
Figure 1. Diabetic kidney damage.
Oxidative stress has been established as a risk factor for the progression of diabetic nephropathy in patients with type 2 diabetes mellitus (T2DM). For example, in patients with T2DM, urinary excretion of 8-oxo-7,8-dihydro-2'-deoxyguanosine is associated with the progression of diabetic nephropathy. Similarly, increased levels of proinflammatory cytokines and chemokines (interleukin 6, interleukin 18, and monocyte chemoattractant protein-1), high-sensitivity C-reactive protein (a marker of subclinical inflammation), or adhesion molecules (soluble vascular cellular adhesion molecule-1 and soluble E-selectin) confer an increased risk for the development of diabetic nephropathy and the progression to severe kidney disease in patients with either T1DM or T2DM.
An abrupt decline in kidney function, onset of overt proteinuria within 5 years of the onset of diabetes, or an active urine sediment with dysmorphic red blood cells and red blood cell casts are suggestive of a nondiabetic etiology of the patient's kidney disease.
Learn more about diabetic nephropathy.
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Cite this: A. Brent Alper. Fast Five Quiz: Diabetic Nephropathy Presentation and Diagnosis - Medscape - Apr 24, 2020.
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