title: Reduction of urine volume ameliorates adriamycin-induced nephropathy.
abstract: 1. Adriamycin, a commonly used antineoplastic antibiotic, induces glomerular lesions in rats, resulting in persistent proteinuria and glomerulosclerosis. 2. The effect of urine volume on the progression of adriamycin-induced nephropathy was studied in 70 male Wistar rats (180-200 g) observed for 30 weeks and separated into 4 groups: healthy control group (HCG, N = 10) inoculated i.v. with 1 ml of saline, and nephrotic groups inoculated iv with a single dose of adriamycin of 3 mg/kg body weight. The nephrotic rats were separated into 3 groups (N = 20): nephrotic control group (NCG) receiving only adriamycin; dehydrated nephrotic group (DNG) water deprived for 36 h within each 48-h period, and furosemide nephrotic group (FNG) treated with 12 mg/dl furosemide, and 0.9 g/dl NaCl in the drinking water. 3. The 30-week survival rates of the DNG (100%) and HCG (100%) were significantly higher than those of the NCG (85%) and FNG (55%). 4. The proteinuria observed in the HCG (range, 7.38 +/- 0.7 to 13.6 +/- 1.27 mg/24 h) was significantly lower than that observed for all the nephrotic groups throughout the experiment. The DNG presented significantly less proteinuria (range, 42.71 +/- 6.83 to 140.10 +/- 19.22 mg/24 h) than the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) from week 10 on. There was no significant difference between the mean 24-h proteinuria of the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) and the FNG (range, 35.82 +/- 7.91 to 221.54 +/- 26.74). 5. The mean frequency of damaged glomeruli was 0.3% +/- 0.3 for HCG, 42% +/- 6% for CNG, 40.8% +/- 8% for DNG, and 47% +/- 14% for FNG. The median value of the tubulointerstitial lesion, evaluated by a semiquantitative method, was 0 in HCG, 10 in CNG, 8.5 in DNG and 9.5 in FNG (P < 0.05 for all groups compared to HCG). 6. The data indicate that reduction of urine volume has a protective effect on adriamycin-induced nephropathy.
authors.affiliation: Departamento de Clínica Médica, Faculdade de Medicina, Universidade Estadual Paulista, Botucatu, SP, Brasil.
authors.forename: V A
authors.initials: VA
authors.lastname: Soares
authors.forename: R M
authors.initials: RM
authors.lastname: Viero
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004317:Doxorubicin / Q000009:adverse effects*; D005665:Furosemide; D005921:Glomerulonephritis / Q000139:chemically induced* / Q000473:pathology / Q000652:urine; D005923:Glomerulosclerosis, Focal Segmental / Q000139:chemically induced / Q000473:pathology / Q000652:urine; D007668:Kidney / Q000473:pathology; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D011507:Proteinuria / Q000139:chemically induced; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014556:Urine; D014868:Water Deprivation
chemical_list: D005665:Furosemide; D004317:Doxorubicin