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Diabetes and Renal Disease

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Type 1 Vs Type 2 DM. 4. Type 1. Young. Thin. Insulin deficient (pancr. islet cell loss) ... Immune destruction of insulin producing cells in pancreas. leading ... – PowerPoint PPT presentation

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Title: Diabetes and Renal Disease


1
Diabetes and Renal Disease
  • Dr Anne Kleinitz
  • KRSS GP
  • 12/11/2009

1
2
Learning Objectives
  • Type 1 vs Type 2 DM
  • Diabetes Management
  • Diabetic Complications
  • Diabetic Nephropathy ESKD

2
3
Type 1 Vs Type 2 DM
3
4
  • Type 1
  • Young
  • Thin
  • Insulin deficient (pancr. islet cell loss)
  • Acute presentation
  • Ketoacidosis
  • Insulin initially
  • Type 2
  • Older
  • Overweight
  • Insulin resistant
  • (excess fat cell mass)
  • Delayed diagnosis
  • Diet pills
  • Insulin later or never

4
5
5
6
6
7
Type 1
  • Immune destruction of insulin producing cells in
    pancreas
  • leading to insulin deficiency.
  • Prevalence
  • General population 12 17
  • Indigenous 1
  • Acute onset, usually early in life

7
8
Type 2
  • Tissue resistance to insulin defects in insulin
    secretion
  • Gradual onset. One end of spectrum
  • Insulin resistance but normal glucose tolerance
  • Impaired fasting glucose (IFG)
  • Impaired glucose tolerance pre-diabetes (IGT)
  • Type 2 DM

8
9
9
10
Q. More common in T2 than T1?
  • Age lt 20 years
  • Overweight
  • High levels of blood insulin
  • Prone to ketoacidosis
  • Albuminuria at time of diagnosis

10
11
Q. More common in T2 than T1?
  • Age lt 20 years NO
  • Overweight YES
  • High levels of blood insulin YES
  • Prone to ketoacidosis NO
  • Albuminuria at time of diagnosis YES

11
12
  • Prevalance (estimated)
  • Australia - 7.5 (but ½ unDx!)
  • Indigenous
  • gt 25 yrs 10 30
  • 3 4 x higher than general population
  • Higher in remote communities
  • Hospital admission for DM more common
  • 12 x higher rates eg. Gestational DM
  • Contributes to CVD 67 with DM died of CVD
    (1997-99)
  • Renal failure is also a common cause of death

12
13
Age-adjusted Percentage of U.S. Adults Who Were
Obese or Who Had Diagnosed Diabetes
Obesity (BMI 30 kg/m2)
Diabetes
CDCs Division of Diabetes Translation. National
Diabetes Surveillance System available at
http//www.cdc.gov/diabetes/statistics
13
14
1994
14
15
1995
15
16
1996
16
17
1997
17
18
1998
18
19
1999
19
20
2000
20
21
2001
21
22
2002
22
23
2003
23
24
2004
24
25
2005
25
26
2006
26
27
2007
27
28
Childhood Diabetes
  • Rising T2DM, parallel with ? obesity
  • 10-14 of new paediatric DM
  • 50 in rural and remote
  • Many likely undiagnosed
  • Indigenous children disproportionately
    represented
  • gt ½ of children with T2DM are indigenous
  • Mx Diet, exercise, Metformin and Insulin

28
29
Gestational diabetes
  • Temporary
  • Occurs in pregnancy and usually disappears after
    delivery
  • Mother has much greater risk of developing
    diabetes later
  • Morbidity

29
30
Metabolic SyndromeSyndrome X
  • Associated with increased risk of CVD, CKD and
    death.
  • DIAGNOSIS
  • Insulin resistance
  • FBG gt 5.6 or T2DM
  • Central Obesity
  • WC gt 94cm
  • Abnormal lipid profile HDL
  • Male lt 1.03, Female lt 1.29
  • Hypertension
  • Sys gt 130, dias gt85

30
31
31
32
32
33
33
34
Treatment Options
34
35
Treatment Options
  • ?Glucose load ? meal size sugars
  • ?Insulin release (secretogogues)
  • sulphonourea eg
    Gliclazide
  • Insulin, Pancreas Tx
  • ?Insulin resistance (insulin sensitizers)
  • Exercise weight
    loss Metformin or glitazones

35
36
Diabetes management
  • Life-style
  • ? physical activity
  • Weight ?
  • Smoking cessation
  • Alcohol reduction
  • Low fat diet
  • Oral Medications
  • Increase insulin production (sulphonoureas)
  • Increase insulin sensitivity (metformin)
  • Insulin

36
37
Short-acting Long-acting Insulin
Breakfast
Lunch
Dinner
Short acting
Plasma insulin
Glargine
400
1600
2000
2400
400
800
1200
800
Time
37
38
Aims in Mx (KAMSC Chronic Disease Protocol)
  • HbA1C lt 7
  • Total cholesterol lt 4 mmol/L
  • HDL gt 1mmol/L, TG lt 2, LDL lt 1.8
  • BP lt 125/80
  • BMI 17-25
  • WC lt 100 cm
  • NO smoking
  • Alcohol max 2 std drinks/day
  • Exercise gt 20 mins gt 4 day/wk
  • ACR lt 3.5 mg/mmol

38
39
Multidisciplinary Team Care
  • Diabetes
  • Endocrinology/Dietetics
  • Microvascular Disease
  • Ophthalmology/Nephrology/Podiatry
  • Macrovascular Disease
  • Vascular Surgery/Cardiology

39
40
Specialised Treatments
  • Insulin Pump
  • Tight BSL control for brittle diabetes
  • Awaiting autofeedback sensors
  • Pancreas Transplantation
  • Insulin independence
  • Operative mortality

40
41
Diabetic Complications
41
42
Diabetic Complications
  • Microvascular
  • Retinopathy
  • Nephropathy
  • Neuropathy
  • peripheral autonomic
  • Macrovascular
  • Cerebrovascular
  • Cardiovascular
  • Peripheral vascular

42
43
43
44
Natural History of Type I
  • 5 stages
  • 1. Hyperfiltration at diagnosis (low s. creat)
  • 2. Microalbuminuria gt 5-10 years (urine ACR)
  • 3. Overt proteinuria with ?BP retinopathy for
    2-5 years, minimal haematuria (MSU)
  • 4. CKD with normal-sized kidneys (renal U/S)
  • 5. ESKD 18-24 months after CKD

44
45
45
46
Natural History of Type II
  • Far commoner than Type I
  • Long asymptomatic phase
  • HPT, nephropathy retinopathy often present at
    time of Dx
  • Degree of proteinuria correlates with general
    vascular risk and 20x CKD risk

46
47
Hyperfiltration Phase
  • Elevated GFR 2o ?BSL/BP/protein/obesity
  • ?Intra-glomerular pressure
  • Too good to be true serum creatinine
  • Accelerated progression to CKD

47
48
Albuminuria then Proteinuria
  • Microalbuminuria first (lower MW)
  • Raised by ?GFR (i.e. ?BSL, ?protein diet, fever,
    exercise)
  • Spot urine ACR or PCR
  • more convenient than 24hr collection
  • more accurate than urinalysis
  • adjusts for fluid intake
  • underestimates the muscular patient

48
49
Diabetic Nephropathy
  • From haemodynamic metabolic stresses
  • Metabolic stress
  • deposition of advanced glycosylation end products
    in connective tissue sml vessels.
  • May take 10-20 yrs but many T2DM asymptomatic for
    several yrs, hence nephropathy may already be
    present at Dx

49
50
  • 1st clinical sign is microalbuminuria (??ACR)
  • Kidney not able to catabolise albumin
  • This can also occur transiently with
  • Fever
  • Exercise
  • Short term hyperglycaemia
  • High protein meal
  • Hence, repeat at a later date/rule out reversible
  • DM HPT, ? x 20 risk of progressive nephropathy
  • DM HPT poor diabetic lipid control, ? x 40
    risk

50
51
Nephropathy Risk Factors
  • DM Type Duration
  • 20 of Type I after 20 years
  • 40 of Type II any duration
  • Poor diabetic control
  • Hypertension
  • Aboriginal gt Indian gt Caucasian
  • Smokers
  • Family history

51
52
Nephropathy Risk Factors
  • Modifiable
  • HbA1c, BP total cholesterol (Odds Ratio 43)
  • Obesity, smoking
  • Non-modifiable
  • Age, ethnicity, male sex

52
53
Delaying Complications
  • Tight diabetic control
  • Prevention of microvascular Cmplx
  • Risk of hypos
  • Tight BP control
  • Prevention and management of micro macro Cmplx
  • Use ACEI, ARBs or both combined

53
54
ACE Inhibitors can prevent progression of renal
failure
Normotensive Type 2 Diabetics
400
110
Proteinuria (mg/day)
Initial GFR
350
105
320
Placebo
100
280
Enalapril
240
95
200
90
160
Placebo
Enalapril
85
120
80
80
0
1
2
3
4
5
6
0
1
2
3
4
5
6
Years
Years
Ann Intern Med 118 577-581.1993
54
55
ACEI/ARB Proteinuria Remission
Protein/Creat Ratio - Urine
1000
mg/mmol
500
H


0
2000
2001
2002
Jan 2000
Creatinine - Plasma
H


H


90
80
70
umol/L
60
50
L


L


40
30
2000
2001
2002
Jan 2000
55
56
Use of ACEi/ARBs
  • BUT
  • ARF risk if underperfused
  • Hyperkalaemia risk with many types of pills
    (spironolactone)
  • SO
  • Check BP electrolytes at 1/12 and 6/12
  • Check all new pills

56
57
Q. Which features are typical of diabetic CKD at
presentation ?
  • Haematuria
  • Small scarred kidneys
  • Progress to ESKD in lt2yrs
  • Associated retinopathy
  • ß-blockers better than ACE-I Rx

57
58
Q. Which features are typical of diabetic CKD at
presentation ?
  • Haematuria NO
  • Small scarred kidneys NO
  • Progress to ESKD in lt2yrs NO
  • Associated retinopathy YES
  • ß-blockers better than ACE-I Rx NO

58
59
Diabetes and ESKD
  • Reducing insulin requirements
  • Difficult vascular access
  • Accelerated macrovascular disease
  • Advanced microvascular disease
  • Frequent sepsis
  • Silent ischaemia
  • 2-3 x death rate vs non-DM patients

59
60
How can DM effect Dialysis?
  • Autonomic neuropathy may suffer hypotension
    increased by large fluid shift in HD
  • Uncontrolled BSLs may absorb some glucose in PD
    fluid
  • Severe PVD difficult to get vascular access for
    HD
  • PVD may also affect peritoneum and reduce PD
    success
  • Increased risk of infections problem in both
  • Transplants new kidneys develop nephropathy,
    hence good glycaemic control important

60
61
Strict BSL Control in early Type I
  • Target HbA1c lt 7
  • For every 1? HbA1c
  • 10 ?CVD
  • 40 ?Microvascular Cmplx
  • BUT
  • Doubles risk of hypoglycaemia
  • Loss of control with DM duration
  • 50 at 3yr
  • 30 at 6yr
  • 15-25 at 9yr ( patients with HbA1c lt 7 on
    Met or OHA alone)

61
62
Strict BSL Control in DM CKD
  • AND
  • Minimal benefit if overt proteinuria
  • Diabetes cured by advancing CKD
  • reduced appetite and CHO intake
  • prolonged insulin half-life
  • false elevation of HbA1c by 0.5-1

62
63
Metformin in CKD
  • No hypos or weight gain
  • Inexpensive
  • BUT
  • Renally-excreted
  • Excess doses ? anorexia, diarrhoea
  • Dose adjust to GFR 2g to 250mg/day
  • Protocol says
  • eGFR 30 59 max 1gm/day
  • cease when eGFR lt30 but
  • Risk of fatal lactic acidosis if unwell

63
64
Glitazones in DM
  • Av.1 fall in HbA1c as monoRx or add-on
  • Preserves beta-cell fn - use early
  • Durable effect gt3yrs
  • BUT
  • 1-2/12 delayed onset
  • Average 4kg SC fat gain, visceral fat loss
  • Oedema (Na/H20, ?vasc. permeability)
  • Expensive

64
65
Strict BP Control at any stage
  • ½s (or even stops) rate of fall in GFR
  • Greater benefit than tight BSL control
  • Falling BP Target 120/70 currently
  • Preferential use of ACEi/ARBs
  • Complete regression of proteinuria possible
  • Helps all micro- macrovascular disease
  • (Parving, UKPDS, Captopril Trial, MicroHOPE,
    IRMA/IDNT, JNC VI)

65
66
Use of ACEi/ARBs actions
  • Antihypertensive
  • ? by salt excess, ?by thiazides
  • need mean of 3 agents in mild CKD
  • Antiproteinuric
  • 30-50? alone, 40-70? together
  • Renoprotective
  • corrects ?GFR, expected 30 ?creatinine

66
67
Combination ACEI/ARBs ? proteinuria by 90
Laverman Kidney Int 2002
67
68
ACEI/ARB Proteinuria Remission
Protein/Creat Ratio - Urine
1000
mg/mmol
500
H


0
2000
2001
2002
Jan 2000
Creatinine - Plasma
H


H


90
80
70
umol/L
60
50
L


L


40
30
2000
2001
2002
Jan 2000
68
69
Use of ACEi/ARBs risks
  • BUT
  • ON-TARGET ? CVD death if no proteinuria
  • Risk of ARF
  • Esp. if dry, in CCF, bilateral RAS, on NSAIDs
  • Risk of hyperkalaemia in diabetic CKD
  • Esp. if high fruit/nut/choc diet, acidotic
  • Esp. if other K-sparing Rx (NSAIDs,
    spironolactone, trimethoprim)

69
70
Use of ACEi/ARBs guidelines
  • SO
  • Always check BP electrolytes 1 month after
    starting or adding thiazide
  • Check after 1 week in high-risk patients
  • Stop temporarily if unwell

70
71
Thank You
  • Questions ?

71
72
References
  • Mark Thomas. Nephrologist. Royal Perth Hospital.
  • Kidney Diseases, 5th Edition. National Kidney
    Foundation. 2009
  • Couzos and Murray. Aboriginal Primary Health
    Care, an evidence based approach. 3rd edition.
    2008
  • Murtagh. Murtaghs General Practice. 4th edition.
    2007

72
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