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ภาวะแทรกซ้อนทางไตในผู้ป่วยเบาหวาน

This document discusses diabetic kidney disease (DKD). It begins by outlining the prevalence and scope of DKD, defining DKD, and listing the optimal management of DKD as topics. It then provides details on the diagnosis of DKD, including the earliest clinical evidence being microalbuminuria. It discusses screening guidelines and measuring urinary protein. It outlines the stages of chronic kidney disease and strategies for treating DKD, including blood glucose control, blood pressure control, and lifestyle modifications. Target HbA1c levels for preventing DKD complications are also discussed.

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DIABETIC KIDNEY DISEASE
 Assist Prof. Warangkana Pichaiwong, MD. Renal Division, Department of Medicine. Rajavithi Hospital, Bangkok. wpichaiw@hotmail.com
! Prevalence and Scope of DKD Definition of DKD Optimal management of DKD Topics
Evolution
The adjusted rate of prevalent rates of 
 ESRD and annual percent change 81 84 87 90 93 96 99 02 05 08 11 Bars:Ratepermillionpopulation 0 100 200 300 400 Symbols:one-year%change -5 0 5 10 15 line: add’l adjustment for Hispanic ethnicity 2013 USRDS. Annual Data Report.
Prevalent counts & adjusted rates of ESRD 
 by primary diagnosis USRDS. Annual Data Report. 2013 USRDS. Annual Data Report. Numberofpatients(inthousands) 0 10 20 30 40 50 81 84 87 90 93 96 99 02 05 08 11 Ratepermillionpopulation 0 50 100 150 200 Counts Rates Diabetes Hypertension GN Cystic kidney
Source: IDF Diabetes Atlas Sixth Edition, International Diabetes Federation 2013 Prevalence of Diabetic Mellitus in Adults (20-75 years) 2013
Source: IDF Diabetes Atlas Sixth Edition, International Diabetes Federation 2013 Prevalence of Diabetic Mellitus in Adults (20-75 years), 2013
Diagnosis of Diabetic Mellitus
Diagnosis of Diabetic Mellitus *In the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing. Diabetes Care. 2013; 36 Suppl 1: S11-66. A1C ≥6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.* OR FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8h.* OR 2-h plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT. The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.* OR In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).
Diabetic Kidney Disease
25–40% of patients with type 1 diabetes 5–40% of patients with type 2 diabetes Diabetic Kidney Disease Ismail N, Becker B, Strzelczyk P, et al. Kidney Int 1999; 55 (1): 1-28. Parving HH, Hommel E, Mathiesen E, et al. BMJ (Clin Res Ed) 1988; 296 (6616): 156-60.
Persistent albuminuria Arterial blood pressure elevation Decline in glomerular filtration rate (GFR) High risk of cardiovascular morbidity and mortality Dignosis of Diabetic Kidney Disease Parving, H, Østerby, R & Ritz, E: Diabetic nephropathy, in The Kidney 2000 edited by Brenner BM, Levine S, Philadelphia, W.B. Saunders, p 1731
DKD in Type 1 DM onset: > 5 years after diagnosis ESRD in overt nephropathy at 10 year 50% at 20 year 75% Molitch ME, et al. American Diabetes Association. Diabetes Care. 2004;27 Suppl 1:S79-83. Natural History of Diabetic Kidney Disease DKD in Type 2 DM onset: at diagnosis ESRD in overt nephropathy at 20 year 20%
Initial screening: 5 years after the diagnosis of type 1 diabetes (A) From diagnosis of type 2 diabetes (B) Screening: ●  Measurements of urinary ACR in a spot urine sample (B) ●  Measurement of serum creatinine and estimation of GFR (B)
 Patients with Diabetes should be Screened Annually for DKD National Kidney Foundation.KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Diabetes and Chronic Kidney Disease. Am J Kidney Dis. 2007;49(2 Suppl 2):S12-154.
The earliest clinical evidence of nephropathy is the appearance of low but abnormal levels (≥ 30 mg/day or 20 μg/min) of albumin in the urine. Natural History of Diabetic Nephropathy Parving, H, Østerby, R & Ritz, E: Diabetic nephropathy, in The Kidney 2000 edited by Brenner BM, Levine S, Philadelphia, W.B. Saunders, p 1731
Urine dipstick ! Detects albumin; insensitive to light chains ! Highly specific ! Positive at 300-500mg/day ! Insensitive to microalbuminuria Measurement of Urinary Protein Qualitative measurement
24-hour urine collection Creatinine is excreted in proportion to muscle mass, and its concentration remains relatively constant on a daily basis. Young and middle-aged men excrete 16 to 26 mg per kg per day Women excrete 12 to 24 mg per kg per day. In malnourished and elderly persons, creatinine excretion may be less. Measurement of Urinary Protein
An alternative to the 24-hour urine specimen determined in a random urine specimen while the person carries on normal activity. urine protein-to-creatinine ratio (UPr/Cr) Correlation between the UPr/Cr ratio and 24-hour protein excretion has been demonstrated in several diseases, including diabetes mellitus, preeclampsia and rheumatic disease. Measurement of Urinary Protein
Recent evidence indicates that the UPr/Cr ratio is more accurate than the 24-hour urine protein measurement. The ratio is about the same numerically as the number of grams of protein excreted in urine per day. a ratio of less than 0.2 is equivalent to 0.2 g of protein per day and is considered normal a ratio of 3.5 is equivalent to 3.5 g of protein per day and is considered nephrotic-range (or heavy) proteinuria. Ruggenenti P, et al. BMJ 1998; 316: 504-9. Measurement of Urinary Protein
A first morning sample most closely estimates 24-hour protein excretion, although a random sample is acceptable if a first morning void is unavailable. Ginsberg JM,et al. N Engl J Med 1983; 309: 1543-6. Urine Protein-to-Creatinine Ratio (UPr/Cr)
The earliest clinical evidence of nephropathy is the appearance of low but abnormal levels (≥ 30 mg/day or 20 μg/min) of albumin in the urine Urine Albumin Level Urine dipstick Normal Negative Positive UACR / 24 hr Urine 30 mg/g 20 μg/min 30 mg/day 300 mg/g 200 μg/min 300 mg/day Microalbuminuria Macroalbuminuria Microalbuminuria -The Earliest Clinical Evidence
High albuminuria and low eGFR: independent risk factors for cardiovascular and renal events in type 2 diabetes Diabetic Kidney Disease Ninomiya T, et al. J Am Soc Nephrol. 2009;20(8): 1813-1821. Cardiovascular death Hazardratio Normo- albuminuria Micro- albuminuria Macro- albuminuria eGFR ≥90 eGFR 60-89 eGFR <60 Baseline eGFRBaseline UACR 0 1 2 3 4 5 6 <60 FR Hazardratio Normo- albuminuria Micro- albuminuria Macro- albuminuria eGFR ≥90 eGFR 60-89 eGFR <60 Baseline eGFRBaseline UACR Renal events 0 5 10 15 20 25 GFR ≥90 GFR 60-89 GFR <60 Baseline eGFR (ml/min/1.73 m2 ) GFR ≥90 GFR 60-89 GFR <60 Baseline eGFR (ml/min/1.73 m2 )2 ) 2 ) rg Cardiovascular death Hazardratio Normo- albuminuria Micro- albuminuria Macro- albuminuria eGFR ≥90 eGFR 60-89 eGFR <60 Baseline eGFRBaseline UACR 0 1 2 3 4 5 6 0 R Hazardratio Normo- albuminuria Micro- albuminuria Macro- albuminuria eGFR ≥90 eGFR 60-89 eGFR <60 Baseline eGFRBaseline UACR Renal events 0 5 10 15 20 25 GFR ≥90 GFR 60-89 GFR <60 Baseline eGFR (ml/min/1.73 m2 ) GFR ≥90 GFR 60-89 GFR <60 Baseline eGFR (ml/min/1.73 m2 )2 ) 2 ) g
Stage Description GFR (mL/min/1.73 m2) Action 1 ไตเริ่ม ผิดปกติ Kidney damage with normal or GFR >90 Diagnosis and treatment Treatment of co-morbid conditions Slowing progression CVD risk reduction 2 ไตเรื้อรัง ระยะเริ่มต้น Kidney damage with mild GFR 60-89 Estimating progression 3 ไตเรื้อรัง ระยะปานกลาง Moderate GFR 30-59 Evaluating and treating complications 4 ไตเรื้อรังเป็นมาก Severe GFR 15-29 Preparation for kidney replacement therapy 5 ไตวาย Kidney failure <15 (or dialysis) Replacement (if uremia present) Stages of CKD
National Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int Suppl. 2013;3:1-150.
Strategies Treatment of Diabetic Nephropathy
Standard Therapy 1. Blood glucose control 2. Blood pressure control 3. Cardiovascular Disease and Risk Management 4. Life style modification Strategies Treatment of Diabetic Nephropathy
Blood Glucose Control
Intensive Diabetes Therapy: Reduced incidence of complications HbA DCCT 9 → 7.2% Kumamoto 9 → 7 UKPDS 8 → 7 Retinopathy 63% 69% 17-21% Nephropathy 54% 70% 24-33% Neuropathy 60% improve - Cardiovascular disease 41% - 16% DCCT Research Group. N Engl J Med. 1993;329:977-986. Ohkubo Y, et al. Diabetes Res Clin Pract. 1995;28:103-117. UKPDS 33: Lancet 1998; 352, 837-853.
Target and Achieved HbA1c Levels in the Intensively and Conventionally Treated Groups of Three Recent Clinical Trials that Examined Different Levels of Glycemic Control in Patients with Type 2 Diabetes Study Intensive Treatment Conventional Treatment Complication Target Achieved Target Achieved Microalbu -minuria Macroalbu -minuria ADVANCE <6.5% 6.5% Unspecified 7.3% 9% 30% ACCORD <6.0% 6.4% 7-9% 7.5% 21% 32% VADT <6.0% 6.9% 9% 8.4% 32% 37% The Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) trial The Action to Control Cardiovascular Risk in Diabetes (ACCORD). The Veterans Affairs Diabetes Trial (VADT) Patel A, et al. N Engl J Med. 2008; 358(24): 2560-2572. Ismail-Beigi F, et al.. Lancet. 2010; 376(9739): 419-430. Duckworth W, N Engl J Med. 2009; 360(2): 129-139. Intensifying glycemic control beyond conventional management did not result in decreased risk of the primary endpoints ! composites of major adverse cardiovascular disease (CVD) events
We recommend a target HbA1c of ~7.0% to prevent or delay progression of the microvascular complications of diabetes, including DKD. (1A) We recommend not treating to an HbA1c target of <7.0% in patients at risk of hypoglycemia. (1B) We suggest that target HbA1c be extended above 7.0% in individuals with co-morbidities or limited life expectancy and risk of hypoglycemia. (2C) Target HbA1c National Kidney Foundation. KDOQI clinical practice guideline for diabetes and CKD: 2012 update. Am. J. Kidney Dis. 2012;60:850–886.
Recommendations for use of Metformin based on eGFR eGFR level (mL/min per 1.73 m Action ≥ 60 No renal contraindication to metformin
 Monitor renal function annually <60 and ≥45 Continue use Increase monitoring of renal function (every 3–6 months) < 45 and ≥ 30 Prescribe metformin with caution Use lower dose (e.g., 50%, or half-maximal dose) Closely monitor renal function (every 3 months) Do not start new patients on metformin < 30 Stop metformin Lipska KJ, et al. Diabetes Care. 2011;34(6):1431-1437.
Dose Adjustment for Insulin Compounds and Oral Medicines for Diabetes in CKD Medication Class and Agents CKD stages 3, 4, and 5 ND First-generation sulfonylureas Avoid use Second-generation sulfonylureas Glipizide No dose adjustment Glimepiride Start conservatively at 1 mg daily Glyburide Avoid use Gliclazide No dose adjustment Thiazolidinediones Pioglitazone No dose adjustment Alpha-glucosidase inhibitors Acarbose Avoid if GFR <30 mL/min/1.73 m
Dose Adjustment for Insulin Compounds and Oral Medicines for Diabetes in CKD Medication Class and Agents CKD stages 3, 4, and 5 ND DPP-4 inhibitor Sitagliptin GFR >50 mL/min/1.73 m2: 100 mg daily GFR 30-50 mL/min/1.73 m2: 50 mg daily GFR <30 mL/min/1.73 m2: 25 mg daily Saxagliptin GFR > 50 mL/min/1.73 m GFR < 50 mL/min/1.73 m Linagliptin No dose adjustment Vildagliptin GFR > 50 mL/min/1.73 m GFR < 50 mL/min/1.73 m Incretin mimetic Exenatide Not recommended in GFR <30 mL/min/1.73 m Liraglutide Not recommended in GFR <60 mL/min/1.73 m
`Blood Pressure Control
95 98 101 104 107 110 113 116 119 r = 0.69; P < 0.05 Mean arterial pressure (mmHg) DeclineinGFR(mL/min/year) 130/85 140/90 Untreated hypertension 0 -2 -4 -6 -8 -10 -12 -14 Bakris et al. Am J Kidney Dis 2000; 36: 646–661. Reduced Blood Pressure Slows The Rate of GFR Decline
9.9 10.0 9.3 24.4 18.6 11.9 0 5 10 15 20 25 30 ≤90 mm Hg ≤85 mm Hg ≤80 mm Hg Target DBP group Major CV events per 1000 patient years All patients (n=18,790) Diabetics (n=1,501) Hansson L, et al. Lancet 1998; 351: 1755–1762. Intensive BP-lowering decreases cardiovascular risk 51% in patients with hypertension, especially diabetes patient Hypertension Optimal Treatment
1. Patients 60 or older, BP goal is 150/90. ! 2. Patients <60y, BP goal is 140/90 ! 3. Patients with CKD, DM and >18y, BP goal is 140/90 ! 4. Start with thiazide diuretic, CCB, ACE or ARB (in general). ! 5. Start with thiazide or CCB in African-American patients ! 6. Start with ACE/ARB for CKD patients. JNC 8
JNC 8
Reduced proteinuria Reduced renal and cardiovascular events ! ! ! ! The superior antiproteinuric effect of dual RAS blockade was expected to translate into effective long-term renoprotection and cardioprotection
The use of a combination of ACE-Is and ARBs
What level of blood pressure should anti-hypertensive therapy be initiated? What is the optimum blood pressure goal? Strategies for the management of hypertension in patients with T2DM are controversial
4,733 participants T2DM HbA1c ≥7.5 %, and established cardiovascular disease or multiple cardiovascular risk factors Intensive BP control SBP<120 mmHg Standard BP control SBP<140 mmHg Outcome: Composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular-related death The ACCORD Study Group. N Engl J Med 2010; 362: 1575-1585. The ACCORD (Action to Control Cardiovascular Risk in Diabetes)
The ACCORD Study Group. N Engl J Med 2010; 362: 1575-1585. Primary outcome Nonfatal MI Nonfatal stroke In T2DM with high risk for cardiovascular events, targeting SBP < 120 mm Hg, as compared with <140 mm Hg, did not reduce the rate of a composite outcome of fatal and nonfatal major cardiovascular events. Effects of Intensive Blood-Pressure Control in T2DM

JNC8. JAMA. 2014;5;311(5):507-20. National Kidney Foundation. KDOQI clinical practice guideline for diabetes and CKD: 2012 update. Am. J. Kidney Dis. 2012;60:850–886. Blood Pressure Target KDIGO JNC 8 Aluminuria < 30 mg/d ≤140 / 90 (1B) ≤ 140 / 90 ! E for SBP A for DBP if over 30 E for DBP if under 30 ! ! ACEI or ARB for all CKD regardless of diabetic or proteinuric status Aluminuria 30-300 mg/d ≤130 / 80 (2D) ACEI or ARB (2D) Aluminuria > 300 mg/d ≤130 / 80 (2C) ACEI or ARB (1B)
Dyslipidemia in DKD
Dyslipidemia in DKD ! LDL Cholesterol Risk factor for CVD
Life-table plot of effects of allocation to simvastatin plus ezetimibe versus placebo on major atherosclerotic events Numbers remaining at risk of a first major atherosclerotic event at the beginning of each year are shown for both treatment groups. Lowering LDL-C reduces cardiovascular events in a wide range of patients with diabetes and CKD Baigent C, et al. Lancet. 2011;377(9784):2181-2192. for triglyceri 3023 (33% dialysis at ra 496 [5%] p cholesterol dialysis tha 2·9 [SD 0·9 of 6247 patie creatinine, Modification 26·6 (SD 13 had Kidney 3 disease ( (43%) stage and 1221 (20 1·73 m²). Am dialysis with creatinine r 30 mg/g, 2 2359 (42%) The medi surviving p period, sligh ezetimibe d simvastatin finding was *In patients initially allocated to simvastatin, no 1-year sample was collected, while samples scheduled for collection at 2·5 and 4 years were collected at 1·5 and 3 years after rerandomisation. Table 2: Average use of study simvastatin plus ezetimibe or non-study statin and average change in plasma LDL cholesterol from baseline, by period of follow-up Figure 2: Life-table plot of effects of allocation to simvastatin plus ezetimibe versus placebo on major atherosclerotic events Numbers remaining at risk of a first major atherosclerotic event at the beginning of each year are shown for both treatment groups. 543210 4620 4650 4204 4271 3849 3939 3469 3546 2566 2655 1269 1265 Years of follow-up Number at risk Placebo Simvastatin plus ezetimibe 0 5 10 15 20 25 Peoplesufferingevents(%) Placebo Simvastatin plus ezetimibe Rate reduction 17% (95% CI 6–26%) Log-rank p=0·0021 Rate Reduction 17%
In nondialysis-dependent CKD statins and statins/ezetimibe compared with placebo CVD events and mortality The beneficial effects do not modified by the presence or absence of diabetes. Statins did not alter kidney disease progression Dyslipidemia in DKD Statins are recommended for all diabetic patients with nondialysis-dependent CKD
In dialysis-dependent CKD Statin - no CVD or survival advantage It is appropriate to consider continuing statin therapy in those who progress to treatment by chronic dialysis. Dyslipidemia in DKD Statins are recommended for all diabetic patients with dialysis-dependent CKD
! People with diabetes, CKD stages 1-4, and LDL-C > 100 mg/dL should be treated with a statin. (B) Target LDL-C in people with diabetes and CKD stages 1-4 should be < 100 mg/dL; <70 mg/dL is a therapeutic option. (B) Treatment with a statin should not be initiated in patients with type 2 diabetes on maintenance hemodialysis who do not have a specific cardiovascular indication for treatment. (A) Atorvastatin treatment in patients with type 2 diabetes on maintenance treatment does not improve cardiovascular outcomes. (Strong) KDIGO-Dyslipidemia in DKD KDOQI US Commentary on the 2013 KDIGO Clinical Practice Guideline for Lipid Management in CKD
1. Smoking cessation 2. Healthy diet 3. Exercise 4. Weight reduction Lifestyle Modifications
Weight Reduction
Visceral obesity RAAS activation SNS activation Insulin resistance Dyslipidemia Tubular NaCl reabsorption Hyperglycemia Inflammation Oxidative Stress Renal vasodilation PGc Macula densa feedback Volume expansion Arterial Hypertension Albuminuria Glomerulopathy Obesity/Diabetes related nephropathy
The scientific evidence confirms 30 min/d of moderate- or high-level physical activity is an effective and safe way to prevent type 2 diabetes in all populations Moderate physical activity increases both nitric oxide (NO) and ROS and decreases oxidative stress. Strenuous exercise increases NO, markedly increases ROS, and increases oxidative stress.
Nutritional Therapy
Gaede P, N Engl J Med. 2003;348(5):383-93. Multifactorial Intervention and Cardiovascular Disease veral k for The enal ntion ntrol, and ents hese after w-up eutic with erse Patientswithdevelopmentorprogression ofdiabetickidneydisease 50 40 30 25 20 15 10 5 0 45 35 3·8 7·8 13·3 Duration of follow-up (years) 24 10 39 20 46 25 RR 0·44 (95% CI 0·25–0·77); p=0·004 Conventional treatment Intensive treatment Residualrenalrisk
“It Just Doesn’t Get Any Better . . . or Does It?”
HbA1c ~7 BP < 140/90 LDL < 100 Life Style Diabetic Nephropathy Optimal Care for Risk Reduction ! Prevent hypoglycemia ACEI or ARB no combination Statin/ ezetimibe Physical activity weight reduction non-smoking
! Early diagnosis of DN remains critical in preventing long term devastating outcomes of renal loss. A significant cause for progressive kidney disease, DN remains an area for active investigation of pathogenesis and possible treatments to prevent and/or reverse disease. Summary of Today Talk about Diabetic Nephropathy
Thank You for Your Attention

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ภาวะแทรกซ้อนทางไตในผู้ป่วยเบาหวาน

  • 1.
    DIABETIC KIDNEY DISEASE
 AssistProf. Warangkana Pichaiwong, MD. Renal Division, Department of Medicine. Rajavithi Hospital, Bangkok. wpichaiw@hotmail.com
  • 2.
    ! Prevalence and Scopeof DKD Definition of DKD Optimal management of DKD Topics
  • 3.
  • 4.
    The adjusted rateof prevalent rates of 
 ESRD and annual percent change 81 84 87 90 93 96 99 02 05 08 11 Bars:Ratepermillionpopulation 0 100 200 300 400 Symbols:one-year%change -5 0 5 10 15 line: add’l adjustment for Hispanic ethnicity 2013 USRDS. Annual Data Report.
  • 5.
    Prevalent counts &adjusted rates of ESRD 
 by primary diagnosis USRDS. Annual Data Report. 2013 USRDS. Annual Data Report. Numberofpatients(inthousands) 0 10 20 30 40 50 81 84 87 90 93 96 99 02 05 08 11 Ratepermillionpopulation 0 50 100 150 200 Counts Rates Diabetes Hypertension GN Cystic kidney
  • 6.
    Source: IDF DiabetesAtlas Sixth Edition, International Diabetes Federation 2013 Prevalence of Diabetic Mellitus in Adults (20-75 years) 2013
  • 7.
    Source: IDF DiabetesAtlas Sixth Edition, International Diabetes Federation 2013 Prevalence of Diabetic Mellitus in Adults (20-75 years), 2013
  • 8.
  • 9.
    Diagnosis of DiabeticMellitus *In the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing. Diabetes Care. 2013; 36 Suppl 1: S11-66. A1C ≥6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.* OR FPG ≥126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8h.* OR 2-h plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT. The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.* OR In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).
  • 10.
  • 11.
    25–40% of patientswith type 1 diabetes 5–40% of patients with type 2 diabetes Diabetic Kidney Disease Ismail N, Becker B, Strzelczyk P, et al. Kidney Int 1999; 55 (1): 1-28. Parving HH, Hommel E, Mathiesen E, et al. BMJ (Clin Res Ed) 1988; 296 (6616): 156-60.
  • 12.
    Persistent albuminuria Arterial bloodpressure elevation Decline in glomerular filtration rate (GFR) High risk of cardiovascular morbidity and mortality Dignosis of Diabetic Kidney Disease Parving, H, Østerby, R & Ritz, E: Diabetic nephropathy, in The Kidney 2000 edited by Brenner BM, Levine S, Philadelphia, W.B. Saunders, p 1731
  • 13.
    DKD in Type1 DM onset: > 5 years after diagnosis ESRD in overt nephropathy at 10 year 50% at 20 year 75% Molitch ME, et al. American Diabetes Association. Diabetes Care. 2004;27 Suppl 1:S79-83. Natural History of Diabetic Kidney Disease DKD in Type 2 DM onset: at diagnosis ESRD in overt nephropathy at 20 year 20%
  • 14.
    Initial screening: 5 yearsafter the diagnosis of type 1 diabetes (A) From diagnosis of type 2 diabetes (B) Screening: ●  Measurements of urinary ACR in a spot urine sample (B) ●  Measurement of serum creatinine and estimation of GFR (B)
 Patients with Diabetes should be Screened Annually for DKD National Kidney Foundation.KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Diabetes and Chronic Kidney Disease. Am J Kidney Dis. 2007;49(2 Suppl 2):S12-154.
  • 15.
    The earliest clinicalevidence of nephropathy is the appearance of low but abnormal levels (≥ 30 mg/day or 20 μg/min) of albumin in the urine. Natural History of Diabetic Nephropathy Parving, H, Østerby, R & Ritz, E: Diabetic nephropathy, in The Kidney 2000 edited by Brenner BM, Levine S, Philadelphia, W.B. Saunders, p 1731
  • 16.
    Urine dipstick ! Detects albumin;insensitive to light chains ! Highly specific ! Positive at 300-500mg/day ! Insensitive to microalbuminuria Measurement of Urinary Protein Qualitative measurement
  • 17.
    24-hour urine collection Creatinineis excreted in proportion to muscle mass, and its concentration remains relatively constant on a daily basis. Young and middle-aged men excrete 16 to 26 mg per kg per day Women excrete 12 to 24 mg per kg per day. In malnourished and elderly persons, creatinine excretion may be less. Measurement of Urinary Protein
  • 18.
    An alternative tothe 24-hour urine specimen determined in a random urine specimen while the person carries on normal activity. urine protein-to-creatinine ratio (UPr/Cr) Correlation between the UPr/Cr ratio and 24-hour protein excretion has been demonstrated in several diseases, including diabetes mellitus, preeclampsia and rheumatic disease. Measurement of Urinary Protein
  • 19.
    Recent evidence indicatesthat the UPr/Cr ratio is more accurate than the 24-hour urine protein measurement. The ratio is about the same numerically as the number of grams of protein excreted in urine per day. a ratio of less than 0.2 is equivalent to 0.2 g of protein per day and is considered normal a ratio of 3.5 is equivalent to 3.5 g of protein per day and is considered nephrotic-range (or heavy) proteinuria. Ruggenenti P, et al. BMJ 1998; 316: 504-9. Measurement of Urinary Protein
  • 20.
    A first morningsample most closely estimates 24-hour protein excretion, although a random sample is acceptable if a first morning void is unavailable. Ginsberg JM,et al. N Engl J Med 1983; 309: 1543-6. Urine Protein-to-Creatinine Ratio (UPr/Cr)
  • 21.
    The earliest clinicalevidence of nephropathy is the appearance of low but abnormal levels (≥ 30 mg/day or 20 μg/min) of albumin in the urine Urine Albumin Level Urine dipstick Normal Negative Positive UACR / 24 hr Urine 30 mg/g 20 μg/min 30 mg/day 300 mg/g 200 μg/min 300 mg/day Microalbuminuria Macroalbuminuria Microalbuminuria -The Earliest Clinical Evidence
  • 22.
    High albuminuria andlow eGFR: independent risk factors for cardiovascular and renal events in type 2 diabetes Diabetic Kidney Disease Ninomiya T, et al. J Am Soc Nephrol. 2009;20(8): 1813-1821. Cardiovascular death Hazardratio Normo- albuminuria Micro- albuminuria Macro- albuminuria eGFR ≥90 eGFR 60-89 eGFR <60 Baseline eGFRBaseline UACR 0 1 2 3 4 5 6 <60 FR Hazardratio Normo- albuminuria Micro- albuminuria Macro- albuminuria eGFR ≥90 eGFR 60-89 eGFR <60 Baseline eGFRBaseline UACR Renal events 0 5 10 15 20 25 GFR ≥90 GFR 60-89 GFR <60 Baseline eGFR (ml/min/1.73 m2 ) GFR ≥90 GFR 60-89 GFR <60 Baseline eGFR (ml/min/1.73 m2 )2 ) 2 ) rg Cardiovascular death Hazardratio Normo- albuminuria Micro- albuminuria Macro- albuminuria eGFR ≥90 eGFR 60-89 eGFR <60 Baseline eGFRBaseline UACR 0 1 2 3 4 5 6 0 R Hazardratio Normo- albuminuria Micro- albuminuria Macro- albuminuria eGFR ≥90 eGFR 60-89 eGFR <60 Baseline eGFRBaseline UACR Renal events 0 5 10 15 20 25 GFR ≥90 GFR 60-89 GFR <60 Baseline eGFR (ml/min/1.73 m2 ) GFR ≥90 GFR 60-89 GFR <60 Baseline eGFR (ml/min/1.73 m2 )2 ) 2 ) g
  • 23.
    Stage Description GFR (mL/min/1.73 m2) Action 1 ไตเริ่ม ผิดปกติ Kidneydamage with normal or GFR >90 Diagnosis and treatment Treatment of co-morbid conditions Slowing progression CVD risk reduction 2 ไตเรื้อรัง ระยะเริ่มต้น Kidney damage with mild GFR 60-89 Estimating progression 3 ไตเรื้อรัง ระยะปานกลาง Moderate GFR 30-59 Evaluating and treating complications 4 ไตเรื้อรังเป็นมาก Severe GFR 15-29 Preparation for kidney replacement therapy 5 ไตวาย Kidney failure <15 (or dialysis) Replacement (if uremia present) Stages of CKD
  • 24.
    National Kidney Disease:Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int Suppl. 2013;3:1-150.
  • 25.
    Strategies Treatment ofDiabetic Nephropathy
  • 26.
    Standard Therapy 1.Blood glucose control 2. Blood pressure control 3. Cardiovascular Disease and Risk Management 4. Life style modification Strategies Treatment of Diabetic Nephropathy
  • 27.
  • 28.
    Intensive Diabetes Therapy: Reducedincidence of complications HbA DCCT 9 → 7.2% Kumamoto 9 → 7 UKPDS 8 → 7 Retinopathy 63% 69% 17-21% Nephropathy 54% 70% 24-33% Neuropathy 60% improve - Cardiovascular disease 41% - 16% DCCT Research Group. N Engl J Med. 1993;329:977-986. Ohkubo Y, et al. Diabetes Res Clin Pract. 1995;28:103-117. UKPDS 33: Lancet 1998; 352, 837-853.
  • 29.
    Target and AchievedHbA1c Levels in the Intensively and Conventionally Treated Groups of Three Recent Clinical Trials that Examined Different Levels of Glycemic Control in Patients with Type 2 Diabetes Study Intensive Treatment Conventional Treatment Complication Target Achieved Target Achieved Microalbu -minuria Macroalbu -minuria ADVANCE <6.5% 6.5% Unspecified 7.3% 9% 30% ACCORD <6.0% 6.4% 7-9% 7.5% 21% 32% VADT <6.0% 6.9% 9% 8.4% 32% 37% The Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) trial The Action to Control Cardiovascular Risk in Diabetes (ACCORD). The Veterans Affairs Diabetes Trial (VADT) Patel A, et al. N Engl J Med. 2008; 358(24): 2560-2572. Ismail-Beigi F, et al.. Lancet. 2010; 376(9739): 419-430. Duckworth W, N Engl J Med. 2009; 360(2): 129-139. Intensifying glycemic control beyond conventional management did not result in decreased risk of the primary endpoints ! composites of major adverse cardiovascular disease (CVD) events
  • 30.
    We recommend atarget HbA1c of ~7.0% to prevent or delay progression of the microvascular complications of diabetes, including DKD. (1A) We recommend not treating to an HbA1c target of <7.0% in patients at risk of hypoglycemia. (1B) We suggest that target HbA1c be extended above 7.0% in individuals with co-morbidities or limited life expectancy and risk of hypoglycemia. (2C) Target HbA1c National Kidney Foundation. KDOQI clinical practice guideline for diabetes and CKD: 2012 update. Am. J. Kidney Dis. 2012;60:850–886.
  • 31.
    Recommendations for useof Metformin based on eGFR eGFR level (mL/min per 1.73 m Action ≥ 60 No renal contraindication to metformin
 Monitor renal function annually <60 and ≥45 Continue use Increase monitoring of renal function (every 3–6 months) < 45 and ≥ 30 Prescribe metformin with caution Use lower dose (e.g., 50%, or half-maximal dose) Closely monitor renal function (every 3 months) Do not start new patients on metformin < 30 Stop metformin Lipska KJ, et al. Diabetes Care. 2011;34(6):1431-1437.
  • 32.
    Dose Adjustment forInsulin Compounds and Oral Medicines for Diabetes in CKD Medication Class and Agents CKD stages 3, 4, and 5 ND First-generation sulfonylureas Avoid use Second-generation sulfonylureas Glipizide No dose adjustment Glimepiride Start conservatively at 1 mg daily Glyburide Avoid use Gliclazide No dose adjustment Thiazolidinediones Pioglitazone No dose adjustment Alpha-glucosidase inhibitors Acarbose Avoid if GFR <30 mL/min/1.73 m
  • 33.
    Dose Adjustment forInsulin Compounds and Oral Medicines for Diabetes in CKD Medication Class and Agents CKD stages 3, 4, and 5 ND DPP-4 inhibitor Sitagliptin GFR >50 mL/min/1.73 m2: 100 mg daily GFR 30-50 mL/min/1.73 m2: 50 mg daily GFR <30 mL/min/1.73 m2: 25 mg daily Saxagliptin GFR > 50 mL/min/1.73 m GFR < 50 mL/min/1.73 m Linagliptin No dose adjustment Vildagliptin GFR > 50 mL/min/1.73 m GFR < 50 mL/min/1.73 m Incretin mimetic Exenatide Not recommended in GFR <30 mL/min/1.73 m Liraglutide Not recommended in GFR <60 mL/min/1.73 m
  • 34.
  • 35.
    95 98 101104 107 110 113 116 119 r = 0.69; P < 0.05 Mean arterial pressure (mmHg) DeclineinGFR(mL/min/year) 130/85 140/90 Untreated hypertension 0 -2 -4 -6 -8 -10 -12 -14 Bakris et al. Am J Kidney Dis 2000; 36: 646–661. Reduced Blood Pressure Slows The Rate of GFR Decline
  • 36.
    9.9 10.0 9.3 24.4 18.6 11.9 0 5 10 15 20 25 30 ≤90mm Hg ≤85 mm Hg ≤80 mm Hg Target DBP group Major CV events per 1000 patient years All patients (n=18,790) Diabetics (n=1,501) Hansson L, et al. Lancet 1998; 351: 1755–1762. Intensive BP-lowering decreases cardiovascular risk 51% in patients with hypertension, especially diabetes patient Hypertension Optimal Treatment
  • 37.
    1. Patients 60or older, BP goal is 150/90. ! 2. Patients <60y, BP goal is 140/90 ! 3. Patients with CKD, DM and >18y, BP goal is 140/90 ! 4. Start with thiazide diuretic, CCB, ACE or ARB (in general). ! 5. Start with thiazide or CCB in African-American patients ! 6. Start with ACE/ARB for CKD patients. JNC 8
  • 38.
  • 39.
    Reduced proteinuria Reduced renaland cardiovascular events ! ! ! ! The superior antiproteinuric effect of dual RAS blockade was expected to translate into effective long-term renoprotection and cardioprotection
  • 40.
    The use ofa combination of ACE-Is and ARBs
  • 41.
    What level ofblood pressure should anti-hypertensive therapy be initiated? What is the optimum blood pressure goal? Strategies for the management of hypertension in patients with T2DM are controversial
  • 42.
    4,733 participants T2DM HbA1c≥7.5 %, and established cardiovascular disease or multiple cardiovascular risk factors Intensive BP control SBP<120 mmHg Standard BP control SBP<140 mmHg Outcome: Composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular-related death The ACCORD Study Group. N Engl J Med 2010; 362: 1575-1585. The ACCORD (Action to Control Cardiovascular Risk in Diabetes)
  • 43.
    The ACCORD StudyGroup. N Engl J Med 2010; 362: 1575-1585. Primary outcome Nonfatal MI Nonfatal stroke In T2DM with high risk for cardiovascular events, targeting SBP < 120 mm Hg, as compared with <140 mm Hg, did not reduce the rate of a composite outcome of fatal and nonfatal major cardiovascular events. Effects of Intensive Blood-Pressure Control in T2DM

  • 44.
    JNC8. JAMA. 2014;5;311(5):507-20. NationalKidney Foundation. KDOQI clinical practice guideline for diabetes and CKD: 2012 update. Am. J. Kidney Dis. 2012;60:850–886. Blood Pressure Target KDIGO JNC 8 Aluminuria < 30 mg/d ≤140 / 90 (1B) ≤ 140 / 90 ! E for SBP A for DBP if over 30 E for DBP if under 30 ! ! ACEI or ARB for all CKD regardless of diabetic or proteinuric status Aluminuria 30-300 mg/d ≤130 / 80 (2D) ACEI or ARB (2D) Aluminuria > 300 mg/d ≤130 / 80 (2C) ACEI or ARB (1B)
  • 45.
  • 46.
    Dyslipidemia in DKD ! LDLCholesterol Risk factor for CVD
  • 47.
    Life-table plot ofeffects of allocation to simvastatin plus ezetimibe versus placebo on major atherosclerotic events Numbers remaining at risk of a first major atherosclerotic event at the beginning of each year are shown for both treatment groups. Lowering LDL-C reduces cardiovascular events in a wide range of patients with diabetes and CKD Baigent C, et al. Lancet. 2011;377(9784):2181-2192. for triglyceri 3023 (33% dialysis at ra 496 [5%] p cholesterol dialysis tha 2·9 [SD 0·9 of 6247 patie creatinine, Modification 26·6 (SD 13 had Kidney 3 disease ( (43%) stage and 1221 (20 1·73 m²). Am dialysis with creatinine r 30 mg/g, 2 2359 (42%) The medi surviving p period, sligh ezetimibe d simvastatin finding was *In patients initially allocated to simvastatin, no 1-year sample was collected, while samples scheduled for collection at 2·5 and 4 years were collected at 1·5 and 3 years after rerandomisation. Table 2: Average use of study simvastatin plus ezetimibe or non-study statin and average change in plasma LDL cholesterol from baseline, by period of follow-up Figure 2: Life-table plot of effects of allocation to simvastatin plus ezetimibe versus placebo on major atherosclerotic events Numbers remaining at risk of a first major atherosclerotic event at the beginning of each year are shown for both treatment groups. 543210 4620 4650 4204 4271 3849 3939 3469 3546 2566 2655 1269 1265 Years of follow-up Number at risk Placebo Simvastatin plus ezetimibe 0 5 10 15 20 25 Peoplesufferingevents(%) Placebo Simvastatin plus ezetimibe Rate reduction 17% (95% CI 6–26%) Log-rank p=0·0021 Rate Reduction 17%
  • 48.
    In nondialysis-dependent CKD statins and statins/ezetimibe compared with placebo CVD events and mortality The beneficial effects do not modified by the presence or absence of diabetes. Statins did not alter kidney disease progression Dyslipidemia in DKD Statins are recommended for all diabetic patients with nondialysis-dependent CKD
  • 49.
    In dialysis-dependent CKD Statin - no CVD or survival advantage It is appropriate to consider continuing statin therapy in those who progress to treatment by chronic dialysis. Dyslipidemia in DKD Statins are recommended for all diabetic patients with dialysis-dependent CKD
  • 50.
    ! People with diabetes,CKD stages 1-4, and LDL-C > 100 mg/dL should be treated with a statin. (B) Target LDL-C in people with diabetes and CKD stages 1-4 should be < 100 mg/dL; <70 mg/dL is a therapeutic option. (B) Treatment with a statin should not be initiated in patients with type 2 diabetes on maintenance hemodialysis who do not have a specific cardiovascular indication for treatment. (A) Atorvastatin treatment in patients with type 2 diabetes on maintenance treatment does not improve cardiovascular outcomes. (Strong) KDIGO-Dyslipidemia in DKD KDOQI US Commentary on the 2013 KDIGO Clinical Practice Guideline for Lipid Management in CKD
  • 51.
    1. Smoking cessation 2.Healthy diet 3. Exercise 4. Weight reduction Lifestyle Modifications
  • 52.
  • 53.
    Visceral obesity RAAS activationSNS activation Insulin resistance Dyslipidemia Tubular NaCl reabsorption Hyperglycemia Inflammation Oxidative Stress Renal vasodilation PGc Macula densa feedback Volume expansion Arterial Hypertension Albuminuria Glomerulopathy Obesity/Diabetes related nephropathy
  • 54.
    The scientific evidenceconfirms 30 min/d of moderate- or high-level physical activity is an effective and safe way to prevent type 2 diabetes in all populations Moderate physical activity increases both nitric oxide (NO) and ROS and decreases oxidative stress. Strenuous exercise increases NO, markedly increases ROS, and increases oxidative stress.
  • 55.
  • 56.
    Gaede P, NEngl J Med. 2003;348(5):383-93. Multifactorial Intervention and Cardiovascular Disease veral k for The enal ntion ntrol, and ents hese after w-up eutic with erse Patientswithdevelopmentorprogression ofdiabetickidneydisease 50 40 30 25 20 15 10 5 0 45 35 3·8 7·8 13·3 Duration of follow-up (years) 24 10 39 20 46 25 RR 0·44 (95% CI 0·25–0·77); p=0·004 Conventional treatment Intensive treatment Residualrenalrisk
  • 57.
    “It Just Doesn’tGet Any Better . . . or Does It?”
  • 58.
    HbA1c ~7 BP< 140/90 LDL < 100 Life Style Diabetic Nephropathy Optimal Care for Risk Reduction ! Prevent hypoglycemia ACEI or ARB no combination Statin/ ezetimibe Physical activity weight reduction non-smoking
  • 59.
    ! Early diagnosis ofDN remains critical in preventing long term devastating outcomes of renal loss. A significant cause for progressive kidney disease, DN remains an area for active investigation of pathogenesis and possible treatments to prevent and/or reverse disease. Summary of Today Talk about Diabetic Nephropathy
  • 60.
    Thank You forYour Attention