The excretion of N-acetyl-beta-glucosaminidase in glomerulonephritis.
The excretion of N-acetyl-beta-glucosaminidase (Nag) was studied in 109 patients with glomerulonephritis. A positive correlation was found between the concentration of albumin and Nag in the urine. Almost all the urinary Nag had the properties of the tissues, not of the serum isoenzyme. The ratio between Nag and albumin in the urine was significantly lower in patients with minimal lesions and in those with focal sclerosis than in those with proliferative, membrano-proliferative and membranous glomerulonephritis. The excretion of Nag per g creatinine differed significantly between the various histologic subgroups of glomerulonephritis but not between groups with various degrees of tubulointerstitial changes. The excretion of Nag in 9 patients with proximal tubular damage induced by exposure to cadmium in the past was only moderate. We suggest that urinary Nag excretion is not caused by an increased glomerular permeability to macromolecules but may instead reflect the activity of renal disease.
D000118:Acetylglucosaminidase / Q000652:urine*; D000419:Albuminuria / Q000652:urine; D002199:Capillary Permeability; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000201:enzymology*; D005923:Glomerulosclerosis, Focal Segmental / Q000652:urine; D006596:Hexosaminidases / Q000652:urine*; D006801:Humans; D007683:Kidney Tubular Necrosis, Acute / Q000652:urine
D006596:Hexosaminidases; D000118:Acetylglucosaminidase