10 Aug Clinical Course of Diabetic Kidney Disease Has Changed Over Past 30 Years

MedicalResearch.com Interview with:

Dr. Ian de Boer

Ian de Boer, MD, MS
Associate Professor of Medicine
Adjunct Associate Professor of Epidemiology
Division of Nephrology and Kidney Research Institute
University of Washington, Seattle, WA

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: From the perspective of patients with diabetes, kidney disease can be a devastating complication, leading to end stage renal disease requiring dialysis or kidney transplantation and markedly increasing the risks heart disease, stroke, peripheral vascular disease, and amputation. From a public health perspective, diabetes is the most common cause of end stage renal disease in the US, so understanding, preventing, and treating diabetic kidney disease is critical to reduce the numbers of people needing dialysis and kidney transplants. There have been major changes in the treatment of patients with diabetes over the last 30 years, so we were interested in evaluating how diabetic kidney disease was changing in this context.

We observed that the clinical manifestations of kidney disease have indeed changed among US adults with diabetes over the last 30 years. Albuminuria, or elevated levels of albumin in the urine, has traditionally been thought of as the first evidence of kidney damage for people with diabetes. Reduced GFR, or a reduced ability of the kidneys to filter out waster products, has typically been thought of as a late stage of diabetic kidney disease. But from 1988 to 2014, we saw a significant decrease in the prevalence of albuminuria accompanied by a significant increase in reduced GFR.

MedicalResearch.com: What should readers take away from your report?

Response: The changes we observed imply that the clinical course of diabetic kidney disease has shifted and the diabetic kidney disease that we as physicians are seeing in the clinic has changed. We don’t know for sure why this is happening. It’s likely related at least in part to better glucose control, better blood pressure control, and more use of renin-angiotensin system inhibitors. It’s also possible that people with diabetes are living longer and developing different forms of kidney damage compared to what was seen 30 years ago.

Now, the “typical” presentation of diabetic kidney disease described in older textbooks and literature may no longer be typical. Patients are presenting with different clinical features than they have in the past. Clinically, it’s important to routinely measure serum creatinine and estimate GFR for patients with diabetes.

Also, while the data suggest that better glucose and blood pressure control have reduced albuminuria, they also suggest that these treatments alone are not enough. We need to do more to understand what’s going on in the kidneys of patients with diabetes and develop new, additional treatments to preserve kidney function.

Finally, it was important that the improvements in albuminuria were only seen for young adults.

MedicalResearch.com: What recommendations do you have for future research as a result of this study?

Response: We need to understand the biology that’s underlying the changes observed in this study. For example, what’s going on in the kidneys of a patient with diabetes who has reduced GFR but no evidence of albuminuria? If we can understand the mechanisms of disease in today’s patients, who are already often treated with good glucose and blood pressure control, then we can develop new, additional interventions to further reduce diabetic kidney disease. Advances in technology, including discovery technologies like proteomics, metabolomics, and genomics, have advanced rapidly and may help us gain this level of understanding. Moving forward will require collaboration of physicians, scientists, funding agencies, industry, and most importantly patients with diabetes who are willing to volunteer and help everyone learn how to better prevent and treat kidney disease.

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Last Updated on August 10, 2016 by Marie Benz MD FAAD