Reciprocal Relationship : Renal Anemia, Diabetes & CVD.

Reciprocal Relationship : Renal Anemia, Diabetes & CVD

Anaemia in diabetic renal disease: an underestimated and unrecognised risk factor?

Diabetes: a worldwide epidemic

Awareness of anaemia in people with diabetes - Europe Questionnaire based interview with 1054 respondents in six European countries to assess the level of understanding and awareness of anaemia and its impact on quality of life amongst people with diabetes 32% had been given information on anaemia, less than 50% were aware of being tested for anaemia and only 14% attributed anaemia to diabetes 132 (12.5%) known to be anaemic –one-fifth were not receiving any treatment –12 received blood transfusions –5 patients were on erythropoietin –Remainder were given iron and/or vitamin supplements Perceived state of health in those with anaemia was worse Stevens et al Curr Med Res Opin 2003; 19: 395-401

Awareness of anaemia in people with diabetes - USA 504 respondents selected from a nationally representative panel of people with diabetes 26% were aware that they were at risk for anaemia 14% were aware that they had been diagnosed with anaemia Of the 86% of patients not diagnosed with anaemia –58% indicated they suffer from one or more symptoms often associated with anaemia 69% attributed the symptoms to diabetes 66% attributed the symptoms to ageing Roper Starch Worldwide 2001

Awareness of anaemia in physicians caring for people with diabetes Unrecognised anaemia in patients with diabetes 1 –cross sectional survey of 820 patients in a diabetic clinic –190 (23%) had unrecognised anaemia by WHO definition and 56 (7%) by KDOQI/EBPG definition –risk of anaemia increased 2-3x in people with diabetes Prevalence and degree of anaemia in diabetic patients with declining renal function 2 –cross sectional survey of 119,730 patients in diabetes clinics and GPs surgeries –3507 (2.93%) had creatinine clearance < 90 ml/min –39.6% men and 43.9% women had unrecognised anaemia by WHO definition and 17.2% men and 25.8% women by KDOQI/EBPG definition 1. Thomas et al Diabetes Care 2003; 26:1164-11692. 2. Hasslacher et al IDF Paris 2003; poster 946

Awareness of anaemia in physicians caring for people with diabetes Anaemia in diabetes – under recognised and under treated –prospective survey of all patients unknown to renal services with serum creatinine >180 µmol/L in men and >135 µmol/L in women over a 2 year period –872 people with diabetes and chronic renal failure (median glomerular filtration rate 29.9 ml/min) –17.7% of patients had not had Hb levels checked at all –of the remainder, 65.7% men and 53.6% women had unrecognised anaemia by WHO definition and 21.5% men and 27.8% women had Hb levels < 11 g/dL John et al IDF Paris, 2003 poster 1315

Increasing awareness of anaemia in diabetic kidney disease The Individualised Risk-profiling In DIabEtes Mellitus (IRIDIEM) study An observational study of patients with diabetes and chronic kidney disease aiming to –document current management of diabetic nephropathy –study the effect of individualised and evidence-based cardio- and reno-protective interventions on cardiovascular and metabolic risk profile and outcomes

IRIDIEM: Study design Phase l Pharmaco-epidemiological assessment (~2500 patients with diabetic nephropathy and risk factors) Phase ll Evidence-based educational guidance for individualising reno- and cardio-protective interventions (~700 patients stage lll or lV CKD and risk factors) Re-assessment of risk factor status 6 and 12 months after enrolment

Why should we be aware of anaemia in diabetic renal disease? The risk of coronary heart disease in people with diabetes is 2-4x higher than the general population and the risk of cerebrovascular disease up to 5x higher Anaemia develops early in chronic kidney disease The risks of cardiovascular disease develop early in the course of chronic kidney disease and are increased by diabetes Combination of anaemia and chronic kidney disease substantially increases stroke risks Anaemia predicts  left ventricular mass, left ventricular dilation, heart failure and death

Anaemia develops early in chronic kidney disease Canadian multicenter cohort study WHO criteria Levin et al, Am J Kidney Dis 1999; 34: 125-134 Prevalence (%) Creatinine clearance (ml/min) 100 40 0 >5035-4925-34<25 25 44 51 87 20 60 80

Anaemia develops early in CKD NHANES III –15,419 non-institutionalised adults over the age of 20 –Prevalence of anaemia (KDOQI) increased from 1% at glomerular filtration rate of 60 ml/min to 9% at 30 ml/min and 33% at 15 ml/min Astor et al, Arch Int Med 2002; 162: 1401-1408 Hb (g/dL) Glomerular filtration rate (ml/min) 5 10 15 20 603015 Hb (men) Hb (women)

Prevalence of anaemia in early renal insufficiency – PAERI study 1716 subjects, mean age 68 Mean serum creatinine 2.2 mg/dL (194 µmol/L) Mean Hb 12 g/dL Odds ratio of Hb < 12 g/dL or < 10 g/dL 1.8x in diabetes vs. no diabetes McClellan et al, ASN 2001

Cardiovascular disease in early chronic kidney disease HDFP study 1 –subjects with serum creatinine >150 µmol/L vs. < 150 µmol/L OR for death after 8 years 2.2 Framingham study 2 –increased incidence of cardiovascular disease in those with renal insufficiency Canadian multicenter cohort 3 –incidence of cardiovascular disease already 35.2% in those with glomerular filtration rate >50 ml/min and rose to 45.3% in those with glomerular filtration rate <25 ml/min 1. Shulman et al Hypertension 1989; 13(5):I80-93 2. Culleton et al Kidney Int 1999; 56: 2214-2219 3. Levin et al, Am J Kidney Dis 1999; 34: 125

Framingham study, N = 6223 Culleton et al Kidney Int 1999; 56: 2214-2219 8% mild CRF (males serum creatinine 136-265, females 120-265 µmol/L) Percentage (%) No renal insufficiency Chronic renal insufficiency ECG LVH=echocardiogram left ventricular hypertrophy CHD=coronary heart disease CHF=congestive heart failure CVD=cardiovascular disease

Canadian multicenter cohort study of chronic kidney disease Prevalence of any cardiovascular disease and left ventricular hypertrophy by creatinine clearance Percentage (%) Levin et al, Am J Kidney Dis 1999; 34: 125-134 Creatinine clearance (ml/min) 60 50 40 30 20 10 0 >50 35-4925-34<25 Cardiovascular disease Left ventricular hypertrophy

SOLVD study 1 –increase relative risk of mortality of 1.44 and relative risk of pump failure of 1.68 in subjects with glomerular filtration rate 60 ml/min HOPE study 2 –cardiovascular disease mortality, myocardial infarction or stroke 22.2% in subjects with serum creatinine 124-200 µmol/L vs. 15.1% in those with serum creatinine < 124 µmol/L Cardiovascular Health Study 3 –OR 2.34 for cardiovascular disease in subjects with serum creatinine > 132 µmol/L in males and > 114 µmol/L in females Cardiovascular disease in early chronic kidney disease 1. Dries et al, J Am Coll Cardiol, 2000; 35 :681-689 2. Mann et al, Ann Int Med, 2001;134:629-36 3. Manjunath et al, Kidney Int, 2003; 63: 1121-1129

Prevalence of cardiovascular abnormalities is higher among diabetic patients with CKD Newfoundland/Montreal study p=0.003 p<0.00001 p=0.04 Prevalence at dialysis start (%) Foley et al Diabetologia 1997; 40: 1307-1312 CLVHIHDCF IHD=ischaemic heart disease CF=cardiac failure CLVH = concentric left ventricular hypertrophy

Relative risk p=0.0003 p=ns p<0.0001 p<0.0001 CV = cardiovascular IHD = ischaemic heart disease CCF = chronic cardiac failure Foley et al Diabetologia 1997; 40: 1307-1312 Prevalence of cardiovascular abnormalities is higher among diabetic patients with CKD Newfoundland/Montreal study

Anaemia, chronic kidney disease and risk of stroke – the ARIC study, n = 13,716 Community based cohort, 9 yr follow up –mean age 54.1 ± 5.7, mean Hb 13.9, 10.6% diabetic –15 percent Cr Cl < 60 ml/min, mean blood pressure 120/71 –85 percent Cr Cl ≥ 60 ml/min, mean blood pressure 121/74 –Use of anti-hypertensives 24.6% & 23.5% Lower Cr Cl associated with higher crude stroke rate –Cr Cl < 60 ml/min, stroke rate 3.7 –Cr Cl ≥ 60 ml/min, stroke rate 2.06 Abramson et al, Kidney Int 2003; 64: 610-615

ARIC study – influence of anaemia (WHO) Stroke rate Abramson et al, Kidney Int 2003; 64: 610-615 Cr Cl ≥ 60 ml/min Cr Cl < 60 ml/min 2.06 3.7 1.52 10.53 2.12 2.85

Effect of 1g/dL fall in Hb 1.6 1.4 1.2 1.0 0.8 0.6 0.4 0.2 0 CLVHLV DilSDFCCFIHDDeath 1 1.49 1.55 1.24 1 1.25 Foley et al Am J Kidney Dis 1996; 28: 53-61. Relative risk CLVH = concentric left ventricular hypertrophy LV Dil = left ventricular dilatation SDF = systolic dysfunction CCF = chronic cardiac failure IHD = ischaemic heart disease

Cause specific death rates for prevalent dialysis patients aged  20 USRDS 1997-1999 0 10 20 30 40 50 60 70 Acute MICardiac arrestCardiac other Deaths per 1000 patient years Diabetes mellitus No diabetes mellitus

Mortality and haematocrit level: First year follow up, all dialysis patients USRDS prevalent patients 1994-1997 Haematocrit 0 50 100 150 200 250 300 350 400 <3030 - <3333 - <3636+ Deaths per 1000 patient years Diabetes mellitus No diabetes mellitus

Conclusions Anaemia is prevalent in people with diabetic kidney disease and is largely unrecognised and untreated Anaemia occurs earlier in diabetic kidney disease than is commonly recognised The association between chronic kidney disease and all forms of cardiovascular disease begins early in the evolution of chronic kidney disease, anaemia significantly amplifies this association Cardiovascular events and mortality in chronic kidney disease are increased in patients with diabetic kidney disease and are closely related to anaemia

Aetiology of anaemia and benefits of early treatment in patients with diabetes

Diabetes and renal disease WHO & IDF estimates suggest that in Europe there are already 32 million adults age 20-79 with diabetes Diabetes is the commonest cause of end stage renal failure worldwide and up to 1 in 4 people with diabetes will develop diabetic kidney disease over the course of 20 years Studies such as the RENAAL 1 and UKPDS 2 clearly demonstrate that the risk of mortality in diabetic kidney disease clearly outweighs the risk of progression to end stage renal disease 1. Keane et al Kidney Int 2003 63:1499-507 2. Adler et al Kidney Int 2003 63:225-32

Cardiovascular risk factors in chronic kidney disease Traditional –older age –male gender –  BP & LVH –  LDL-C  HDL-C –diabetes –smoking –inactivity –menopause CKD related –RAS activity –ECFV overload –Ca/PO 4 abnormalities –anaemia –MIA syndrome –oxidative stress –  Homocysteine –thrombogenic factors –  GFR

Diabetic kidney disease and anaemia Anaemia is prevalent in people with diabetic kidney disease and is largely unrecognised and untreated Anaemia occurs earlier in diabetic kidney disease than is commonly recognised The association between chronic kidney disease and all forms of cardiovascular disease begins early in the evolution of chronic kidney disease; anaemia significantly amplifies this association Cardiovascular events and mortality in chronic kidney disease are increased in patients with diabetic kidney disease and are closely related to anaemia

Potential causes of anaemia in chronic kidney disease Decreased erythropoietin production Shortened red blood cell survival Iron deficiency Inhibition of erythropoiesis Malnutrition and other deficiencies Chronic inflammation

Anaemia in diabetic nephropathy Aetiology Decreased erythropoietin levels resulting from: Tubulointerstitial damage Autonomic dysfunction Use of ACE inhibitors? Reviewed in Bilous Acta Diabetol 2002; 39: S15-19

Erythropoietin (EPO) Produced predominantly by peritubular fibroblasts in the kidneys and released in response to anaemia and hypoxia Release is modulated through the sympathetic nervous system (ß-adrenergic receptors) Anaemia associated with EPO deficiency usually occurs at a glomerular filtration rates below 35-40 ml/min but may occur at higher levels in diabetic kidney disease

Anaemia occurs early in diabetic nephropathy and is more severe than non- diabetic patients Bosman et al Diabetes Care 2001; 24: 495-499 DN anaemic*DN normalGNNon-DN anaemic Serum creatinine (mmol/l) 110 (63–160) 88 (64–133) 93 (49–180) 68 (59–148) Proteinuria (g/day) 2.5 (0.1–5.2) 0.6 (0.1–2.9) 1.9 (0.3–5.0) Hb (g/dl) 10.6 (8.7–12.0) 13.7 (11.8–15.1) 13.7 (11.6–16.3) 9.3 (6.9–11.6) Erythro- poietin (IU/l) 8.1 (2.5–19.0) 8.5 (2.5–17.5) 8.5 (2.5–17.0) 57.7 (29.2–195.8) *Anaemia <11.5 g/dl women, <12.0 g/dl men DN=diabetic nephropathy; GN=glomerulonephritis

Low serum erythropoietin levels cause anaemia and may predict the severity of diabetic nephropathy Bosman et al Diabetes Care 2001; 24: 495-499 0 2 4 6 6 810121416  Non-anaemia and microcytic anaemic control subjects, n=32 Diabetic nephropathy, n=26 Hb (g/dl) ln EPO

Erythropoietin-deficiency anaemia in diabetic nephropathy Underlying autonomic neuropathy 15 type 1 diabetic patients with severe complications including autonomic neuropathy and normal (<122 µmol/L) serum creatinine Compared with 18 controls matched for age and duration of diabetes but not for renal function Winkler et al Diabetic Med 1999; 16: 813-819 Diabetes + AN Diabetes Number of patients 1518 Duration (y)22.725.2 Hb (g/dl)11.113.7 (p<0.01) Serum creatinine (µmol/L) 86.966.4 Proteinuria3 micro- albuminuria; 12 proteinuria 3 micro- albuminuria AN = autonomic nephropathy

Erythropoietin-deficiency anaemia in diabetic nephropathy: Underlying autonomic neuropathy 0 2 4 6 6810121416 Hb (g/dl) ln EPO  Iron deficient and normals, n=32 Diabetic nephropathy, n=26 Winkler et al Diabetic Med 1999; 16: 813-819

Iron deficiency and anaemia in chronic kidney disease WomenMen  (g/dL) P P Fer ≥ 100 ng/mL & TSAT ≥ 20% reference Fer < 100 ng/mL & TSAT ≥ 20% - 0.20.002- 0.10.30 Fer ≥ 100 ng/mL & TSAT< 20% - 0.30.001- 0.40.004 Fer < 100 ng/mL & TSAT < 20% - 0.6<0.0001- 0.8<0.0001 Hsu et al, J Am Soc Nephrol 2002;13:2783-86 Fer=ferritin TSAT=transferrin saturation

Iron deficiency and anaemia in diabetes Unrecognised anaemia in patients with diabetes Cross sectional survey of 820 patients in a diabetic clinic Mean Hb 13.9 g/dL (men) & 12.9 g/dL (women) 190 (23%) had unrecognised anaemia by WHO definition and 56 (7%) by KDOQI/EBPG definition Most powerful predictors were transferrin saturation and glomerular filtration rate accounting for 22% and 10% of the variance in Hb respectively Thomas et al, Diabetes Care 2003;26:1164-1169

Why do we treat renal anaemia? Subjective 1 –well-being –life satisfaction –happiness –psychological affect Objective 1 –energy level –functional ability –activity level –health status Others –  cardiac status 2 –  blood transfusions 3 –  hospitalisation 4 –  mortality 5 1. Evans et al J Am Med Soc. 1990; 263:825-830 2. Winearls Nephrol Dial Transplant 1995; 10(suppl10):3-9 3. Fellner et al Kidney Int; 1993; 44:1309-1315 4 Churchill et al Clin Nephrol 1995; 43:184-188 5. US Renal Data System 1998

What do we hope to achieve by the early treatment of renal anaemia? Increased exercise capacity, improved quality of life, cognitive function and sexual function Regression of left ventricular hypertrophy Reduced mortality and hospitalisation Reduced transfusion requirements ?Regression of chronic renal failure progression

Epoetin improves quality of life in predialysis patients 83 predialysis patients entered into a parallel-group, open-label clinical trial and randomised to –epoetin –no treatment Epoetin treatment significantly improved anaemia and –energy –physical function –home management –social activity –cognitive function Revicki et al Am J Kidney Dis 1995; 25: 548-554

QOL following correction of anaemia Moreno et al, Am J Kidney Dis 1996;27:548-56 Karnofsky scale score Age <60 years Age >60 years 50 60 70 80 90 Basal6 months

QOL following correction of anaemia Moreno et al, Am J Kidney Dis 1996;27:548-56 Age <60 years Age >60 years Sickness impact profile score 0 5 10 15 20 25 30 35 Basal6 months

Correction of anaemia improves left ventricular hypertrophy in dialysis patients 22 dialysis patients studied by echocardiogram before and after correction of their anaemia with epoetin Hb increased at least 3.0 g/dL over baseline Correction of anaemia produced: –decrease in left ventricular mass (p = 0.0004) –decrease in left ventricular end-diastolic volume (p <0.0001) Adapted from Silverberg et al. Can J Cardiol 1990; 6: 1-4

Adapted from Portolés et al Am J Kidney Dis 1997; 29: 541-548 Partial correction (n=11) Reduction in LVMI with partial anaemia correction in predialysis patients LVMI (g/m 2 ) Baseline Hb = 9.0 g/dl 0 100 140 180 220 260 Epoetin p < 0.05 178.2 147.3 6 Months Hb = 11.7 g/dl LVMI = left ventricular mass index

Mean value 111.2 p=0.0108 Epoetin 0 20 40 60 80 100 120 140 160 180 200 140.6 126.9 Complete correction (n=9) Baseline PartialNormal Hct = 23.6% Hct = 32.1% Hct = 39.1% LVMI (g/m 2 ) Reduction in LVMI with complete anaemia correction in predialysis patients Adapted from Hayashi et al Am J Kidney Dis 2000; 35: 250-256 LVMI = left ventricular mass index

Building the evidence: Mortality & hospitalisation Lombardy registry 1 –all cause mortality and hospitalisation risks reduced with Hct levels >32% compared with <27% (n=5302) Ma et al 2 –RR mortality reduces as Hct rises, 1.51 at Hct < 27% to 0.9 at Hct 33-36% (n=96,369) Xia et al 3 –hospitalisation risks lowest in patients with Hct 33-36% (n=71,717) 1. Lombardy registry Nephrol Dial Transplant 1998;13:1642-44 2. Ma et al J Am Soc Nephrol 1999;10:610-619 3. Xia et al J Am Soc Nephrol 1999;10:1309-1316

Building the evidence: Mortality & hospitalisation Collins et al 1 –Relative risk of death and/or hospitalisation lowest at Hct levels of 36-39% Fink et al 2 –Pre-dialysis epoetin treatment leads to a relative risk of mortality of 0.8 (n=4866, 1107 epoetin) 1. Collins et al J Am Soc Nephrol November 2001 2. Fink et al Am J Kidney Dis 2001;37:348-355

Epoetin therapy correlates with reduced mortality and less hospitalisation Adapted from Locatelli et al Nephrol Dial Transplant 1998 Hct < 27% Patients with diabetes = 7.6% Hospitalisation days per patient-year Adjusted general mortality (n=5302) Odds ratio Adjusted CV mortality (n=5302) rh EPO-treated haemodialysis patients Untreated haemodialysis patients 0.8 0.6 0.4 0.2 0 1 p <0.001 p <0.05 Hct 27–32% Hct >32%

Adapted from Ma et al. J Am Soc Nephrol 1999; 10: 610-619 Mortality adjusted for risk factors [without severity of disease] Relative risk of mortality according to haematocrit in US patients with end stage renal disease 0.51.01.5 33-36 30-33 27-30 <27 Haematocrit (%) Relative risk (0.90) (1.00) (1.20) (1.51) 2.0 n = 96,369 Diabetes = 50%

Mortality, hospitalisation, and economic associations in HD patients aged  65 years Incident Medicare HD cohort 1/1/1996 to 30/6/1998 Follow-up period: one year Variables –age, gender, race, renal diagnosis, comorbidity, number of transfusions, number of access procedures, number of hospital days Hct groups: <30, 30<33, 33<36, 36<39, 39+ Outcome: risk of death and first hospitalisation Collins et al, ASN 2001

0.0 0.5 1.0 1.5 2.0 2.5 Relative risks of death and 95% CI < 30 30-<33 33-<36 36-<39  39 All-cause Cardiac Infection reference Collins et al, ASN 2001 Haematocrit Relative risk

Relative risks of hospitalisation & 95% CI Collins et al, ASN 2001 <3030-<3333-<3636-<39 >=39 All-cause Cardiac Infection reference Haematocrit Relative risk 0.0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6 1.8 2.0

Reduced mortality with anaemia treatment pre-dialysis 4,866 patients, median follow up 26.2 months 1,107 treated with epoetin pre-dialysis Relative risk of death for epoetin-treated pre-dialysis = 0.8 Most significant survival benefit was in those with the highest haematocrit Concluded that epoetin use pre-dialysis confers survival benefit Fink et al, Am J Kid Dis 2001;37:348-355

Reversal of anaemia by epoetin can retard progression of chronic renal failure Adapted from Kuriyama et al Nephron 1997; 77: 176-185 Cumulative renal survival rate (%) 20 0 40 60 80 100 0510152025303540 p=0.0024 p=0.3111 p=0.0003 Months of follow-up Hct <30%, treated with epoetin Hct >30%, untreated Hct <30%, untreated n=108

Building the evidence: delaying progression of chronic renal failure 63 patients (serum creatinine > 300 μmol/L, creatinine clearance < 15 mL/min/1.73 m 2 ) 20 with Hb 10 g/dL= control group Significant reduction in rate of progression of chronic renal failure in study group, no change in control group Jungers et al Nephron Dial Transplant 2001; 16: 307-312

Trials in treatment of CKD anaemia CREATE trial (Cardiovascular risk Reduction by Early Anaemia Treatment with Epoetin beta) CHOIR trial (Correction of Haemoglobin and Outcomes In Renal Insufficiency) ACORD (Anaemia CORrection in Diabetes) Aims of the studies : to establish whether early intervention –prevents development of left ventricular hypertrophy –reduces cardiovascular mortality and morbidity –delays progression of chronic renal failure –reduces stroke and heart failure related hospitalisations

Time or creatinine CREATE trial (Cardiovascular risk Reduction by Early Anaemia Treatment with Epoetin beta) Hb (g/dl) 15 12.5 10 Group 1 (Hb 13-15 g/dl) Group 2 (Hb 10.5-11.5 g/dl) 600 subjects glomerular filtration rate 15-35 ml/min randomised to 2 groups, early intervention and standard practise

Time or creatinine CHOIR trial (Correction of Haemoglobin and Outcomes In Renal Insufficiency) Hb (g/dl) 15 12.5 10 Group 1 (Hb 13-13.5 g/dl) Group 2 (Hb 10.5-11.0 g/dl) 2000 subjects GFR 15-50 ml/min randomised to 2 groups

The Anaemia CORrection in Diabetes (ACORD) study The ACORD study is investigating the effects of anaemia correction with subcutaneous epoetin beta on –cardiac structure –cardiac function In patients with early diabetic nephropathy Primary endpoint –effect of early anaemia treatment on left ventricular hypertrophy as a cardiovascular risk marker

Hb (g/dl) 16 14 12 10 8 6 16 14 12 10 8 6 Early intervention Target Hb: 13–15 g/dl Standard treatment Target Hb: 10.5–11.5 g/dl Inclusion: Hb 10.5–13.0 g/dl Creatinine clearance ≥30 ml/min m f Time n = 160 Randomisation ACORD: Study design

European recommendations for optimising treatment of renal anaemia Indication for start of epoetin therapy: –repeated Hb measurements <11g/dL –after exclusion of non-renal causes of anaemia (bleeding, nutritional deficiencies, hypothyroidism, iron deficiency, haemolysis) Target haemoglobin: –general: Hb >11 g/dL (no upper limit) –in CHD: Hb 11-12 g/dL Administration of epoetin: –SC dosing preferred; IV dosing also an option in HD patients –the goal is to increase Hb levels by 1–2 g/dL per month van Ypersele de Strihou Nephrol Dial Transplant 1999; 14 (suppl 2): 37-45

Iron stores Target –serum ferritin > 100  g/l (aim for 200-500) –hypochromic red blood cell count 20% (aim for < 2.5% & 30-40%) Level B Treatment strategies –predialysis and CAPD oral  intravenous –HD will need intravenous Level B

How should epoetin be administered to predialysis patients with diabetes and anaemia? EBPG & KDOQI recommend epoetin treatment for anaemia due to CKD when Hb < 11 g/dL Hb correction should be gradual to avoid: –exacerbation of hypertension –increased viscosity with adverse haemodynamics Guidelines recommend an increase of Hb 0.5 g/dL every 2 weeks Common practice suggest a target Hb of 11–12 g/dL (or ?12-13 g/dL)

Conclusions Anaemia is prevalent in diabetic kidney disease and occurs earlier than is commonly recognised Proven benefits of treatment of anaemia with epoetin (± intravenous iron) include –improved quality of life and performance status –regression of left ventricular hypertrophy –reduced transfusion requirements Potential benefits of early anaemia treatment include –reduced cardiovascular mortality and morbidity –delayed progression of chronic renal failure –reduced stroke and heart failure related hospitalisations

Reciprocal Relationship : Renal Anemia, Diabetes & CVD.

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