 10 days and returned progressively to base-line level. The
kallikrein content in the tissue was significantly increased immediately after
sodium chromate administration and recovered normal values 12 days later. The increase of
kallikrein in the tissue is more likely unspecific due to impaired protein transport than a specific stimulation of renal
kallikrein biosynthesis. The decreased UKE may indicate a distal tubular reversible dysfunction in this ARF model. These reductions in
electrolyte excretion, glomerular filtration and UKE were associated with selective morphological lesions. Whereas the glomeruli were intact, important damages affected proximal tubule cells which appeared necrotic and showed presence of vacuoles, liquefaction of cytoplasmic material and lost of microvilli. Less marked lesions were however observed in distal tubules, particularly large vacuoles were present at the apical poles of the tubule cells, the sites of
kallikrein secretion. These distal damages may be involved in the increase of tissue concentration and in the decrease of UKE.(ABSTRACT TRUNCATED AT 250 WORDS)