Diabetes Dateline
NIDDK Researchers Seek Model for Reversing Kidney Damage
The 1990s saw significant advances in the understanding and treatment
of chronic renal failure in general and diabetic nephropathy in particular.
At the beginning of the decade, scientists knew that antihypertensive
drugs could slow the progressive decline of renal function caused by diabetic
nephropathy. In 1993, the Collaborative Study Group, funded by the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), found
that captopril, a member of the class of antihypertensives known as angiotensin-converting
enzyme (ACE) inhibitors, protected renal function in patients with type
1 diabetes better than other medicines that provided the same level of
blood pressure control. Subsequent studies have shown that the protection
conferred by ACE inhibitors extends to patients with other types of renal
disease, although it has not been determined in large populations whether
the protection of renal function goes beyond that attributable to lowering
blood pressure. Still, in all of these studies, treatment merely slows
the progression of the disease; it does not reverse or stop it.
More recently, NIDDK-funded researchers have been exploring possible
ways to actually reverse the damage done by diabetic and other nephropathies.
In July 1998, one group of researchers reported observing the reversal
of the lesions of diabetic nephropathy after a pancreas transplant. While
the study is based on only eight cases and improvement was not observed
until 10 years after transplantation, the study provides hope of reversing
renal disease in patients with type 1 diabetes.
The researchers explain that diabetic nephropathy results from a buildup
of extracellular material in the mesangium and membranes of the kidney
filters that decreases filtration surface. In people who do not have diabetes
or hyperglycemia, the volume of this extracellular material stays constant
throughout their adult lives, reflecting a balance between the production
of extracellular material and its removal. In some people with diabetes,
hyperglycemia causes this extracellular material to build up until diabetic
nephropathy results. However, since many people with diabetes do not develop
nephropathy, the researchers theorize that some genetic mechanism is responsible
for the different renal reactions to hyperglycemia.
In patients who achieved 10 years of good glycemic control after receiving
a pancreas transplant, the volume of extracellular material had decreased,
indicating a shift in the balance between the buildup and removal of this
substance in and around the glomeruli.
The researchers point out that neither the mechanism that reverses extracellular
buildup after a pancreas transplant nor the genetic mechanism that protects
some people with diabetes from nephropathy is well understood. They assert
that further research in this area will result in a greater understanding
of the mechanisms that protect and restore renal function and in powerful
tools for treating a range of renal diseases.
For information on upcoming diabetes-related meetings, workshops, programs,
and events, check the National Diabetes Education Program's 2000 Diabetes
Calendar at ndep.nih.gov/new/nltr/nltr_index.htm
on the Internet.
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