The 1/serum creatinine slope was significantly (P < 0.01) higher in AST-120–treated subjects (0.0043 ± 0.0036 dl · mg−1 · week−1) than in control subjects (−0.0174 ± 0.0043 dl · mg−1 · week−1). AST-120 did not affect HbA1c levels (control subjects: before 7.4 ± 0.2%, after 6 months 7.5 ± 0.2%, NS, vs. AST-120–treated subjects: before 7.0 ± 0.4%, after 6 months 6.8 ± 0.4%; NS) or systolic and diastolic blood pressure levels (control subjects: before 136.4 ± 4.9/67.0 ± 4.4 mmHg, after 6 months 136.1 ± 3.6/70.9 ± 1.9 mmHg, NS, vs. AST-120–treated subjects: before 131.5 ± 4.3/63.8 ± 5.5 mmHg, after 6 months 130.3 ± 2.5/69.8 ± 3.0 mmHg, NS).
Since AST-120 in the gut did not adsorb creatinine in the blood, and there is no exchange of serum creatinine levels between the gut and blood (3), the observed attenuation of increase of serum creatinine levels by AST-120 should not be attributable to the excretion of creatinine into the feces. Although the results are limited because of the nonrandomized self-selection study design, our findings indicate that AST-120 should contribute to the delay of the development of renal dysfunction in type 2 diabetic patients.
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