Urinary acidic hydrolases in renal diseases in children.
Acidic hydrolases were assayed in urines of 19 normal children, 33 children with idiopathic nephrotic syndrome of childhood (INS), 21 children with glomerulonephritides (GN) and 7 children with persistent proteinuria/hematuria, and in plasma of 10 children each with INS or GN. Both plasma and urinary acidic hydrolases were studied in intermittent orthostatic proteinuria. Cbeta-galactosidase and Cbeta-N-hexosaminidase were done in normals and children with active renal disease. Significantly (P less than 0.01) elevated urinary acidic hydrolases excretion in active renal diseases, both in INS and GN, returned to a normal range with regression of the diseases. Increased postural proteinuria was associated with normal urinary acidic hydrolases. Both beta-galactosidase and beta-N-hexosaminidase excretion was higher than similar mol wt proteins in normals and increased further in active renal diseases. The data suggests that increased urinary acidic hydrolases is related to the activity of the renal disease, and not to urinary WBC, hematuria or proteinuria. The likely source of urinary acidic hydrolases thus appears to be the injured renal parenchyma itself.
D001192:Arylsulfatases / Q000652:urine; D002648:Child; D005921:Glomerulonephritis / Q000201:enzymology*; D006417:Hematuria / Q000201:enzymology*; D006596:Hexosaminidases / Q000097:blood / Q000652:urine; D006801:Humans; D006867:Hydrolases / Q000097:blood / Q000652:urine*; D008361:Mannosidases / Q000097:blood; D009404:Nephrotic Syndrome / Q000201:enzymology*; D011507:Proteinuria / Q000201:enzymology*; D005644:alpha-L-Fucosidase / Q000097:blood / Q000652:urine; D001616:beta-Galactosidase / Q000097:blood / Q000652:urine
D006867:Hydrolases; D001192:Arylsulfatases; D006596:Hexosaminidases; D008361:Mannosidases; D001616:beta-Galactosidase; D005644:alpha-L-Fucosidase