1 diabetes and renal disease dr anne kleinitz krss gp 12/11/2009
TRANSCRIPT
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Diabetes and Diabetes and Renal DiseaseRenal Disease
Dr Anne KleinitzDr Anne Kleinitz
KRSS GPKRSS GP
12/11/200912/11/2009
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Learning ObjectivesLearning Objectives
• Type 1 vs Type 2 DM• Diabetes Management• Diabetic Complications• Diabetic Nephropathy & ESKD
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Type 1 Vs Type 2 DMType 1 Vs Type 2 DM
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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
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Type 1 Type 2
Onset Acute (symptomatic)
Slow or insidious
Clinical features Weight lossPolyuriaPolydipsia
Obese/over wtStrong FHx EthnicityPCOS
Ketosis Often present Usually absent
Insulin (endog) Low or absent Normal or
Antibodies + ve ve
Assoc. autoimmune disorders
Yes No
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Type 1Type 1
• Immune destruction of insulin producing cells in pancreasleading to insulin deficiency.
• Prevalence– General population 12 – 17% – Indigenous 1%
• Acute onset, usually early in life
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Type 2Type 2
• Tissue resistance to insulin + defects in insulin secretion
• Gradual onset. One end of spectrum:– Insulin resistance but normal glucose
toleranceImpaired fasting glucose (IFG)Impaired glucose tolerance “pre-diabetes”
(IGT)Type 2 DM
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Normal IFG IGT Diabetes
Fasting <5.5 5.5 – 6.9 and
< 7 and ≥ 7.0
2 hr post 75g glucose
<7.8 <7.8 7.8 – 11 ≥11.1
Random < 5.5 ≥ 11.1
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Q. More common in T2 than T1?Q. More common in T2 than T1?
• Age < 20 years• Overweight• High levels of blood insulin• Prone to ketoacidosis• Albuminuria at time of diagnosis
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Q. More common in T2 than T1?Q. More common in T2 than T1?
• Age < 20 years NO**• Overweight YES• High levels of blood insulin YES• Prone to ketoacidosis NO• Albuminuria at time of diagnosis YES
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• Prevalance (estimated)– Australia - 7.5% (but ½ unDx!)
• Indigenous– > 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
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Age-adjusted Percentage of U.S. Adults Who Were Obese or Who Had Diagnosed Diabetes
Obesity (BMI ≥30 kg/m2)
Diabetes
1994
1994
2000
2000
2007
2007
No Data <14.0% 14.0-17.9% 18.0-21.9% 22.0-25.9% >26.0%
No Data <4.5% 4.5-5.9% 6.0-7.4% 7.5-8.9% >9.0%
CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available at http://www.cdc.gov/diabetes/statistics
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1994
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1995
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1996
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1177
1997
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1998
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1999
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2000
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2001
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2002
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2003
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2004
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2005
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2006
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2007
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Childhood DiabetesChildhood Diabetes
• Rising T2DM, parallel with obesity• 10-14% of new paediatric DM• ~ 50% in rural and remote• Many likely undiagnosed• Indigenous children disproportionately
represented– > ½ of children with T2DM are indigenous
• Mx – Diet, exercise, Metformin and Insulin
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Gestational diabetesGestational diabetes
• Temporary• Occurs in pregnancy and usually
disappears after delivery• Mother has much greater risk of
developing diabetes later• Morbidity
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Metabolic SyndromeMetabolic Syndrome“Syndrome X”“Syndrome X”
• Associated with increased risk of CVD, CKD and death.
• DIAGNOSIS1. Insulin resistance
• FBG > 5.6 or T2DM
2. Central Obesity • WC > 94cm
3. Abnormal lipid profile: HDL • Male < 1.03, Female < 1.29
– Hypertension• Sys > 130, dias >85
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Treatment OptionsTreatment Options
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Treatment OptionsTreatment 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
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Diabetes managementDiabetes management
• Life-style– physical activity– Weight ↓– Smoking cessation– Alcohol reduction– Low fat diet
• Oral Medications– Increase insulin production (sulphonoureas)– Increase insulin sensitivity (metformin)
• Insulin
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4:00 16:00 20:00 24:00 4:00
Breakfast Lunch Dinner
8:0012:008:00
Time
Glargine
Short acting
Pla
sma insu
linShort-acting & Long-acting InsulinShort-acting & Long-acting Insulin
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Aims in Mx Aims in Mx (KAMSC Chronic Disease Protocol)(KAMSC Chronic Disease Protocol)
• HbA1C < 7%• Total cholesterol < 4 mmol/L• HDL > 1mmol/L, TG < 2, LDL < 1.8• BP < 125/80• BMI 17-25• WC < 100 cm• NO smoking• Alcohol – max 2 std drinks/day• Exercise > 20 mins > 4 day/wk• ACR < 3.5 mg/mmol
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Multidisciplinary Team CareMultidisciplinary Team Care
• Diabetes:– Endocrinology/Dietetics
• Microvascular Disease:– Ophthalmology/Nephrology/Podiatry
• Macrovascular Disease:– Vascular Surgery/Cardiology
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Specialised TreatmentsSpecialised Treatments• Insulin Pump
– Tight BSL control for brittle diabetes– Awaiting autofeedback sensors
• Pancreas Transplantation– Insulin independence– Operative mortality
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Diabetic ComplicationsDiabetic Complications
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Diabetic ComplicationsDiabetic Complications
• Microvascular– Retinopathy– Nephropathy– Neuropathy
• peripheral & autonomic
• Macrovascular– Cerebrovascular– Cardiovascular– Peripheral vascular
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Natural History of Type INatural History of Type I
5 stages
1. Hyperfiltration at diagnosis (low s. creat)
2. Microalbuminuria > 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
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Stage Diabetes Duration
Manifestations
1 0 – 3-5 Renal hypertrophy GFR
2 3-5 + Basement M thickeningMesangial expansion
3 7-15 + MicroalbuminuriaHPT
4 15-20 + ProteinuriaHPT↓ GFR
5 15 – 25+ ESKD
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Natural History of Type IINatural 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
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Hyperfiltration PhaseHyperfiltration Phase
• Elevated GFR 2o ↑BSL/BP/protein/obesity
• ↑Intra-glomerular pressure
• “Too good to be true” serum creatinine
• Accelerated progression to CKD
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Albuminuria then ProteinuriaAlbuminuria 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
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Diabetic NephropathyDiabetic 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
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• 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
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Nephropathy Risk FactorsNephropathy Risk Factors
• DM Type & Duration– 20% of Type I after 20 years– 40% of Type II any duration
• Poor diabetic control• Hypertension• Aboriginal > Indian > Caucasian• Smokers• Family history
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Nephropathy Risk FactorsNephropathy Risk Factors
• Modifiable– HbA1c, BP & total cholesterol (Odds Ratio 43)
– Obesity, smoking
• Non-modifiable– Age, ethnicity, male sex
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Delaying ComplicationsDelaying Complications
• Tight diabetic control– Prevention of microvascular Cmplx
• Risk of hypos
• Tight BP control– Prevention and management of micro &
macro Cmplx– Use ACEI, ARB’s or both combined
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ACE Inhibitors can prevent ACE Inhibitors can prevent progression of renal failureprogression of renal failure
120
160
200
240
280
320
350
400
800 1 2 3 4 5 6
Years
Ann Intern Med 118 577-581.1993
Placebo
Enalapril 85
90
95
100
105
110
800 1 2 3 4 5 6
Years
Placebo
Enalapril
Normotensive Type 2 Diabetics
Proteinuria
(mg/day)
% Initial GFR
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ACEI/ARB Proteinuria ACEI/ARB Proteinuria RemissionRemission
H
L
H
L
30
40
50
60
70
80
90
2000Jan 2000
2001 2002
Creatinine - Plasma
umol
/L
H 0
500
1000
2000Jan 2000
2001 2002
Protein/Creat Ratio - Urine
mg/
mm
ol
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Use of ACEi/ARBsUse 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
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Q. Which features are typical of Q. Which features are typical of diabetic CKD at presentation ?diabetic CKD at presentation ?
• Haematuria• Small scarred kidneys• Progress to ESKD in <2yrs• Associated retinopathy• β-blockers better than ACE-I Rx
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Q. Which features are typical of Q. Which features are typical of diabetic CKD at presentation ?diabetic CKD at presentation ?
• Haematuria NO• Small scarred kidneys NO• Progress to ESKD in <2yrs NO• Associated retinopathy YES• β-blockers better than ACE-I Rx NO
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Diabetes and ESKDDiabetes 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
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How can DM effect Dialysis?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
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Strict BSL Control in early Type IStrict BSL Control in early Type I
• Target HbA1c < 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 < 7% on Met or OHA
alone)
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Strict BSL Control in DM CKDStrict 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%
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Metformin in CKDMetformin 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 <30 but…
– Risk of fatal lactic acidosis if unwell
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Glitazones in DMGlitazones in DM
• Av.1% fall in HbA1c as monoRx or add-on• Preserves beta-cell fn - use early • Durable effect >3yrs
BUT:– 1-2/12 delayed onset – Average 4kg SC fat gain, visceral fat loss
– Oedema (Na+/H20, ↑vasc. permeability)
– Expensive
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Strict BP Control at any stageStrict BP Control at any stage
• ½’s (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)
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Use of ACEi/ARBs: actionsUse 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
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Laverman Kidney Int 2002
Combination ACEI/ARBs ↓ proteinuria by 90%
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ACEI/ARB Proteinuria ACEI/ARB Proteinuria RemissionRemission
H
L
H
L
30
40
50
60
70
80
90
2000Jan 2000
2001 2002
Creatinine - Plasma
umol
/L
H 0
500
1000
2000Jan 2000
2001 2002
Protein/Creat Ratio - Urine
mg/
mm
ol
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Use of ACEi/ARBs: risksUse 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)
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Use of ACEi/ARBs: guidelinesUse 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
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Thank YouThank You
Questions ?Questions ?
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ReferencesReferences
• 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. Murtagh’s General Practice. 4th edition. 2007