Diabetes Nephropathy Flashcards
T or F: DN is the most common cause of ESRD
T
T or F: Development is strongly genetic
T: only 17 % risk if no family history
Describe the early changes assc with DN (pathogenesis, clinical, histo)
hyperfiltraion resulting in glomerular hypertrophy
clinically manifests as microalbuminemia
histo: inc mesangial matrix, glomerular collapse, glomerularsclerosis
Describe the progression of DN.
microalbuminemia –> proteinuria –> inc Sr Cr –> ESRD
What is the clinical defn of DN?
long standing DM (+/-retinopathy)
Macroalbuminemia
HTN
What usually develops at the same time as DN?
retinopathy
What are the 5 stages of DN kidney disease?
- hyperfiltration (inc GFR)
- microalbuminemia
- more proteinuria, more Sr Cr, inc BUN, +/- HTN
- GFR <10 ml/min
How long can it take to get to ESRD?
long time (avg 23 yrs)
What causes the damage in DN?
inc blood glc, inc Ang II causes hyperfiltration –> inc glomerular pressure –> hypertrophy of epithelium and endothelium –> accerlation of cell failure and premature glomerulosclerosis
Is there inflammation assc with progression of DN?
no, TGF-B secreted by the tubuloepithelial cells causes thickening of GBM, hypertrophy, mesangial matrix expansion
What are AGEs? What is their role in DN? How are they formed?
advanced glycosylation products –> accelerates cell injury
*long term hyperglycemia forms them from non-enzymatic glycosylation of capillary BM
Are AGEs normal?
yes, there are just more of them in DN pts
What is the tx for DN? Why?
CONTROL DM!! (slows progression)
ARBs and ACE-Is (only drugs that dec glomerular pressure = relax both aff and eff tone)
What is a good marker for the progression of DN towards ESRD?
degree of proteinuria
What are some complications of DN?
pyelonephritis
papillary necrosis
RTA type 4
neurogenic bladder