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Flashcards in Diabetes Nephropathy Deck (24)
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1
Q

T or F: DN is the most common cause of ESRD

A

T

2
Q

T or F: Development is strongly genetic

A

T: only 17 % risk if no family history

3
Q

Describe the early changes assc with DN (pathogenesis, clinical, histo)

A

hyperfiltraion resulting in glomerular hypertrophy

clinically manifests as microalbuminemia

histo: inc mesangial matrix, glomerular collapse, glomerularsclerosis

4
Q

Describe the progression of DN.

A

microalbuminemia –> proteinuria –> inc Sr Cr –> ESRD

5
Q

What is the clinical defn of DN?

A

long standing DM (+/-retinopathy)
Macroalbuminemia
HTN

6
Q

What usually develops at the same time as DN?

A

retinopathy

7
Q

What are the 5 stages of DN kidney disease?

A
  1. hyperfiltration (inc GFR)
  2. microalbuminemia
  3. more proteinuria, more Sr Cr, inc BUN, +/- HTN
  4. GFR <10 ml/min
8
Q

How long can it take to get to ESRD?

A

long time (avg 23 yrs)

9
Q

What causes the damage in DN?

A

inc blood glc, inc Ang II causes hyperfiltration –> inc glomerular pressure –> hypertrophy of epithelium and endothelium –> accerlation of cell failure and premature glomerulosclerosis

10
Q

Is there inflammation assc with progression of DN?

A

no, TGF-B secreted by the tubuloepithelial cells causes thickening of GBM, hypertrophy, mesangial matrix expansion

11
Q

What are AGEs? What is their role in DN? How are they formed?

A

advanced glycosylation products –> accelerates cell injury

*long term hyperglycemia forms them from non-enzymatic glycosylation of capillary BM

12
Q

Are AGEs normal?

A

yes, there are just more of them in DN pts

13
Q

What is the tx for DN? Why?

A

CONTROL DM!! (slows progression)

ARBs and ACE-Is (only drugs that dec glomerular pressure = relax both aff and eff tone)

14
Q

What is a good marker for the progression of DN towards ESRD?

A

degree of proteinuria

15
Q

What are some complications of DN?

A

pyelonephritis
papillary necrosis
RTA type 4
neurogenic bladder

16
Q

What are the 3 main types of DN? (and their subtypes)

A
  1. glomerular: diffuse and nodular
  2. papillary: pyelonephritis and papillary necrosis
  3. tubulointersitial: tubular BM thickening and intersitial fibrosis
17
Q

What is the most common type of DN?

A

diffuse

**earlier and less severe

18
Q

Describe the appearance of diffuse DN histologically

A

thickening of GBM and mesangial matrix expansion

19
Q

When does nodular type appear?

A

> 10 yrs of DM

= correlates with ESRD/need for dialysis

20
Q

What are the histological features of nodular DN

A

kimmelsteil wilson nodules and hyaline sclerosis od afferent and efferent arterioles

21
Q

What are kimmelstiel wilson nodules?

A

spherical hyaline deposits of mucopolysacchairdes, lipids, and fibrillary proteins within the mesangium or glomerular tuft

*they eventually squeeze capillaries shut

22
Q

What are the 2 types of exudative lesions and which one occurs only in DN?

A
fibrin caps
capsular drops (only DN)
23
Q

What are fibrin caps and capsular drops?

A

firbin caps: crescentric deposits of condened leaked plasma proteins overlying the peripheral capillaires (can be subspi or sub endo)

Capsular drops: deposits of partly plasma proteins and BM in parietal later of Bowman’s capsule (protrudes into urinary space)

24
Q

The end stage of DN looks just like __disease_ (describe gross and microscopic appearance too)

A

hypertensive nephropathy

  • gross, diffuse fine granularity of cortical surface
  • *microscpoic: fibrosis and sclerosis –> globally sclerotic glomeruli, dilated tubules, tubules resembling thyroid follicles and interstitial fibrosis