Week 3 of learning about diabetic nephrology...and cheering on the Hawks of course! Today we are going to learn about some of the aspects that influence and damage the kidney. There are some great videos that explain more about the subject and are really informative below!
Etiology
The exact cause of diabetic nephropathy is unknown. Various health concerns like genetic factors and smoking contribute to the development of the disease. However, the most significant indicators are high blood glucose levels and hypertension (high blood pressure). Genetically speaking...if a family member has diabetic nephropathy you are five times more likely to develop the disease. Smoking is also a severe risk factor for developing kidney disease because it increases blood pressure. High glucose levels, HgA1C levels above 8.0%, are the strongest causative factor for developing diabetic nephropathy. High glucose levels damage the smaller blood vessels in the kidney leading to the destruction of the filtration process. High blood pressure has both a cause and effect on diabetic nephropathy. High blood pressure impedes filtration in the kidney and contributes to downhill progression of renal damage.
Pathophysiology
The key event in kidney degradation and diabetic nephropathy is basement membrane damage. What does that even mean?! Damage to the basement membrane means there is inflammation and and disruption in the filtration process in the kidney. The declined flow of blood being filtered causes cell death and eventually kidney degradation.
Here are some GREAT videos breaking down diabetic nephropathy pathophysiology! Just click on the title and the video will open up! I hope this will make it clear and easy to understand!
Diabetic Nephropathy Pathophysiology
I hope this week's blog was helpful! Join me next week to learn more about diabetic nephropathy!
American Diabetes Association: Position statement: Diabetic nephropathy. Diabetes Care 22 (Suppl 1):S66-69, 1999.
Evans, Timothy; Campbell, Peter. Clinical Diabetes: Diabetic Nephropathy. 18:1, 2008.
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