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Diabetic Nephropathy

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Nitin on Aug 26, 2009 Says :

It will help to prepare lecture for my MBBS final year students.

Nitin on Aug 26, 2009 Says :

It will help to prepare lecture for my MBBS final year student.

IBRAHIM on Aug 23, 2009 Says :

THANK U VERY MUCH

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excellent

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life is good.

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this slide will be used for scientific purposes.

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Notes

Show Notes

Slide 1 :

Diabetic Nephropathy Dr. Salwa Ibrahim, MD. MSc MMedSCI (UK), MRCP (UK) September 2004

Slide 2 :

Definition DN is microvascular complication Presence of albuminuria Elevated blood pressure Declining glomerular function

Slide 3 :

Historic note ROLO (1798) reported the presence of protein in the urine of DM patients Bright (1836) described the seriousness of protein in the urine of DM patients Kimmelstiel, Wilson (1936 ) described Nodular glomerular lesions in DM

Slide 4 :

The Rising Tide DN is the most common cause of ESRD world wide Accounts for >40% of patients starting RRT in the US in 2002 (USRDS, 2002)

Slide 5 :

Percent of incident patients with diabetes, 2001

Slide 6 :

The number of patients initiating RRT for ESRD related to DM, 1984-2001 USA

Slide 7 :

The number of persons who began treatment for ESRD attributable to diabetes increased with age up to +75 years between 1984-2001

Slide 8 :

Causes of ESRD in HD patients in KSA, as on December 2003

Slide 9 :

Why we are seeing more Increased prevalence of type 2 diabetes 100 million people worldwide have diabetes in 1997 300 million people will have type 2 DM by 2025 (World Health Organization-1998 Report) Increased life expectancy of diabetics Decrease cardiovascular morbidity and mortality Wider acceptance of diabetics in ESRD treatment programs

Slide 10 :

Risk factors Genetic Predisposition ACE polymorphism sodium-lithium counter transport Hyperglycaemia Hypertension Age Gender Smoking Ethnicity (native Americans, Mexican Americans, African Americans)

Slide 11 :

Clinical Stages of DN Renal enlargement and hyperfiltration Microalbuminuria, incipient nephropathy (10-15 Y) 30-299 ug/mg creatinine 30-299 mg/24 h collection Macroalbuminuria, overt nephropathy (11-20 Y) >300 ug/mg creatinine >300 mg/24 h collection Progressive renal failure and severe proteinuria (15-25 Y)

Slide 12 :

Natural Course of DN This clinical course is well defined in type 1 DM, develops in close to 40% of patients Renal involvement is early in type 2 DM, occurs in 5 to 40% of patients In type 2 DM, it is not always clear whether renal failure is due to or caused by diabetes (insidious onset, advanced age, coexisting vascular disease, hypertension)

Slide 13 :

Pathogenesis Altered renal hemodynamics due to hyperglycaemia Increased renal blood flow Glomerular hyperfiltration Altered renal homodynamics increases the shear stress on endothelial and mesangial cells with increase Renal growth factors (AII, TGF-b, IGF-I,PDGF), cytokines and extracellular matrix production Systemic hypertension Hyperlipidemia Proteinuria Genetic factors

Slide 14 :

Morphologic changes in DN Glomerular and tubular hypertrophy Thickening of GBM,TBM A B A .Normal capillary wall thickness B. Severe capillary wall thickening in DN

Slide 15 :

Mesangial expansion is the morphological lesion that closely related to the evolution of the GFR

Slide 16 :

Nodular lesion in Type 1 DM

Slide 17 :

Morphologic features Diffuse glomerulosclerosis Arteriosclerosis and hyalinosis of a.a & e.a Tubulointerstitial fibrosis

Slide 18 :

Screening Screening for microalbuminuria provides unique window of opportunity for early intervention, particularly administration of ACE inhibitors Should be performed annually From the onset in type 2 5 years after onset of type 1 Morning or spot albumin- creatinine ratio is the most reliable test (NKF)

Slide 19 :

Slide 20 :

Primary prevention Tight glycemic control Tight blood pressure control

Slide 21 :

Glycemic control DCCT. 1,441 type 1 DM patients, half had mild retinopathy, were randomized to intensive (A1C 7%) and conventional (AIC 9%) insulin therapy and followed for 6.5% years. Intensive glycemic control reduced the frequency of microalbuminuria by 34% in patients without retinopathy and 43% in retinopathy. Macroalbuminuria reduced by 56%

Slide 22 :

Cumulative incidence of clinical proteinuria (AER >200 ug/min) (broken curve) & microalbuminuria (solid curve) in type 1 DM A- No Retinopathy B- With Retinopathy

Slide 23 :

Slide 24 :

UK Prospective Diabetes Study multi-centre randomised controlled trial of different therapies of Type 2 diabetes 5102 newly diagnosed Type 2 diabetic patients

Slide 25 :

Blood Glucose Control Study Aim To determine whether improved glucose control of Type 2 diabetes will prevent clinical complications

Slide 26 :

HbA1c cross-sectional, median values

Slide 27 :

Microalbuminuria Urine albumin >50 mg/L 0.9% reduction in A1C was associated with 34% reduction in the development of Microalbuminuria over 12 years

Slide 28 :

Blood Pressure Control Study : Aims to determine whether Tight blood pressure control policy can reduce morbidity and mortality in Type 2 diabetic patients ACE inhibitor (captopril) or Beta blocker (atenolol) is advantageous in reducing the risk of development of clinical complications

Slide 29 :

UKPDS Event Rates for Select Endpoints With Tight vs. Less Tight Blood Pressure Control Any diabetes-related endpoint Diabetes- related death Stroke Microvascular complications Events per 1000 patient yrs P=0.005 P=0.02 P=0.01 P=0.009 Less tight (n=390) mean achieved BP 154/87 mmHg Tight (n=758) mean achieved BP 144/82 mmHg

Slide 30 :

Benefit of Beta-Blockers in DiabetesUKPDS Captopril and atenolol were equally effective in reducing blood pressure to a mean of 144/83 mmHg and 143/81 mmHg, respectively, and had a similar effect on diabetic complications

Slide 31 :

Blood pressure goalPrimary prevention ADA (2003), JNCIIV (2003) <130/80 ACEI or ARBs NKF 2000 <130/80 ACEI 1st (ARBs if not tolerated)

Slide 32 :

Secondary prevention Hypertension control to mid-normal range (<125/75), by use of ACEI, ARBs (NKF, 2002) Tight glycemic control (HbA1c 7%) Reduce proteinuria to <1 g/day Smoking cessation Protein restriction Treatment of dyslipidemia Prevention of contrast nephropathy Avoid drug nephrotoxicity

Slide 33 :

ACEI, ARBsClass effect Reduces intraglomerular pressure Antigrowth effect

Slide 34 :

AER and MABP in IDDM e microalbuminuria in European Microalbuminuria captopril study group Captopril 50 mg placebo

Slide 35 :

Probability of progression to clinical proteinuria in IDDM with proteinuria in the European Microalbuminuria Captopril Study Group trial

Slide 36 :

Cumulative incidence of events in IDDM with Clinical nephropathy in captopril & placebo treated groups 48% reduction of doubling S.Creatinine 50% reduction in death or requirement of RRT Lewis et al, 1993

Slide 37 :

Meta-analysis of ACEI Trials in normotensive IDDM with microalbuminuria AER was 50% lower in ACE group as compared to placebo

Slide 38 :

Benefit of ARBs in Diabetes:Important Findings of 3 Major Clinical Trials RENAAL (2001) The losartan compared to placebo reduced the risk of diabetic nephropathy developing to renal failure IRMA II (2001) Higher doses of irbesartan reduced the risk of progression of renal insufficiency IDNT (2001) irbesartan compared to the calcium channel blocker amlodipine provided better renal protection in hypertensive type 2 diabetics, reducing the chance of diabetic nephropathy developing to renal failure

Slide 39 :

The Reduction of Endpoints in NIDDM With the Angiotensin II Antagonist Losartan Study RENAAL Population 1,513 patients (31 to 70 years old) Diagnosed type 2 diabetes and nephropathyy albumin/creatinine ratio ?300 mg/g serum creatinine between 1.3–3.0 mg/dL

Slide 40 :

RENAAL Study Design *†In combination with open-label diuretic, calcium channel blocker, beta-blocker, alpha-blocker, and/or centrally acting agent Losartan 100 mg qd† Maintain antihypertensive therapy* (excluding ACE inhibitors & angiotensin II receptor antagonists) Losartan 100 mg qd† Placebo† Trough Blood Pressure Goal <140/<90 mmHg n=1,513 Placebo† Losartan 50 mg qd† Placebo†

Slide 41 :

RENAAL Trends in Blood Pressure and Pulse Pressure Months 751 673 562 371 101 762 658 532 313 71 Systolic Diastolic Mean arterial pressure (P<0.001 at 12 months) 0 12 24 36 48 60 80 100 120 140 160 Pulse pressure Blood Pressure and Pulse Pressure (mmHg) Placebo* (n) Losartan* (n) *In combination with open-label diuretic, calcium channel blocker, beta-blocker, alpha-blocker, and/or centrally acting agent

Slide 42 :

RENAAL Impact of Losartan on Secondary Endpoints 35% average reduction in the level of proteinuria (P<0.001 for the overall treatment effect) 18% reduction in the decline of renal function (P=0.01)

Slide 43 :

The Irbesartan Microalbuminuria in Type 2 DM Hypertensive Patients Study IRMA II Objectives Randomized, double-blind, placebo-controlled study to evaluate the renal protective effect of irbesartan in hypertensive patients with type 2 DM and microalbuminuria Population 590 patients (30 to 70 years old) Type 2 diabetes Hypertension Persistent microalbuminuria Serum creatinine concentration of no more than 1.5 mg/dL for men and 1.1 mg/dL for women

Slide 44 :

IRMA II Study Design 1,469 patients screened 590 patients randomized and followed Placebo n=201 Irbesartan 150 mg/qd n=195 Irbesartan 300 mg/qd n=194 18 died or had adverse events 18 had adverse events 11 died or had adverse events Follow-up of 2 years 171 completed study 168 completed study 174 completed study Target Blood Pressure* <135/85 mmHg *3 months after randomization

Slide 45 :

IRMA II Irbesartan vs. Placebo Primary Endpoint at 2 Years

Slide 46 :

The Irbesartan in Diabetic Nephropathy Trial IDNT overview Randomized, double-blind trial to determine if irbesartan and amlodipine slow the progression of nephropathy in type 2 diabetics Population 1,715 patients (30 to 70 years old) Diagnosed type 2 diabetes Hypertension Nephropathy (urinary protein excretion of at least 900 mg/24hrs and serum creatinine between 1.0–3.0 mg/dL in women, and 1.2–3.0 mg/dL in men)

Slide 47 :

IDNT Study Design 1,715 patients randomized and followed Placebo n=569 Amlodipine 10 mg/qd n=567 Irbesartan 300 mg/qd n=579 Average follow-up of 2.6 years Target Blood Pressure =135*/ =85 mmHg Potential participants discontinue ACEIs, ARBs and CCBs at least 10 days prior to screening Screening phase of up to 5 weeks

Slide 48 :

IDNT Average Systolic, Mean Arterial and Diastolic Blood Pressures Blood pressure (mmHg) Months of Follow-up 0 6 12 18 24 30 36 42 48 54 Irbesartan Amlodipine Placebo Systolic Mean Arterial Pressure (P=0.001 for both treatment groups compared to placebo for visits after baseline) Diastolic

Slide 49 :

IDNT Summary of Important Findings Irbesartan reduced the incidence of a doubling of serum creatinine, ESRD 23% vs. amlodipine (P=0.006) and 20% vs. placebo (P=0.02) Proteinuria was reduced 33% in the irbesartan group compared to 10% with placebo

Slide 50 :

ACEI in Type 2 DM ACEi have not shown any renal protective advantage in type 2 DM compared to others in some studies (UKPDS,REIN studies)

Slide 51 :

MICRO-HOPE Study The diabetes substudy of the Heart Outcomes Prevention Evaluation (HOPE) study showed that at similar blood pressures, ACE inhibitor resulted in a 24 percent greater decrease in the rate of progression to overt nephropathy than did placebo in patients with type 2 diabetes and norm or microalbuminuria ACEi have well documented cardioprotective effect in type 2 DM (HOPE, ABCD studies)

Slide 52 :

Dual Blockade of RAS Using both in combination proved to be more effective in reducing BP and proteinuria (Mogensen et al, 2000, Rossing et al, 2003)

Slide 53 :

Albuminuria and BP after blockade of the renin-angiotensin system (RAS) in 18 type 1 diabetic patients with diabetic nephropathy Jacobsen et al, J Am Soc Nephrology, 2003

Slide 54 :

Average Number of Anti-Hypertensive Agents Used to Achieve Target BP

Slide 55 :

Side Effects of ACEi & ARBs Hyperkalemia has been attributed to the use of ACE inhibitors in 10 to 38 percent of hospitalized patients with this complication Hyperkalemia develops in approximately 10 percent of outpatients within a year after these drugs are prescribed

Slide 56 :

Protein Restriction Small studies 0.6 gram/kg/day retarded the GFR fall rate modestly

Slide 57 :

Protein Restriction MDRD. No clear benefit of dietary protein restriction (3% of study population are diabetics) 0.8 g/kg/day in overt nephropathy 0.6 g/kg/day in diabetics with falling GFR

Slide 58 :

Nephrology Referral GFR <70 ml/m/1.73 m2 Serum creatinine >2 mg/dl Difficulties in managing Hypertension Hyperkalemia

Slide 59 :

Early Referral ACE started and metformin D/C ACE started, BP control Statin started, ACE prescribed Burton, QJM,2000

Slide 60 :

RRT Vascular access should be established at GFR 25 ml/m RRT should start at GFR 15-20 ml/m TX (renal/pancreas) should be considered in all type 1 DM patients

Slide 61 :

Outcome of RRT in DM DM on RRT have a 22 percent higher mortality at one year and a 15 percent higher mortality at five years than patients without DM 32 % of type 2 DM ESRD patients died in 211 days (Chantrel 1999) Survival is as poor as gastrointestinal carcinoma

Slide 62 :

Late referral 80% of type 2 DM with ESRD required emergency dialysis due to late referrals to the nephrology service (Chantrel et al, 1999)

Slide 63 :

Summary Annual screening for microalbuminuria ACEI, ARBs in albuminuria regardless BP level BP control <135/80- <125/75 (2-3 drugs) Intensive glycemic control (HB A1c <7%) Smoking cessation Prevent radiocontrast nephropathy Restrict dietary protein (0.8-0.6 g/kg/d) Control dyslipidemia (LDL- C <100 mg/dl) Timely Nephrology referral

Slide 64 :

Sugarman et al, 1999 In a survey including more than 3.400 type 2 DM, only 27 % of patients received any type of renal testing in a 1-year period !!!!!

	salwaibrahim@hotmail.com 1 Years ago. Category: Internal Medicine

Tags:	Internal Medicine

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