Comparison of the Urinary Excretion of Aspartate Aminotransferase, Lactic Dehydrogenase, Alkaline and Acid Phosphatase and β-Galactosidase During Nephrotoxic Serum Glomerulonephritis and Mercuric Chloride Tubulonephritis in the Rat

Abstract

During tubulonephritis, we observed one sharp excretion peak of all 5 enzymes on day 1. During regeneration of tubular epithelium, lysosomal enzymes decreased below normal level. Isoenzyme analysis gave most interesting results for aspartate aminotransferase: on the first days, while total activity was increased in urine and serum, 2 fractions were found in serum and 3 in urine while only one (cytoplasmic) in normal rat serum; the mitochondria! fraction appeared indicative of tissue necrosis; the third fraction only found in urine migrated towards the anode faster than albumin at pH 8.6 and was never detected in serum. Serum lactic dehydrogenase activity was increased and its isoenzyme pattern was reversed on day 1 when isoenzyme 1 characteristic of kidney cortex predominated. Lactic dehydrogenase isoenzymes 1 and 2 predominated in urine. Urinary enzyme activities after tubular necrosis seem to originate mainly in the cortical tubules. During glomerulonephritis we observed increased urinary activities of the 5 enzymes which culminated during the 2 periods of highest proteinuria: 1) the heterologous phase limited to the first days 2) the autologous phase maximum at the second week. A significant diminution was noted in serum, for alkaline phosphatase during the autologous phase. The only isoenzyme of aspartate aminotransf erase detected in urine at the periods of high enzymuria appeared identical to the isoenzyme present in serum. Urinary enzyme activities during glomerulonephritis appear to originate mainly in the plasma or in the glomeruli.

Enzymuria as an index of renal damage in canine leishmaniasis

“…Three important factors need to be taken into account in assessing the renal status of dogs with canine leishmaniasis: the deposition of antibodies and immune complexes in the glomerular basement membrane (Poli and others 1988, Mancianti and others 1989), tubulonephrosis, especially in the proximal tubule (García and Martín 1991), and proteinuria (Palacio and others 1995). An increase in urinary enzyme excretion has been shown to be a consequence of the deposition of immune complexes in the glomerular basement membrane (Sternberg and others 1974). Tubulonephrosis in the proximal tubule also causes enzymes to be released from this site.…”