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Diabetic nephropathy

Diabetic nephropathy. Diabetes is common in Saudi Arabia This mainly related to genetic factors as well as the life style 40% of patients with ERSD are diabetics. The Kidney’s. وظيفة الكلية. *التخلص من المواد الضارة الناتجة عن الاحتراق والطاقة * التحكم في كمية السوائل بداخل الجسم

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Diabetic nephropathy

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  1. Diabetic nephropathy • Diabetes is common in Saudi Arabia • This mainly related to genetic factors as well as the life style • 40% of patients with ERSD are diabetics

  2. The Kidney’s

  3. وظيفة الكلية • *التخلص من المواد الضارة الناتجة عن الاحتراق والطاقة • * التحكم في كمية السوائل بداخل الجسم • * انتاج فيتامين "د" وتقوية العظام • * المساعدة في تكوين كريات الدم الحمراء ومنع الانيميا

  4. أسباب الفشل الكلوي • مرض السكر ارتفاع ضغط الدم • امراض الكلى الوراثية • التهابات الكلى المزمنة • التناول الخاطئ لبعض الادوية خاصة المخفضة للالام والاعشاب المستخدمة لتخفيف الوزن

  5. ارتفاع ضغط الدم • يحصل الفشل الكلوي اذا ارتفع ضغط الدم الى مستوى كبير جدا على فترة زمنية طويلة • * اذا عولج ارتفاع ضغط الدم بطريقة صحيحة فأنه لايسبب الفشل الكلوي • * اذا علولج ارتفاع ضغط الدم بعد وجود قصور في وظائف الكلى فان الوظائف تتحسن وقد تعود الى طبيعتها

  6. مرض السكر • *يسبب مرض السكر الفشل الكلوي بعد مرور عشرين سنة او اكثر ويحصل ذلك اكثر عند وجود بعض العوامل الوراثية واهمال العلاج وارتفاع ضعط الدم • * يمكن تلافي ذلك بالمحافظة على مستوى السكر بالدم بشكل دقيق مع المحافظة على ضغط الدم بمستوى طبيعي • * اذا اكتشفت الحالة مبكرة يمكن اعطاء بعض العقاقير التي تمنع ذلك

  7. الفشل الكلوي المزمن • اعراضه . • يسمى الفشل الكلوي القاتل الصامت إلا ان هناك بعض الاعراض منها التعب والإجهاد ووجود دم في البول واضطراب في الدورة الشهرية لدى النساء مع فقر الدم • * في الحالات المبكرة قد يكون هناك زلال وتورم في القدمين مع ارتفاع في ضغط الدم • * في الحالات المتقدمة يوجد غثيان مع قيء ثم صعوبة في التنفس وقد يؤدي الى تشنجات

  8. علاج الفشل الكلوي • في الحالات المبكرة نركز على التحكم في الضغط والسكر وهناك حالات تستجيب لعقارالكورتيزون او ادوية اخرى • في الحالات المتقدمة يركز على نفس النقاط بالاضافة الى حمية عن البروتينات • * في الحالات المتقدمة جدا قد نحتاج الى غسيل كلوي مزمن او زراعة كلية

  9. زراعة الكلى • تتم الزراعة اما عن طريق قريب او تؤخذ من شخص متوفي دماغيا • * لابد ان يكون المتبرع خالي من الامراض خاصة السكر والضغط ولايقل سنه عن 18 سنة ولايزيد عن 65 سنة ولايكون حاملا لاي فيروس او بكتيريا • * لابد ان يكون المتلقي ايضا خال من امراض القلب والامراض المزمنة وغير حامل للفيروسات

  10. زراعة الكلى • تبلغ نسبة نجاح زراعة الكلى اكثر من 90% • *يتراوح متوسط عمر الكلية المزروعة من 12الى 15 سنة وقد تكون اطول من ذلك بكثير او اقصر بكثير • * يستطيع المريض المتلقي للكلية ان يعيش حياة طبيعية ويمارس نشاطاته بشكل عادي كما يمكنه الانجاب سواء كان ذكر او انثى * يظل المريض المتلقي للكلية يتناول ادوية مخفضة للمناعة لمنع رفض الكلية المزروعة طوال حياته • * لاتوجد اضرار معروفة للمتبرع اذا كان الاختيار صحيحا

  11. P a t i e n t ' s K i d n e y T r a n s p l a n t K i d n e y ( e x t r a - p e r i t o n e a l l y ) B l a d d e r Transplantation Advantages • Most like your own kidney • No dialysis needed • No access needed • Normal Diet (-sodium) • More “normal” life style Disadvantage • Risks of major surgery • Risk of body rejecting kidney • Possible side effects of drugs • Lower resistance to illness • Body image changes.

  12. ارشادات عامة حول الكلى • * ننصح الجميع الاكثار من شرب السوائل بحيث تكون كمية البول اكثر من لتر ونصف يوميا • * الدقة في مراجعة الحمل واكثشاف اي تشوهات جنينية مبكرة • * عند وجود اي اعراض مثل حرقة البول او دم في البول وكثرة التردد بمراجعة "استشاري الكلى "لتقييم الحالة وإعطاء الادوية قبل تطور المرض

  13. Renal impairment: Prevalence • The progression of renal impairment can lead to end-stage renal disease which has huge medical, social and financial consequences • End-stage renal disease is particularly prevalent in: • The elderly • African-Americans • Patients with diabetes • Nearly half of the hypertensive population displays some abnormality of renal function

  14. Progression to end-stage renal disease In type 1 diabetes, progression to end-stage renal disease has been sequenced into five stages: • Early hypertrophy of renal tissue and increased glomerular filtration rate (GFR) • Development of glomerular lesions without any clinically appreciable disease (GFR remains increased) • Incipient nephropathy with microalbuminuria (GFR normal or slightly increased) • Clinical nephropathy with marked proteinuria and decreased GFR • GFR continues to decrease and end-stage renal disease develops

  15. Type 1 • Strict glycaemic control can decrease the nephropathy and progression of renal diseases

  16. Type one DM It hasbeen suggested that 25 to 45 percent of these patients will, during their lifetime, develop clinically evident disease

  17. Strict blood pressure control is very important • Genetic factors play major role in diabetic nephropathy • Most patients have retinopathy • Most are asymptomatic

  18. Nutrition

  19. Alternatives to Avoid

  20. Nutrition in Patients with CRF Classes of nutrients • - carbohydrates • - fats • - proteins • - vitamins • - minerals • - water Essential nutrients • - amino-acids • - essential fatty acids • - vitamins, elements • Without these, an individual • cannot function • Dietary protein provide • amino acids - body proteins • Without sufficient dietary • protein and energy, no growth • or repair

  21. Recommended Protein & Energy Intakes Protein Energy (g/kg BW/day) (kcal/kg BW/day) Healthy adults > 0.75#>35 CRF patients (non-dialyzed) ? 0.60 (high quality) >35 HD patients > 1.2 >35 CAPD patients > 1.2 >35 #safe for 97.5 % of the population (WHO 1985) CRF patients with GFR 30-20 ml/min reduce protein and energy intake (MDRD study) Protein and energy intake lower than recommended in a large proportion (20-60%?)of HD and CAPD patients

  22. Serum albumin alone is neither necessary nor sufficient to indicate malnutrition

  23. 20 Relative Death Risk 10 0 >4.5 <=2.5 2.5-3.0 3.0-3.5 3.5-4.0 4.0-4.5 Serum Albumin (mg/dl) Serum Albumin and Death RiskHaemodialysis Patients Lowrie et al, 1990

  24. Urinary albumin excretion Normal excretion<30 mg/24 hrs (<20 µg/min) Microalbuminuria30–300 mg/24 hrs (20–200 µg/min) Clinical proteinuria>300 mg/24 hrs (>200 µg/min) Mogensen CE et al. Lancet 1995; 346: 1080–1084

  25. Microalbuminuria: Prevalence and predictive power in diabetics • Type 1 diabetes • Prevalence: 50% • Predictive value for the development of nephropathy: 75% • Type 2 diabetes • Prevalence: 25–60% (depending on ethnic origin) • Predictive value for the development of nephropathy: 25% Savage MW et al. Br J Hosp Med 1995; 54: 429–435 Viberti GC et al. In: International Textbook of Diabetic Medicine, 1992

  26. Serum creatinine level of 1.4 mg/dl:What is the renal function? 12 10 8 6 4 2 0 Large muscular male Normal male Small female Serum creatinine (mg/dl) 120 60 30 15 GFR (ml/min) 100 50 25 0 Fraction of normal renal function (%) Sica DA. Unpublished data

  27. Therapeutic options in hypertension ACE inhibitors Angiotensin II antagonists a1-antagonists Hypertension Diuretics b-blockers Calcium antagonists

  28. ACE inhibitors in hypertension and heart failure In hypertension, ACE inhibitors • Lower blood pressure • Reduce the progression of end-organ damage In heart failure, ACE inhibitors • Improve cardiovascular hemodynamics • Improve symptomatolgy and exercise capacity • Decrease morbidity and mortality

  29. ACE inhibitors and renal impairment: Considerations ACE inhibitors ACE inhibitors show renoprotective effects over and above blood pressure control Dose modifications are a consideration in patients with renal impairment (except for fosinopril) Occasional cases of renal impairment and hyperkalemia have been reported with ACE inhibitors

  30. Adrenergic agents and renal impairment: Considerations Adrenergic agents There is no evidence of renoprotective effects over and above blood pressure control Modification of initial dosing is a consideration for hydrophilic b-blockers Post-dose temporary reduction in renal blood flow and GFR

  31. Calcium antagonists and renal impairment: Considerations Calcium antagonists There is no evidence of a class-specific renoprotective effect over and above blood pressure control The effect of renal impairment on metabolism of some active metabolites of calcium antagonists (e.g. diltiazem, verapamil) is unknown

  32. Diuretics and renal impairment: Considerations Diuretics There is no evidence of renoprotective effects over and above blood pressure control Thiazides may decrease renal blood flow and GFR Efficacy may be reduced in renal impairment

  33. Antihypertensive treatment in diabetes: Additional considerations Adapted from Cziraky MJ et al. Ann Pharmacother 1996; 30: 791–801

  34. Schematic diagram of ACE inhibition and renal function Normotensive Hypertensive Hypertensive treatedwith an ACE inhibitor Renal function (%) Time (years)

  35. Renoprotection: ACE inhibitors vs. other antihypertensives Calcium antagonists ACE inhibitors Diuretics and/or b-blockers Urinary protein Mean systemic blood pressure 0 –10 –20 –30 –40 –50 Decrease from baseline (%) Böhlen L et al. Am J Hypertens 1994; 7: 84S–92S

  36. ACE inhibitors are renoprotective ACE inhibitors have demonstrated renoprotective potential in: • Patients with type 2 diabetes • Patients with type 1 diabetes • Non-diabetic patients with nephropathy • Non-diabetic patients with hypertension and nephropathy • Non-diabetic hypertensive patients without pre-existing nephropathy

  37. ACE inhibition: Renoprotection in type 2 diabetes Placebo (years 1–5) and ACE inhibitor (years 6 and 7) Placebo (years 1–7) ACE inhibitor (years 1–5) and placebo (years 6 and 7) ACE inhibitor (years 1–7) 105 100 95 90 85 80 Initial value of reciprocal creatinine (%) 0 1 2 3 4 5 6 7 Treatment (years) Ravid M et al. Arch Intern Med 1996; 156: 286–289

  38. ACE inhibition: Renoprotection in type 1 diabetes 50 40 30 20 10 0 Placebo Captopril Died or needed dialysis or transplantation (%) p=0.006 0 1 2 3 4 Follow-up (years) Placebo n=202 198 192 186 171 121 100 59 26 Captopril n=207 207 204 201 195 140 103 64 37 Lewis EJ et al. N Engl J Med 1993; 329: 1456–1462

  39. ACE inhibition: Renoprotection in non-diabetic nephropathy 100 90 80 70 60 50 Patients not reaching an endpoint (%) Placebo Benazepril 0 1 2 3 Treatment (years) Adapted from Maschio G et al. N Engl J Med 1996; 334: 939–945

  40. ACE inhibition: Renoprotection in hypertension and nephropathy 100 90 80 70 60 50 Cumulative survival rate (%) Placebo ACE inhibitor Log rank test p<0.05 0 5 10 15 20 25 30 35 Treatment (months) Hannedouche T et al. Br Med J 1994; 309: 833–837

  41. ACE inhibition: Renoprotection in hypertensive patients Time (months) 0 6 12 18 24 30 36 0 –1 –2 –3 –4 –5 –6 –7 Decrease in GFR (ml/min/1.73 m2) ACE inhibitor b-blocker Himmelmann A et al. Am J Hypertens 1996; 9: 850–853

  42. Dosing of different ACE inhibitors depending on renal function Sica DA. J Cardiovasc Pharmacol 1992; 20(Suppl 10): S13–S20

  43. Microalbuminuria: Prevalence and predictive power in non-diabetics • Non-diabetics • Prevalence: 25–40% (depending on level of antihypertensive control) • Predictive value for the development of nephropathy: Thought to be lower than in diabetic patients Bigazzi R et al. Nephron 1992; 61: 94–97 Ljungman S. Am J Hypertens 1990; 3: 956–960

  44. ACE inhibitors are renoprotective ACE inhibitors have demonstrated renoprotective potential in: • Patients with type 2 diabetes • Patients with type 1 diabetes • Non-diabetic patients with nephropathy • Non-diabetic patients with hypertension and nephropathy • Non-diabetic hypertensive patients without pre-existing nephropathy

  45. ACE inhibition: Renoprotection in type 1 diabetes 50 40 30 20 10 0 Placebo Captopril Died or needed dialysis or transplantation (%) p=0.006 0 1 2 3 4 Follow-up (years) Placebo n=202 198 192 186 171 121 100 59 26 Captopril n=207 207 204 201 195 140 103 64 37 Lewis EJ et al. N Engl J Med 1993; 329: 1456–1462

  46. ACE inhibition: Renoprotection in hypertension and nephropathy 100 90 80 70 60 50 Cumulative survival rate (%) Placebo ACE inhibitor Log rank test p<0.05 0 5 10 15 20 25 30 35 Treatment (months) Hannedouche T et al. Br Med J 1994; 309: 833–837

  47. Correlation between beneficial renal effects and albuminuria * 0.4 0 –0.4 –0.8 Controls ACE inhibitors Change in GFR (ml/min/1.73 m2/month) <30 30–300 >300 Baseline albuminuria (mg/day) *p=0.02 vs. controls Lebovitz HE et al. Kidney Int 1994; 45(Suppl 45): S150–S155

  48. Dosing of different ACE inhibitors depending on renal function Sica DA. J Cardiovasc Pharmacol 1992; 20(Suppl 10): S13–S20

  49. Simplifying antihypertensive treatment in the presence of renal failure If a patient presents with hypertension Hypertension accelerates the decline in GFR and many hypertensive patients have some degree of renal impairment WHY? Consider that the patient may have renal impairment Measure renal function ACE inhibitors are the only antihypertensives with established renoprotective potential If some degree of renal dysfunction is found, consider treatment with an ACE inhibitor WHY? If you consider treatment with an ACE inhibitor, consider dual and compensatory elimination

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