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Renal Week 3 > Diabetic Renal Disease > Flashcards

Diabetic Renal Disease Flashcards

1
Q

What defines Diabetes in a patient?

A
  • Fasting Blood Glucose greater than 126 mg/dL

* Random Blood Glucose greater than 200 mg/dL and confirmed on more than 1 occasion

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2
Q

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

A

True

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3
Q

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

A

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

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4
Q

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

A
  • Metabolic
  • Macrovascular
  • Microvascular
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5
Q

What are the diabetic microvascular complications?

A

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

Note: Retinopathy and Nephropathy = close tie in type I

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6
Q

What are the diabetic macrovascular complications?

A

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

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7
Q

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

A

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

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8
Q

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

A

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

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

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9
Q

How do you make the Clinical Diagnosis of Diabetic Retinopathy?

A
  • 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
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10
Q

What defines microalbuminuria?

A

30-300 mg/day excretion of albumin

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11
Q

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

A

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

Structural:
• Increase in Basement membrane Thickness
• Mesengial Expansion

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12
Q

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

A

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

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13
Q

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

A

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)

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14
Q

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

A

True

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15
Q

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.

A

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

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16
Q

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

A

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
Q

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

A

Angiotensin II leads to RELEASE of TGF-ß

18
Q

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

A

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

TGF-ß also acts as a Metalloprotease inhibitor

19
Q

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

A
  • 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
Q

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

A
  • Tubuloepithelial Hypertrophy
  • Mesangial Proliferation
  • Glomerular Scarring

Via stimulation of Collagen Deposition and MMP inhibition

21
Q

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

A

• HTN see in Stage 4 - ADVANCED CLINICAL NEPHROPATHY

22
Q

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

A
  • TGF-ß stimulates tubuloepithelial hypertrophy

* Lots of PROXIMAL tubular damage

23
Q

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

A

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

24
Q

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?

A

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
Q

How does HTN progress as diabetic nephropathy progresses?

A

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

Later HTN = Volume dependent - as glomerular filtration rate decreases

26
Q

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

A

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
Q

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?

A
  • PREGNANCY

* Beta blockers and non-dihydropyridine Calcium Channel Blockers

28
Q

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

A

• Avoid EtOH, Salt, Loss Wt. and Excercise

29
Q

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

A

TRUE

30
Q

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

A

STD drugs = INCREASE proteinuria because you have increased GFR

31
Q

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

A

TRUE

32
Q

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

A

• 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
Q

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

A

True

34
Q

Why are diabetics at an increased risk for PAPILLARY NECROSIS?

A

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

35
Q

Is neurogenic bladder associated with diabetes?

A

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

36
Q

Why is RTA 4 associated with acidosis and hyperkalemia?

• how does this relate to diabetes?

A

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*

Renal Week 3 (16 decks)

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