Up to 40% of diabetics may develop kidney disease, and since the patient’s genetics are an important causal factor, controlling blood sugar is a less effective way to prevent diabetic nephropathy than it is for preventing other complications. (A. McKnight, et al., “Genetics of Diabetic Nephropathy: A Long Road of Discovery,” Current Diabetes Reports, 15 (7) 41 (2015))
There is, however, one adjunctive therapy that can delay the progression of diabetic nephropathy, and that is a form of modified charcoal, AST-120 (Kremezin) that has been used in Japan, Korea, and the Philippines as a standard treatment for this condition since the 1990s. There have been numerous scientific studies of its effects, and it seems to work by absorbing the toxins left circulating in the body because of declining renal function, which in turn worsen the health of the kidneys, in a vicious cycle which accelerates their decline. Because the chemically modified charcoal in AST-120 absorbs these toxins, the vicious cycle is interrupted. Here is an example of one study of its effects:
Diabetes Res Clin Pract. 2008 Sep;81(3):310-5. doi: 10.1016/j.diabres.2008.04.024. Epub 2008 Jun 11.
AST-120 (Kremezin) initiated in early stage chronic kidney disease stunts the progression of renal dysfunction in type 2 diabetic subjects.
Konishi K1, Nakano S, Tsuda S, Nakagawa A, Kigoshi T, Koya D.
There is little clinical evidence when AST-120 should be prescribed for subjects with early stage overt diabetic nephropathy. We therefore designed a prospective, randomized, controlled study for subjects with type 2 diabetes (serum creatinine <1.5mg/dl and urinary protein >0.5g/day) in November, 2001. The primary end point was defined as exceeding 2mg/dl of serum creatinine, and the secondary end point was defined as introducing a hemodialysis. Twenty-two subjects were selected, and after excluding 6 drop-out subjects, 16 subjects (10 in the control group; 6 in the KRM group) finally entered the study. Mean follow-up periods were 37 and 34 months in the control and KRM groups, respectively. There was no difference in clinical characteristics including renal dysfunction at baseline between the two groups. There was a significant reduction in urinary indoxyl sulfate at month 12 in the KRM group than in the control group. A significant difference was observed in changes in mean levels of serum creatinine versus time between the two groups. The primary end points were counted in 7 (70%) of the control subjects, while only 1 (17%) of the KRM group, and the Kaplan-Meier analysis was statistically significant. Although 4 (40%) of the control group and 1 (17%) of the KRM group were initiated hemodialysis as the secondary end point, the difference did not reach a statistical significance. Thus, we concluded that administration of AST-120 initiated in early stage overt diabetic nephropathy stunts the progression of renal dysfunction.
Although AST-120 is available only with a doctor’s prescription in Japan, outside Japan it can be ordered without a prescription. It seems to be effective in slowing all forms of renal disease, since by absorbing the toxins associated with declining renal function it interrupts the accelerative process by which all renal diseases cause kidney failure.