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Diabetes and Renal Disease

Diabetes and Renal Disease. Dr Anne Kleinitz KRSS GP 12/11/2009. 1. Learning Objectives. Type 1 vs Type 2 DM Diabetes Management Diabetic Complications Diabetic Nephropathy & ESKD. 2. Type 1 Vs Type 2 DM. 3. Type 2 Older **** Overweight Insulin resistant (excess fat cell mass)

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Diabetes and Renal Disease

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

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

  3. Type 1 Vs Type 2 DM 3

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

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

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

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

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

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

  13. No Data <4.5% 4.5-5.9% 6.0-7.4% 7.5-8.9% >9.0% No Data <14.0% 14.0-17.9% 18.0-21.9% 22.0-25.9% >26.0% 2000 2000 2007 1994 1994 2007 Age-adjusted Percentage of U.S. Adults Who Were Obese or Who Had Diagnosed Diabetes Obesity (BMI ≥30 kg/m2) Diabetes CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available at http://www.cdc.gov/diabetes/statistics 13

  14. 1994 14

  15. 1995 15

  16. 1996 16

  17. 1997 17

  18. 1998 18

  19. 1999 19

  20. 2000 20

  21. 2001 21

  22. 2002 22

  23. 2003 23

  24. 2004 24

  25. 2005 25

  26. 2006 26

  27. 2007 27

  28. Childhood Diabetes • Rising T2DM, parallel with  obesity • 10-14% of new paediatric DM • ~ 50% in rural and remote • Many likely undiagnosed • Indigenous children disproportionately represented • > ½ of children with T2DM are indigenous • Mx – Diet, exercise, Metformin and Insulin 28

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

  30. Metabolic Syndrome“Syndrome X” • Associated with increased risk of CVD, CKD and death. • DIAGNOSIS • Insulin resistance • FBG > 5.6 or T2DM • Central Obesity • WC > 94cm • Abnormal lipid profile: HDL • Male < 1.03, Female < 1.29 • Hypertension • Sys > 130, dias >85 30

  31. 31

  32. 32

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  34. Treatment Options 34

  35. Treatment Options • ↓Glucose load: ↓ meal size & sugars • ↑Insulin release (“secretogogues”) • sulphonourea eg Gliclazide • Insulin, Pancreas Tx • ↓Insulin resistance (“insulin sensitizers”) • Exercise & weight loss Metformin or glitazones 35

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

  37. Short-acting & Long-acting Insulin Breakfast Lunch Dinner Short acting Plasma insulin Glargine 4:00 8:00 12:00 16:00 20:00 24:00 4:00 8:00 Time 37

  38. Aims in Mx (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 38

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

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

  41. Diabetic Complications 41

  42. Diabetic Complications • Microvascular • Retinopathy • Nephropathy • Neuropathy • peripheral & autonomic • Macrovascular • Cerebrovascular • Cardiovascular • Peripheral vascular 42

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  44. Natural 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 44

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

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

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

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

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

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