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SM 207 Diabetic Nephropathy Flashcards

1
Q

What is Diabetes Mellitus?

A

Diabetes Mellitus is a disorder that results in hyperglycemia due to insulin deficiency (Type I) and/or resistance (Type II)

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2
Q

What is Type I Diabetes?

A

A form of DM that presents at birth or within months of development characterized by no insulin due to destruction of pancreatic islet cells

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3
Q

What is Type II Diabetes?

A

A form of DM that presents later in life due to insulin resistance and eventual deficiency

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4
Q

What is the pathophysiological cause of Type I Diabetes?

A

Autoimmune destruction of pancreatic islet cells early in life

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5
Q

When and how does Type I Diabetes present?

A

Type I Diabetes presents early in childhood with severe illness, due to autoimmune destruction of pancreatic islet cells

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6
Q

Which occurs first in Type II Diabetes, Insulin Resistance or Insulin deficiency?

A

Insulin Resistance first manifests in Type II Diabetes, due to high secretion of Insulin desensitizing cells

Insulin deficiency occurs later

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7
Q

What is the major risk factor for Type II Diabetes?

A

Obesity

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8
Q

What factor about Type II Diabetes effects Diabetic Nephropathy?

A

Duration - long-standing DIIM has a greater likelihood of developing Diabetic Nephropathy

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9
Q

Is Diabetes Mellitus curable?

A

Only if it’s Type I, with a pancreas transplant

Type II cannot be cured and is only managed

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10
Q

What do the microvascular consequences of Diabetes Mellitus refer to?

A

Nephropathy, Retinopathy, Neuropathy

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11
Q

What do the macrovascular consequences of Diabetes Mellitus refer to?

A

Cardiovascular risk (MI, Stroke)

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12
Q

How does Diabetes Mellitus effect the extremities?

A

Peripheral Vascular Disease, Amputations

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13
Q

Which races are more at risk for Diabetes?

A

Hispanics and African Americans

Increased DIIM risk predisposes kidney disease risk

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14
Q

What is the leading cause of ESRD?

A

Diabetes

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15
Q

What is the leading cause of Blindness in adults?

A

Diabetes

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16
Q

Is Diabetic Nephropathy inevitable in patients with Diabetes?

A

No, about 1/3 develop Diabetic Nephropathy

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17
Q

Why is the natural history of Diabetic Nephropathy more predictable in patients with Type I DM than those with Type II DM?

A

Type I DM has a clear time of onset, while Type II DM may be long-standing, and the duration of Diabetic damage sets the course of Diabetic Nephropathy

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18
Q

What are the 4 stages of Diabetic Nephropathy?

A

Hyperfiltration (Silent)
Microalbuminuria (Incipient)
Macroalbuminuria (Overt)
Advanced Nephropathy

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19
Q

What lab abnormalities are found in the Hyperfiltration stage of Diabetic Nephropathy?

A

None - Hyperfiltration stage is not detectable on labs

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20
Q

What effect does the Hyperfiltration have on GFR during Diabetic Nephropathy?

A

During the Hyperfiltration stage, single Nephron GFR increases

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21
Q

Which stage of Diabetic Nephropathy is the first that can be detected in clinic on urine?

A

Microalbuminuria (Incipient)

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22
Q

Silent Diabetic Nephropathy is also known as?

A

Hyperfiltration

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23
Q

Incipient Diabetic Nephropathy is also known as?

A

Microalbuminuria

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24
Q

Overt Diabetic Nephropathy is also known as?

A

Macroalbuminuria

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25
Q

What functional changes occur during the Silent phase of Diabetic Nephropathy?

A

Silent = Hyperfiltration stage

Increase in GFR (always, not normally measured)
Increase in Kidney Size (sometimes, seen on ultrasound)

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26
Q

What structural changes occur during the Silent phase of Diabetic Nephropathy?

A

Silent = Hyperfiltration stage

Glomerular Hypertrophy (no cell proliferation)
Glomerular Basement Membrane Thickening
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27
Q

What is the first sign of Diabetic Nephropathy that can be detected, ever?

A

Glomerular basement thickening, in the Silent Stage

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28
Q

What are the functional changes that accompany Incipient Diabetic Nephropathy?

A

Incipient = Microalbuminuria

Microalbuminuria develops
Normal GFR
Microvascular complications (Eyes, Feet, Sensation)

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29
Q

Is GFR normal in the Incipient stage of Diabetic Nephropathy?

30
Q

What is Microalbuminuria?

A

30 - 300mg of albumin in urine

31
Q

Is Albuminuria the same as Proteinuria?

A

NO; proteinuria is all protein except Albumin and can have up to 150mg of protein normally

32
Q

Is Diabetic Retinopathy a predictor of Diabetic Nephropathy?

A

Yes; patients with Diabetic Retinopathy tend to have Diabetic Nephropathy

33
Q

What structural changes accompany Incipient Nephropathy?

A

Mesangial Matrix expansion

34
Q

What is the hallmark of Diabetic Nephropathy?

A

Mesangial Matrix expansion

35
Q

What is Mesangial Matrix expansion?

A

Mesangial space expanding due to increased ECM proteins like collagen and fibronectin

36
Q

How does Mesangial Matrix expansion effect the kidney?

A

ECM expansion causes loss of filtration capacity and the glomerulus loses normal function, leading to nodules known as Kimmelsteil-Wilson lesions

37
Q

What are Kimmelsteil-Wilson lesions pathopneumonic for?

A

Pathopneumonic for Diabetic Nephropathy

38
Q

What causes Kimmelsteil-Wilson lesions?

A

Mesangial Matrix expansion in Incipient Diabetic Nephropathy

39
Q

What functional changes accompany Overt Nephropathy?

A

Overt = Macroalbuminuria

Albuminuria > 300mg/day
GFR declines rapidly (6-12 ml/min/year)
Hypertension

40
Q

Which stage of Diabetic Nephropathy reflects the first decline in GFR?

A

Overt Nephropathy (Macroalbuminuria)

41
Q

What is nephrotic range proteinuria?

42
Q

How rapidly does GFR decline in Incipient Nephropathy?

A

It doesn’t, compensation still holds

43
Q

Why does HTN occur during Overt Diabetic Nephropathy?

A

Sodium and fluid retention

44
Q

What are the pathogenic factors that drive tissue injury in Diabetic Nephropathy?

A

Hyperfiltration
Proteinuria
Intraglomerular HTN
Mesangial Matrix Expansion

45
Q

What 3 factors cause Hyperfiltration in Diabetic Nephropathy?

A

Glomerular Hypertrophy leading to increased capillary surface area
Afferent Arteriolar Vasodilation
Efferent Arteriolar Vasoconstriction

46
Q

What causes Afferent Arteriolar Vasodilation in Diabetic Nephropathy?

A 
Less NaCl to the Macula Densa 
= Less ATP
= Less Adenosine
= Less Vasodilation of Afferent Arteriole
= Vasodilation of Afferent Arteriole
47
Q

What causes Efferent Arteriolar Vasoconstriction in Diabetic Nephropathy?

A

Less NaCl to the Macula Densa causes Vasoconstriction due to Angiotensin II

48
Q

What causes Proteinuria in Diabetic Nephropathy?

A

GBM thickens but loses quality due to hyperglycemia
Podocyte abnormalites as foot processes detach
Hemodynamic effects as Intraglomerular HTN worsens

49
Q

Why does Intraglomerular HTN worsen albuminuria?

A

Intraglomerular HTN = high pressure that drives protein efflux into urine

50
Q

How does Mesangial Matrix Expansion correlate with GFR?

A

Inversely; the expanding matrix impinges capillaries and lowers surface area for filtration

51
Q

What effects do cytokines like TGF-Beta have in Diabetic Nephropathy?

A

Cytokines are Inflammatory and Pro-Fibrotic

52
Q

What pathways does hyperglycemia trigger?

A

Advance Glycation End-product formation (AGE)
Signaling Pathways (MAPK, HIF)
ROS release

53
Q

What do cytokines do to urine protein?

A

Cytokines alter hemodynamics and promote albuminuria

54
Q

What is the primary goal in Diabetic Nephropathy treatment?

A

Intensive glycemic control down to Hb1AC < 7%

55
Q

What is the risk with pursuing intensive glycemic control in treating Diabetic Nephropathy?

A

Intensive glycemic control risks Hypoglycemia

56
Q

Does Intensive Glycemic control improve microvascular complications in Diabetic Nephropathy?

A

Yes, but no evidence for benefit of Macrovascular complications

57
Q

Does Intensive Glycemic control improve macrovascular complications in Diabetic Nephropathy?

A

No, but it does benefit Microvascular complications

58
Q

What is the most important risk factor for progressive GFR decline in diabetes?

A

Hypertension

59
Q

What is the blood pressure target in diabetic patients?

A

Since they have a CV risk factor, aim for 130/80, which may require multiple anti-hypertensives

60
Q

Which classes of anti-hypertensive are first-line in diabetes?

A

ACE-inhibitors and ARB’s, because they have renoprotective effects

61
Q

What are the renoprotective effects of ACEi/ARB’s?

A

They not only control BP but also relax the efferent Arteriole to decrease intraglomerular pressure and lower protein being pushed into urine

Also block profibrotic effects of Angiotensin II

62
Q

Which component of the RAAS pathway is pro-fibrotic in the glomerulus?

A

Angiotensin II

ACEi and ARB can block the pro-fibrotic effects, making them first line anti-HTN drugs in diabetics

63
Q

Which is better for managing Diabetic Nephropathy, ACEi or ARB?

A

No evidence one is better than the other

Risk of cough in ACEi

64
Q

Should you use both an ACEi and an ARB in managing Diabetic Nephropathy?

A

NO, risk of AKI and Hyperkalemia

65
Q

What are SGLT inhibitors?

A

Inhibitors of the Na/Glucose transporter in the PCT

66
Q

What is the suffix for SGLT inhibitors?

A

-gliflozins

67
Q

How do SGLT inhibitors treat Diabetic Nephropathy?

A

Promote urinary glucose loss and reduce both microvascular and macrovascular complications in Diabetes

68
Q

Do SGLT inhibitors prevent macrovascular or microvascular complications?

69
Q

How do SGLT inhibitors work?

A

They block the Na/Glucose transporter in the PCT to improve Na delivery to the Macula Densa and decrease RAAS activation, lessening Glomerular HTN and diabetes-induced hyperfiltration

70
Q

What class of drugs reduces diabetes-induced hyperfiltration?

A

SGLT inhibitors

71
Q

What clinical indicators should be tracked in diabetic nephropathy?

A

Albuminuria, Kidney Function, Blood Pressure

Renal (19 decks)

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