On May 19, 2001, the long‐awaited results of the irbesartan and losartan trials of type 2‐related diabetic nephropathy were presented in San Francisco. The results showed that these types of antihypertensive agents (angiotensin receptor blockers, or ARBs), given in addition to other medications, improved renal survival (as measured by serial serum creatinine concentrations done over the 2.5–3.5 years of the studies), compared to regimens that did not include an ARB, ACE inhibitor, or dihydropyridine calcium channel blocker. There was no blood pressure difference between groups. Diabetes is the most common cause of end‐stage renal failure in the U.S. and many other countries. 1 These reports are good news. The www.theheart.org Web site provides an executive summary of these trials while we await peer‐reviewed publication.
Built into that news story is the potential savings in dollars for treating each hypertensive diabetic patient with proteinuria and an elevated creatinine level. The figures are impressive. More good news.
However, the struggle to prevent renal failure in diabetes is far from over. Although we have newer ammunition (vis‐à‐vis these studies) and newer strategies to employ the ammunition, the enemy is growing. Diabetes is increasing in prevalence, possibly because of an increase in obesity and a change in definition—i.e., a blood glucose of >126 mg/dL, rather than >140 mg/dL, is now considered “diabetic.” The growth in numbers of diabetics on dialysis or in renal transplant programs is also increasing. 1
The use of ARBs reduced the rate of, but did not halt, the progression of kidney failure. We still have a lot to learn about the mechanisms through which kidney failure progresses, the optimal degree of blood pressure reduction, the role(s) of comorbidities, and the most advantageous time in the course of diabetes to initiate cardiovascular risk‐reducing therapy. The upcoming NIH‐sponsored trial of chronic renal insufficiency, in which 50% of the subjects will be diabetic, will address several of these issues. 2
In the meantime, we have effective tools to reduce blood pressure, blood sugar, and blood cholesterol. While we await newer pathogenesis and treatment insights, the goals of cardiovascular risk‐reducing therapy in diabetes have become something of a moving target. At this time we should be aiming for a blood pressure of <130/80 mm Hg, a HbA1c of <7%, and an LDL of <100 mg in the diabetic patient. The key is actually achieving treatment goals (we tend to be “under‐achievers” in this regard) and maintaining patients at these goals. Treating patients to goal, and maintaining them at goal, is a continuing challenge. However, articles like those of Jones et al. 3 provide a wealth of practical, office‐based advice to complement the incorporation of these new treatment strategies into our battle against diabetic nephropathy.
References
- 1. National Institutes of Health‐National Institute of Diabetes, Digestive and Kidney Diseases. U.S . Renal Data System 2000 Annual Data Report. Bethesda, MD: National Institutes of Health‐National Institute of Diabetes, Digestive and Kidney Diseases; 2000. [Google Scholar]
- 2. National Institutes of Health . Questions and Answers from the Applicant Information Forum. RFA: DK‐01‐005. Prospective Cohort Study of Chronic Renal Insufficiency. Available at: http://www.niddk.nih.gov/fund/crfo/qarfa01005.htm. Accessed December 11, 2000. [Google Scholar]
- 3. Jones D, Basile J, Cushman W, et al. Managing hypertension in the southeastern United States: applying the guidelines from the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). Am J Med Sci. 1999;318:357–364. [PubMed] [Google Scholar]