Diabetic Renal Disease Flashcards Preview

Renal Week 3 > Diabetic Renal Disease > Flashcards

Flashcards in Diabetic Renal Disease Deck (36):
1

What defines Diabetes in a patient?

• Fasting Blood Glucose greater than 126 mg/dL
• Random Blood Glucose greater than 200 mg/dL and confirmed on more than 1 occasion

2

T or F: Diabetes is the biggest cause of Chronic Kidney Failure.

True

3

Who is at the greatest risk of experiencing kidney failure as a result of diabetes?

Anyone who's not Caucasian

Minorities with diabetes have a greater challenge in preventing kidney disease, since African Americans, Hispanics, and American Indians experience higher rates of kidney disease than Caucasians.

40% of new cases of chronic kidney disease may be attributed to Diabetes

4

What are the 3 types of complications that result from diabetes?

• Metabolic
• Macrovascular
• Microvascular

5

What are the diabetic microvascular complications?

Diabetic Microvascular complications
• Diabetic Nephropathy
• Diabetic Neuropathy
• Diabetic Retinopathy (including Diabetic Macular Edema)

Note: Retinopathy and Nephropathy = close tie in type I

6

What are the diabetic macrovascular complications?

Diabetic Macrovascular complications
• Coronary artery disease – most common reason for extremity amputation
• Cerebrovascular disease
• Peripheral vascular disease

7

What is the overall risk of a diabetic developing a neuropathy?
• how do the two types differ?

30-40% chance of any give diabetic developing Nephropathy

83% of TYPE II diabetics with 1st degree relatives who experienced nephropathy also wound up with a nephropahy compared to 13% of TYPE I diabetics

8

What is the VERY FIRST abnormality detected in diabetic nephropathy? Lab value? specimen?
• Followed by?

***First overall sign of pathology is THICKENING of the basement membrane**

1st. = MICROALBUMINEMIA => overt proteinuria => Reduced GFR => HYPERTENSION

9

How do you make the Clinical Diagnosis of Diabetic Retinopathy?

• Microalbuminemia - Must be measure using 24 hr. collection or with ratio to creatinine

• Retinopathy may also indicate that there are issues with the small vessels

10

What defines microalbuminuria?

30-300 mg/day excretion of albumin

11

What functional and structural changes occur during the progression of Diabetic Nephropathy?

Functional:
• Increase in GFR
• Reversible Albuminuria
• Increase in Kidney Size

Structural:
• Increase in Basement membrane Thickness
• Mesengial Expansion

12

What characteristics define stage 0 (onset of diabetes) through stage 2 of diabetic nephropathy?
• when do they occur?

Stage 0 = Kidney Enlargement

Year 2 = Stage 1 = HYPERFILTRATION with INCREASED GFR (2cm inc. in kidney size)

Year 5 = Stage 2 = MICROALBUMINEMIA and possibly HTN

13

What characteristics define stage 3 through stage 5 diabetic nephropathy?
• when do they occur?

Year 11-23 = stage 3 = ALBUMINUREA

Year 13-25 = Stage 4 = ADVANCED CLINICAL NEPHROPATHY - GFR below 75 ml/min

Year 15-27 = Stage 5 = END STAGE KIDNEY DISEASE - GFR below 10 ml/min (require dialysis or transplantation)

14

T or F: by controlling glucose you can control the rate at which Diabetic Nephropathy progresses

True

15

T or F: Diabetic nephropathy is the biggest single for people to reach end stage renal disease and conversely end stage renal disease is the leading cause of death in diabetic nephropathy.

FALSE, ONLY a small percentage of diabetic patients live long enough to reach end stage renal disease.

16

Why is there increased filtration (hyperfiltration) in diabetic nephropathy?
• when does this occur?

HYPERFILTRATION:
• results from high glucose concentration in the blood leading to increased filtered load TOO MUCH IS FILTERED INTO THE PROXIMAL TUBULE TO ALL BE REABSORBED BY GSLT1/2 so it remains in the nephron as an osmotically active agent

• Macula Densa detect low Chloride and secrete Renin to increase filtration by allowing Angiotensin II to act on the Efferent arteriole

17

Besides contributing to Glomerular Hyperfiltration, what other deleterious does Angiotensin II have?

Angiotensin II leads to RELEASE of TGF-ß

18

What makes the angiotensin II mediated release of TGF-ß so detrimental?

TGF-ß causes SCARING i.e. increased MATRIX, FIBROBLASTS, and TUBULOEPITHELIAL CELLS

TGF-ß also acts as a Metalloprotease inhibitor

19

What causes the thickening of the glomerular basement membrane in diabetic nephropathy?

• Non-enzymatic Glycosylation leads to CROSSLINKED AGEs (advanced glycosylation end products) which lead to COLLAGEN synthesis

• Angiotensin II (activated in hyperfiltration process) also acts DIRECTLY to stimulate TGF-ß production which PROMOTES Scaring and Matrix deposition while Inhibiting Matrix Metalloproteases (MMPs)

20

What tissues are affected by angiotensin II stimulation of TGF-ß in the glomerulus?

• Tubuloepithelial Hypertrophy
• Mesangial Proliferation
• Glomerular Scarring

Via stimulation of Collagen Deposition and MMP inhibition

21

At what stage of diabetic nephropathy do we invariably see Hypertension?

• HTN see in Stage 4 - ADVANCED CLINICAL NEPHROPATHY

22

What are some of the causes of tubular damage in diabetic nephropathy?

• TGF-ß stimulates tubuloepithelial hypertrophy
• Lots of PROXIMAL tubular damage

23

What are the short and long term effects on microalbuminuria with intensive control of blood glucose?

BOTH short term and LONG term patients experience overall slower progression to macroabluminuria

24

What drugs are the best at acting directly to preserve glomerular health in diabetics?
• what changes in lab values should you expect when starting a patient on these drugs?

ACE Is and ARBs are the best because they relieve the increased Glomerular Pressure created by constriction of the efferent arteriole

Lab Values:
• Serum Creatinine will INCREASE because you will reduce glomerular filtration as a result of efferent arteriolar relaxation

25

How does HTN progress as diabetic nephropathy progresses?

Initially HTN = Renin Dependent - with increased Osmotic diuretic effect from glucose overload

Later HTN = Volume dependent - as glomerular filtration rate decreases

26

ACE Is and ARBs increase serum creatinine, indicating decreased kidney function. So why are they use in diabetic nephropathy?

SHORT TERM:
• Reduction in GFR by reducing Hydrostatic pressure in the glomerulus (Pg)

LONG TERM:
• Decrease membrane damage and by reducing glomerular pressure, long term benefit = rise in GFR because INCREASE Kf (you don't ruin the surface area of the capillaries)

27

In what situation can you not use an ACE I or ARB to treat a diabetic with diabetic nephropathy?
• what alternative groups of drugs could you consider for patients not able to take ACE Is or ARBs for diabetic nephropathy?

• PREGNANCY

• Beta blockers and non-dihydropyridine Calcium Channel Blockers

28

In addition to administering an ACE I, what advice should you give to diabetics who are experiencing diabetic nephropathy?

• Avoid EtOH, Salt, Loss Wt. and Excercise

29

T or F: microalbuminuria is a marker of CV risk.

TRUE

30

compare the use of standard blood pressure drugs to ACE Is and ARBs in diabetic nephropathy.

STD drugs = INCREASE proteinuria because you have increased GFR

31

T or F: the higher your proteinuria, the greater the chance is that you'll move on to end stage renal disease.

TRUE

32

Why do we see increased CV benefits when we control proteinuria?

• Increase water retention due to reduced GFR and and salt retention as a result of Renin, angiotensin, aldosterone leads to INCREASED PRELOAD on the heart

33

T or F: diabetics have a much greater chance of having pyelonephritis

True

34

Why are diabetics at an increased risk for PAPILLARY NECROSIS?

• Papillary Necrosis results from decreased blood supply to the medulla that is a result of HYALINE arteriolosclerosis seen in diabetes

35

Is neurogenic bladder associated with diabetes?

YES, this is related to the peripheral nephropathy seen in diabetes

36

Why is RTA 4 associated with acidosis and hyperkalemia?
• how does this relate to diabetes?

RTA 4

• RTA 4 is HYPOALDOSTERONISM which leads to HYPERKALEMIA because there is no aldosterone to cause K+ efflux from the Distal Tubule

• Increase K+ leads to more K+ INflux through NKA which causes increased INflux through the Na+/H+ exchanger on NORMAL BODY CELLS

• Increased flow through Na+/H+ EXPORTS H+ into the plasma while importing Na+

***These factors are what causes HYPERKALEMIA with ACDIOSIS****


Relationship to Diabetes:
*****HYALINE arteriolosclerosis eventually damages the efferent and afferent arterioles to the point where they can no longer detect aldosterone****