Effect of oral adsorbent (AST-120) on renal function, acquired renal cysts and aortic calcification in rats with adriamycin nephropathy.
OBJECTIVE
The effect of oral adsorbent, AST-120, on the experimental renal disease induced by adriamycin, uninephrectomy and high protein diet proposed as a model of acquired cystic disease of the kidney was investigated.


METHODS
3 mg of adriamycin was injected into the tail vein of rats and 4 weeks later right-side nephrectomy was performed, 2 weeks thereafter 26 rats with urinary protein excretion between 100 and 358 mg/day were selected from 60 rats. Two groups, 13 rats in each group, namely the AST-120-treated group and control group, both of which had equal renal damage before the administration of AST-120 or placebo. AST-120 (0.4 g/100 g BW/day) was administered for 19 weeks.


RESULTS
Serum creatinine and BUN in the AST-120-treated group were significantly lower (serum creatinine: 3.3 +/- 2.1 vs. 7.1 +/- 2.7 mg/dl, p < 0.003) and creatinine clearance was higher (0.62 +/- 0.49 vs. 0.29 +/- 0.30 ml/min, p < 0.05) at the final examination than in the control group. Survival rate which was examined using another set of 9 rats was higher in AST-120-treated rats than in AST-120-untreated rats. Serum indoxyl sulfate was significantly lower at all times after using AST-120 in the AST-120-treated group than in contrast to the control group. Histological examination revealed less severe interstitial and cystic changes in the AST-120-treated group. This suggests that AST-120 can prevent or retard the development of acquired renal cystic disease in this model. Aortic calcification tended to be less severe in the AST-120-treated group because of less serum Ca x P products.


CONCLUSIONS
The AST-120-treated group significantly decreased serum creatinine and increased creatinine clearance with less severe renal cystic changes in this model during the later weeks of administration of AST-120 or at death, accompanied with the tendency of less severe aortic calcification.
Ishikawa
Isao
I
Division of Nephrology, Department of Internal Medicine, Kanazawa Medical University, Uchinada, Kahoku, Ichikawa 920-0293, Japan. isikawai@kanazawa-med.ac.jp
Araya
Mitsuru
M
Hayama
Tomoyuki
T
Sugano
Mikio
M
Yamato
Hideyuki
H
Ise
Michihito
M
D000284:Administration, Oral; D000327:Adsorption; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000473:pathology; D002114:Calcinosis / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology; D002244:Carbon / Q000008:administration & dosage*; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D004317:Doxorubicin / Q000633:toxicity*; D007668:Kidney / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D007674:Kidney Diseases / Q000139:chemically induced* / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D052177:Kidney Diseases, Cystic / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D009392:Nephrectomy; D010087:Oxides / Q000008:administration & dosage*; D051381:Rats
D010087:Oxides; D002244:Carbon; D004317:Doxorubicin; C040896:AST 120; D003404:Creatinine