ΑΝΤΙΜΕΤΩΠΙΣΗ ΝΕΦΡΙΚΗΣ ΑΝΕΠΑΡΚΕΙΑΣ ΣΕ ΑΣΘΕΝΗ ΜΕ ΚΑ

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1 ΑΝΤΙΜΕΤΩΠΙΣΗ ΝΕΦΡΙΚΗΣ ΑΝΕΠΑΡΚΕΙΑΣ ΣΕ ΑΣΘΕΝΗ ΜΕ ΚΑ Δημήτριος Β. Βλαχάκος Καθηγητής Παθολογίας - Νεφρολογίας Υπεύθυνος Νεφρολογικής Μονάδας Β Προπαιδευτική Παθολογική Κλινική Πανεπιστημιακό Νοσοκομείο «ΑΤΤΙΚΟΝ» Χαϊδάρι

2 CO 5 L/min 30 kg 1 L/min 300 g 1 L/min

3 180 L/ημ = 125 ml/min

4 60 ml/min Damage Disease Stage I Stage II Stage III Stage IV Stage V normal Mild Moderate Severe failure Glomerular filtration rate (ml/min/1.73m 2 ) National Kidney Foundation. Am J Kidney Dis 2002; 39(2 Suppl 1):S1 S266

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6 Glomerular Filtration Rate in ml/min = (140 - ηλικία) Χ Βάρος σε Kg (72 ή 85 ) Χ Creat,mg%

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9 CRS

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11 OBESITY EPIDEMICS CHF ESRD

12 % of patients with renal dysfunction 60% 40% 20% Clinical trials (patients with severe RD excluded) GFR <60 21% SOLVD-P SOLVD-T NYHA I IINYHA II III (n=3673) 1 (n=2161) 1 GFR <60 36% GFR % GFR % GFR <45 VALIANT (post AMI, CHF / LVD) (n=14,527) 2 GFR >90 Real life GFR GFR GFR <30 ADHERE (acute, decompensated HF) (n=118,465) 3 1. Dries DL et al. J Am Coll Cardiol 2000;35: Anavekar NS et al. N Engl J Med 2004;351: Heywood JT et al. J Card Fail 2007;13: GFR, glomerular filtration rate

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14 40 Prevalence of Anaemia in a CHF Outpatient Clinic (Hgb < 12 g/dl) Male 82% Female 18% N = 193 Prevalence (%) % 9% 17% 26% 0 Class I Class II Class III Class IV NYHA Class Tanner H et al. Int J Cardiol 2002

15 Mechanisms of Anaemia in CHF Haemodilution Plasma Volume Forward failure Bone Marrow (BM) - dysfunction Chronic immune activation TNFα - production of Epo - Epo activity in BM Drugs ACEi/ARB - Epo synthesis - RBC production in BM Iron deficiency Fe ++ uptake malabsorption chron. bleeding (Aspirin) Chronic kidney failure Production of Epo Uremic Toxins Silverberg DS et al. J Am Coll Cardiol 2000

16 ADH SNS RAAS

17 Volpe et al. Am J Cardiol 1994

18 Vasopressin in heart failure

19 Figure 3. Distribution of central venous pressure (CVP) and the relationship between CVP and estimated GFR in 2557 patients. Bock J S, Gottlieb S S Circulation 2010;121: Copyright American Heart Association

20 Volpe et al. Am J Cardiol 1994

21 Volpe et al. Am J Cardiol 1994

22 Vlahakos et al. AJKD 2010 Renal Hypoperfusion (Hypoxia) Renin Release Erythropoetin Secretion Angiotensinogen Angiotensin I Angiotensin II Erythroid Progenitors Increased RBC Mass

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24 AII ACEi/ARB

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26 SOLVD Database Ishani et al. JACC, 2005

27 Young and Zaritsky, Clin J Am Soc Nephrol, 2009

28 Etiology of Anemia in Patients With Advanced Heart Failure 37 advanced CHF pts; NYHA IV; mean LVEF: 22%. Nanas J et al. J Am Coll Cardiol 2006

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30 Οι κατευθυντήριες οδηγίες για τα επίπεδα φερριτίνης και TSAT(%) KDIGO 2012 Αντιμετώπιση όλων των αιτιών της αναιμίας (σιδηροπενίας και φλεγμονής) πριν την έναρξη της θεραπείας με ESA Xορήγηση αρχικής δόσης (φόρτιση) με 1g Fe. Επανάληψη της δόσης σε περίπτωση αποτυχίας να αυξηθούν τα επίπεδα της Hb και/ή να μειωθεί η δόση των ESAs, και εάν το TSAT 30% και η φερριτίνη ορού 500 μg/l

31 Ferric Carboxymaltose in Patients with Heart Failure and Iron Deficiency Anker et al. NEJM Nov 2009 Enrolled 459 patients with chronic heart failure of New York Heart Association (NYHA) functional class II or III, a left ventricular ejection fraction of 40% or less (for patients with NYHA class II) or 45% or less (for NYHA class III), iron deficiency (ferritin level <100 µg per liter or between 100 and 299 µg per liter, if the transferrin saturation was <20%), and a hemoglobin level of 95 to 135 g per liter and no hepatic or renal insufficiency. Patients were randomly assigned, in a 2:1 ratio, to receive 200 mg of intravenous iron (ferric carboxymaltose) or saline (placebo). The primary end points were the self-reported Patient Global Assessment and NYHA functional class, both at week 24. Secondary end points included the distance walked in 6 minutes and the health-related quality of life.

32 Self-Reported Patient Global Assessment and New York Heart Association (NYHA) Functional Class at Week 24, According to Assigned Study Treatment Anker S et al. N Engl J Med 2009

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34 Additive prognostic value of GFR and Ht in CHF (LVEF< 30%) Mitchel J. Am J Cardiol 2007;99:15D 20D

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36 Kaplan-Meier Plot of the Time to the Primary Composite Event between Randomization and Termination: ITT Population 30% Randomized Treatment 125 Kaplan-Meier Failure Estimate (%) 25% 20% 15% 10% Hemoglobin Target 13.5 g/dl Hemoglobin Target 11.3 g/dl Hazard ratio (1.025, 1.743) P= % At risk 0% Months from Randomization Primary Composite Endpoint: Death, MI, CHF hosp (no RRT) and/or stroke Singh et al,new Engl J Med 2006; 355:

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39 Balance the potential benefits of reducing blood transfusions and anemia-related symptoms against the risks of harm in individual patients (e.g., stroke, vascular access loss, hypertension). (1B) Use ESA therapy with great caution, if at all, in CKD patients with active malignancy in particular when cure is the anticipated outcome (1B), a history of stroke (1B), or a history of malignancy (2C). For adult CKD ND patients with Hb concentration >10.0 g/dl, we suggest that ESA therapy not be initiated. (2D) For adult CKD ND patients with Hb concentration <10.0 g/dl we suggest that the decision whether to initiate ESA therapy be individualized based on the rate of fall of Hb concentration, prior response to iron therapy, the risk of needing a transfusion, the risks related to ESA therapy and the presence of symptoms attributable to anemia. (2C) Individualization of therapy is reasonable as some patients may have improvements in quality of life at higher Hb concentration and ESA therapy may be started above 10.0 g/dl (100 g/l). (Not Graded) Initiating ESA therapy

40 Maintaining ESA therapy In general, we suggest that ESAs not to be used to maintain Hb concentration above g/dl in adult patients with CKD. (2C) Individualization of therapy will be necessary as some patients may have improvements in quality of life at Hb concentration above 11.5 g/dl and will be prepared to accept the risks. (Not Graded) In all adult patients, we recommend that ESAs not be used to intentionally increase the Hb concentration above 13 g/dl (130 g/l). (1A)

41 Aρχίσατε με χαμηλή δόση κατά 30-50% και αυξήσατε ανάλογα με το GFR, και την κλινική εικόνα του ασθενούς.

42 PGI 2 AII NSAIA s ACEi or ARB

43 Δώσατε οδηγίες στους ασθενείς και να σας ειδοποιούν όταν: Να διακόπτουν τα διουρητικά και τα φάρμακα του ΣΡΑ όταν έχουν μεγάλη εφίδρωση, πυρετό, εμέτους ή διάρροιες. Να πίνουν τουλάχιστον 1 L αν χρειάζεται στέρηση υγρών λόγω ΚΑ ή 2 L σε κάθε άλλη περίπτωση. Να ενημερώνουν τον χειρουργό, οδοντίατρο, ορθοπεδικό κλπ για την κατάσταση τους και να του αναφέρουν τα φάρμακα που λαμβάνουν. Να αποφεύγουν ΜΣΑΦ, συμπληρώματα ή τροφές με πολύ κάλιο.

44 RAAS ΑΛΑΣ

45 Moderation of dietary sodium potentiates the renal and cardiovascular protective effects of angiotensin receptor blockers Hiddo J Lambers Heerspink et al KI 2012

46 WKD 2011 Logo Protect your kidneys, Save your heart ΕΥΧΑΡΙΣΤΩ ΠΟΛΥ ΓΙΑ ΤΗΝ ΠΡΟΣΟΧΗ ΣΑΣ!

47 ΕΚΤΙΜΗΣΗ ΤΗΣ ΝΕΦΡΙΚΗΣ ΚΑΘΑΡΣΕΩΣ ΣΤΗΝ..OΞΕΙΑ ΝΕΦΡΙΚΗ ΑΝΕΠΑΡΚΕΙΑ.. NON-STEADY-STATE CONDITIONS

48 Εκτίμηση της νεφρικής λειτουργίας στην οξεία νεφρική ανεπάρκεια Ρυθμός μεταβολής της κρεατινίνης από ημέρασε-ημέρα: < 1 mg/dl = όχι πλήρης ανεπάρκεια 1-3 mg/dl = πλήρης ανεπάρκεια δηλαδή GFR < 10 ml/min > 3 mg/dl = ραβδομυόλυση

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50 ΚΛΟΑ Υποογκαιμικός Υπερυδατωμένος Πίεση Ενσφήνωσης

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52 <<<Na <<H20 >>Na >>>>H20 Na >>H20

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54 Ευχαριστώ για την προσοχή σας!!