la gestione del paziente con scompenso cardiaco quando...

La gestione del paziente con scompenso cardiaco Quando chiamare il nefrologo può essere utile?

Aggiornamenti in nefrologia, ipertensione arteriosa e diabete XI Edizione – Isola d’Elba 4 ottobre 2014

Michele Emdin, Roberta Poletti Fondazione Toscana G. Monasterio, Pisa

Things you can read on scientific journals …

«How to motivate nephrologist to think more cardiac and cardiologist to think more renal?»

«Cardiologists and nephrologists: time for a more integrated approach»

«What have cardiologists and nephrologists learnt each other?» «Cardiologists and Nephrologists must realise they need do work in

tandem”


Caro Collega, vorrei capire, ma il problema in questione lo vediamo allo stesso modo?

Le «nostre insufficienze» hanno una fisiopatologia in comune»? Il nostro approccio nosografico e terapeutico si basa sugli stessi

principi?

“L’insufficienza cardiaca congestizia rappresenta una sindrome complessa caratterizzata da alterazioni della funzione ventricolare sinistra e della regolazione neuro-ormonale , che si associano ad intolleranza allo sforzo, ritenzione idrica e ridotta longevità” Packer M., in Braunwald E., Textbook of cardiology, 8th edition, 2007.

Definizione di scompenso cardiaco - oggi -

La malattia renale cronica è definita come una alterazione della struttura o della funzionalità renale, presente da oltre tre mesi, tale da avere implicazioni sullo stato di salute

Clinical Practical Guidelines for the Evaluation and Management of Chronic Kidney Disease - KDIGO, 2012

CKD - definizione

DANNO RENALE

> 3

mes

i

•albuminuria

•alterazioni sedimento urinario

•alterazioni elettrolitiche dovute a mal tubulari

•alterazioni strutturali (imaging)

•alterazioni istologiche (biopsia)

•pregresso trapianto renale

GFR < 60 ml/min/1.73 m2 < 15 ml/min/1.73 m2 kidney failure

FUNZIONE RENALE

Malattie autoimmuni

Malattie vascolari

Ipertensione

Malattia aterosclerotica

Diabete mellito

Malattie glomerUlari

Malattia congenita/

cistica

Malattie chirurgiche

Tossica/Post-chemiotp

CDM

Malattie valvolari

Malattie Tubulo-

interstiziali

Malattia congenita

CKD CHF

La malattia renale cronica (CKD) e lo scompenso cardiaco cronico (CHF) sono un diffuso problema di sanità pubblica, la cui incidenza e prevalenza sono stimate aumentare nei prossimi anni, con importanti costi socio-sanitar i.

0

510

15

20

2530

35

40

I (> 90ml/Kg/min)

II (90-60ml/Kg/min)

III IV (30-15ml/Kg/min)

V (<15ml/Kg/min)eGFR < 15 ml/ min/ 1.73m2 NFK stage 5

2%

eGFR 15-29 ml/ min/ 1.73m2 NFK stage 4

7%


36%


30 %

eGFR > 90 ml/ min/ 1.73m2

NFK stage 1

25%

Prevalenza CHF-CKD

996 pazienti con CHF, FTGM Pisa

Peggioramento della funzione renale (WRF)

>26.5 mmol/L (0.3 mg/dL) increase in serum creatinine

Damman K, et al, Renal impairment, WRF, and outcome in HF patients. Eur Heart J, 2014.

23% AHF 25% CHF

49890 CHF pt mean follow-up of 448+569

(range 10–2555) days

mortality rates: 36 (WRF) vs 32% (no WRF) OR 1.81, 95% CI 1.55–2.12, P = 0.001

Cardiac mortality (p<0.001 Log Rank Mantel Cox)

Mortalità Cardiaca nei pazienti con CHF- sottogruppi di GRF

I (GFR ≥ 90) 440/1465 (30%)

IV + V GFR (<30): 87/1465 (6%)

II GFR (60-89): 440/1465 (30%)

III GFR (30-59): 498/1465 (34%)

Predittori indipendenti di mortalità cardiaca nei paz con GFR < 60 ml/min/1.73 m2

Poletti R et al, International Journal Cardiology 2013

HF-REF

•Sintomi tipici di scompenso

•Segni tipici di scompenso

•Ridotta funzione sistolica VS

HF-PEF

•Sintomi tipici di scompenso

•Segni tipici di scompenso

•Normale o solo lievemente

ridotta funzione sistolica VS

•Alterazioni strutturali

rilevanti (es IVS) e/o

disfunzione diastolica

ESC Acute and Chronic Guidelines 2012

CHF - diagnosi

FUNZIONE Disf. Sistolica VS

Disf. Diastolica VS

Asincronia VS

Disfunzione Vd

CLASSIFICAZIONE ACC-AHA L’ A-B-C-D DELLO SCOMPENSO

SCOMPENSO PRE-CLINICO

SCOMPENSO CONCLAMATO

M. Jessup et al. N Engl J Med 2003; 348:2007-1

Stadi dello SC e Approccio Terapeutico

Modello di inizio e progressione della malattia renale cronica, Kidney Disease Outcome Quality Initiative (K/DOQI), 2002

Fattori di rischio per CKD :

•di suscettibilità età, familiarità, riduzione massa renale, ect

•di inizio diabete, ipertensione, malattie autoimmuni, ect

•di progressione elevata proteinuria, scarso controllo PA/glicemia

•end-stage Bassa resa dialitica, anemia, ipoalbuminemia, ect

Stadio A

Stadio B

Stadio C

Stadio D


C: Caro Collega, ma secondo te esiste una sindrome cardio-renale?

N: sì!

Cardiorenal syndrome definition and classification

Pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction

of 1 organ may induce acute or chronic dysfunction of the other

Traditionally renal insufficiency was thought to be secondary to heart failure, but nowadays several

possibility of interplay have been recognized

New classification of CR syndrome

Cardio-renal syndrome:

a classification

Taub PR et al, 2012


C: Caro Collega, ma secondo te esiste una sindrome cardio-renale?

N: ni!


C: Caro Collega, ti dico cosa pensano i cardiologi dello SC…

From risky conditions, through acute damage and ventricular silent dysfunction, up to overt heart failure

GENETICS -COMORBIDITY

ANP

BNP

NEPI

RENIN

A II

ALDOST.

ANP

BNP

>> pl. Vol

> CO

>> MAP > CO

>> HR

- Na H20 retention – vasoconstriction

LV

DYSFUNCTION

dyspnoea

oedema

arrhythmias sudden death

fatigue


arrhythmogenesis – remodeling

- Sympathetic RAA activation

< baroreflex > chemoreflex

- BNP ANP system activation

NEURO-HORMONAL BALANCE IN HEART FAILURE

< baroreflex

Neurohormonal imbalance & HF treatment LV

dysfunction

> chemoreflex

Sympathetic and RAAS activation

BNP – ANP system activation

>> pl. Vol > CO

>> MAP > CO

>> HR


dyspnoea oedema

arrhythmias sudden death

Fatigue Cheyne –Stokes resp.

- Na H20 retention – vasoconstriction arrhythmogenesis – tissue ischaemia

Beta-blockers ACE-I / ARBs Spironolactone Aerobic training

CRT

ICD

Clark H et al, 2014

Neurohormonal antagonism in HF and CKD: similar therapy for similar diseases?

wor

kloa

d (w

atts

)

80

120

Peak

VO

2 (m

l/min

/kg)

12

18

Hea

rt ra

te(b

.p.m

.)

60

80

BN

P(n

g/L)

100

250

NT-

proB

NP

(ng/

L)

900

1700

Nor

epin

ephr

ine

(ng/

L)

400

700

Baseline 3rdmonth

9thmonth Baseline 3rd

month9th

month

***#

** **

*

**

**

*

*

***#

***##

** #

CHF: miglioramento clinico e neuro-endocrino dopo 9 mesi

Passino C et al.

JACC, 2006

M F Piepoli, BMJ 2004;328:189

Prognosi

Mechanism of action Valsartan blocks the angiotensin II receptor type 1 (AT1) and thereby causes vasodilatation and increases excretion of sodium and water via the kidneys (by reducing aldosterone production). The latter mechanism leads to a reduction in blood volume.

Sacubitril is a prodrug that is activated to LBQ657 by de-ethylation via esterases. LBQ657 inhibits the enzyme neprilysin, which is responsible for the degradation of atrial and brain natriuretic peptide, two blood pressure lowering peptides that work mainly by reducing blood volume.

http://en.wikipedia.org/wiki/Valsartan

http://en.wikipedia.org/wiki/Angiotensin_II_receptor_type_1

http://en.wikipedia.org/wiki/Vasodilatation

http://en.wikipedia.org/wiki/Sodium

http://en.wikipedia.org/wiki/Aldosterone

http://en.wikipedia.org/wiki/Sacubitril

http://en.wikipedia.org/wiki/Prodrug

http://en.wikipedia.org/w/index.php?title=LBQ657&action=edit&redlink=1

http://en.wikipedia.org/wiki/Ethyl_group

http://en.wikipedia.org/wiki/Esterase

http://en.wikipedia.org/wiki/Neprilysin

http://en.wikipedia.org/wiki/Atrial_natriuretic_peptide

http://en.wikipedia.org/wiki/Brain_natriuretic_peptide

http://en.wikipedia.org/wiki/Peptide


C: Caro Collega, ma i diuretici fanno bene al mio pz con CHF?

Severity of fluid retention

Diuretic Dose (mg)

comments

Moderate symptoms

Furosemide or Bumetanide or Torasemide

20-40 0,5 – 1 10 – 20

oral or i.v. and titrate dose according to initial clinical response Monitor K, Na, creatinine, blood pressure

Severe Furosemide or Bumetanide or Torasemide

40-100 iv. 1-4 20-100

Furosemide infusion(5 – 40 mg / h) better than very high bolus doses

Refractory to loop diuretics

add HCTZ or MTZ or Spironolactone

25 – 50 bid 2,5-10 QD 25-50 /day

Combination better than very high dose of loop diuretics Spironolactone best unless renal failure & normal or low K+

Refractory to loop diuretics and thiatzides

add dopamine (renal vasodilation) or dobutamine

Consider ultrafiltration or hemodialysis if coexisting renal failure

Diuretic dosing and administration

ESC Task Force on Acute Heart Failure

State of Data on Loop Diuretics

• The Good –Induce hypotonic urine, reducing total body congestion

• The Bad –Direct Activation of RAA –Loss of K, Mg, Ca, secondary myocyte Ca loading –Reduction of Cardiac Output –Increased Total Systemic Vascular Resistance

• The Ugly –Associated with enhanced morbidity –Associated with increased mortality

L’altro ieri….

• Donato L, Biagini A, Contini C, L'Abbate A, Emdin M, Piacenti M, Palla R. Treatment of end-stage congestive heart failure by extracorporeal ultrafiltration. Am J Cardiol. 1987 Feb 1;59(4):379-80.


Caro Collega, mi puoi aiutare con un mio caro paziente con end-stage HF?

Stage D Therapy

Meticulous identification and control of fluid retention is recommended in patients with refractory end-stage HF.

Control of Fluid Retention

I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III I I I IIa IIa IIa IIb IIb IIb III III III IIa IIa IIa IIb IIb IIb III III III

Managing Resistance to Diuretics • Volume repletion in cases of hypovolaemia • Restrict Na & H2O intake and follow electrolytes • Increase dose and/or frequency of administration of

diuretic • Use intravenous administration as bolus, or as infusion • Combine diuretic therapy

– furosemide + HCTZ – furosemide + spironolactone – metolazone + furosemide (active also in renal failure)

• Combine diuretic therapy with dopamine, or dobutamine • Reduce the dose of ACE-inhibitor or use very low doses • Consider ultrafiltration or dialysis

Acute Heart Failure ESC Guidelines, Eur Heart J 2005; 26:384

Controllo del volume nel paziente con scompenso cronico: la dialisi peritoneale

SOD Dialisi Peritoneale

Azienda ospedaliero-universitaria Pisana

Daniela Palmarini 19 Giugno 2014

Il primo autore che ha descritto l’uso della DP nell’edema cardiogeno è stato Schneierson nel 1949

Ha riportato un marcato decremento ponderale del paziente ed una ripresa della risposta alla terapia diuretica dopo la DP

Pazienti candidati alla DP

EDTA 2008

Nello scompenso cardiaco cronico sono coinvolti citochine e fattori umorali (PNA, TNF-α, IL-1, IL-6) che inducono l’apoptosi dei cardiomiociti ed esercitano un effetto inotropo negativo

E’ noto che PNA e TNF-α hanno una clearance transperitoneale

La rimozione di fluidi con soluzioni a lunga permanenza (icodestrina) permette alti volumi di UF e clearance più elevate di sodio, tossine uremiche, citochine infiammatorie e sostanze cardiodepressive

D, Imholtz AL et al. Appearance of tumor necrosis factor-alpha and soluble TNF-receptors I and II in peritonel effluent of CAPD. Kidney Int 1994; 46: 1422-1430 Fincher ME et al. ANP is removed by peritoneal dialysis in humans. Adv Perit Dial 1989; 5: 16-19 Qi H et al. Comparison of icodextrin and glucose solutions for long dwell exchange in peritoneal dialysis: a meta-analysis of randomized controlled trials. Perit Dial Int. 2011;31:179-88

Utilizzo dell’icodestrina in dialisi peritoneale e nello scompenso cardiaco

Studio monocentrico, prospettico, non-randomizzato 20 pz con scompenso cardiaco classe NYHA IV, FE basale < 35%, eGFR (MDRD) medio basale 15 ml/min, età media 65 anni, Charlson's comorbidity index medio 7.8 Inizialmente trattati con 2-5 sessioni di CVVH fino al raggiungimento del peso secco e successivamente con 3 APD/settimana (8 h ciascuna), utilizzando 15-20 l di soluzione per DP (glucoso 1,5% + 4,25%) 1 anno di follow-up Valutazione dei parametri emodinamici e dello stato di idratazione toracico mediante cardio-bioimpedenziometria transtoracica

Risultati dopo 1 anno di follow-up Tutti i pazienti hanno avuto una regressione dalla classe NYHA IV alla classe I

Ripresa della funzione ventricolare sn

La mortalità a 1 anno era del 10% (più bassa di quella attesa in base all’indice di comorbidità) Il numero dei giorni di ospedalizzazione era 13 vs 157 (p<0.001)


E’ opportuna la correzione dell’anemia Con quali valori target?

turbe metaboliche - cachessia

BPCO

Cheyne-Stokes

Comorbosità

anemia

insufficienza renale

ipertensione

polmonare

Diabete mellito

Ipertensione arteriosa

TARGETS TO TREAT

IN HFS

THE HEART SYSTOLE

DIASTOLE RV

EPICARDIAL CORONARY ARTERIES CORONARY MICROCIRCULATION

HEART RATE SV ARRHYTHMIA

V ARRHYTMIA ASYNCHRONY

VALVULAR FAILURE V REMODELING

CARDIAC METABOLISM

THE BODY CACHEXIA –NUTRITIONAL THERAPY

SKELETAL MUSCLES - PHYSICAL ACTIVITY

THE SOUL LIFE STYLE – SMOKING HABIT/DIET/AE.PH.

ACTIVITY DEPRESSION

END-LIFE ISSUES (PALLIATION)

THE ENVIRONMENT (FAMILY) CAREGIVER

THE SPECIALIST –GENERALIST (ABSENT) ALLIANCE REGULATORY –ECONOMICAL CONSTRAINTS

THERAPY ITSELF AVOID UNNECESSARY

CONTROL-TREAT COLLATERAL EFFECTS MIND INTERACTIONS

CONSIDER/INCREASE COMPLIANCE

ORGAN PROTECTION KIDNEY COPD

(SLEEP) APNEA ANEMIA

SYMPTOMS SALT WATER RITENTION

ETIOLOGY

RISK FACTORS HT - DIABETES -…

THE VESSELS AFTERLOAD

PRELOAD PULMONARY VASCULAR SYSTEM

THE REGULATORY SYSTEM RAAS ACTIVATION

SYMPATHETIC ACTIVATION PARASYMPATHETIC WITHDRAWAL

GALECTIN-3 OVEREXPRESSION CARDIAC ENDOCRINE FUNCTION

LOW T3 SYNDROME

CARDIO-RENAL ANEMIA SYNDROME

Silverberg D. et al, NDT 2003

L’insufficienza cardiaca congestizia, l’insufficienza renale cronica e l’anemia danno origine ad un circolo vizioso

nel quale ciascuna condizione può causare o essere causata dall’altra.

Anemia, rene e scompenso cardiaco Conti Paolo

U.O.C. Nefrologia Dialisi Azienda U.S.L. 9 - Grosseto

34 studies, comprising 153.180 patients

37.2 % were anemic

Minimum FU: 6 months

46.8% of anemic patients died compared to 29.5% of non anemic

J Am Coll Cardiol. 2008 Sep 2; 52(10): 818-27

Groenveld HF et al J Am Coll Cardiol. 2008 Sep 2; 52(10): 818-27

Lower risk of anemic

Higher risk

OVERALL 1.96 (1.74, 2.27)

After Adjustment: HR of 1.46 (1.26, 1.69; p<0.001)

Risk of All-Cause Mortality of Anemic Vs Nonanemic CHF Patients

Conclusioni

E’ opportuna la correzione della anemia severa, senza però dover raggiungere livelli di normalità dell’emoglobina

Il target consigliato è il raggiungimento di un valore di emoglobinemia pari a 11-12 g/dl

L’indicazione deve però poter tenere conto delle condizioni cliniche di ogni paziente, adeguando e modulando l’intervento terapeutico ad ogni soggetto


Caro Collega, ma la mia terapia neuroormonale può essere dannosa nei pazienti con CKD?

Trattare gli scompensi e le comorbidità

Antagonismo del RAAS: protezione per cuore e rene

Stefano Bianchi, Livorno

Basal aldosterone (pg/ml)

Bas

al p

rote

inur

ia

(g

/g cr

eatin

ine)

Regression line between baseline plasma aldosterone levels and proteinuria in 165 subjects with chronic kidney disease

r=0.766 P<0.0001

Long-Term Effects of Spironolactone on Proteinuria and Kidney Function in Patients with Chronic Kidney Disease

Bianchi S et al. Kidney Int, 2006


Caro Collega, negli ultimi anni ho imparato che i biomarkers possono essere di grande ausilio, tu li usi? Li possiamo interpretare insieme?

preproBNP (134 aa)

Signal Peptide (26 aa)

proBNP (108 aa)

NT-proBNP 1-76 BNP (32 aa)

BNP

Ventricular Cardiomyocyte

PLASMA

NT-proBNP

BNP Production and Secretion

Intact proBNP Half-life > 60’

Median 41 ng/L Range 7-220 ng/L

Half-life 15-20’ Median 7 ng/L

Range 0-65 ng/L

BNP (mean±95% CI) in healthy subjects and HF patients w ith stages C to D (NYHA Class I-IV)

1 0

1 8

3 2

5 6

1 0 0

1 7 8

3 1 6

5 6 2

1 0 0 0

5.6

3.2

NYHA class Normal Subjects

I II III IV

BN

P, n

g/L

(log

scal

e)

(332)

(35)

(141)

(97)

(38) (N=362)

Compensatory Phase

Congestive Phase

cut-off value

Why does NP production/level raise?

Renal failure BB ACEi –ARBs-

ALDOb - -

-

BB-ACEi –ARBs-ALDOb CRT

- - -

Why does NP production/level decrease?

La concentrazione del BNP: che vuol dire? “The endocrine paradox”

Artificial kidney

BNP & NT-proBNP increment vs healthy controls (n=182)

top: HF stage A to D (n=820) bottom: C-D stage NYHA I to IV (n=479)

BNP vs NT-proBNP preclinical HF (stage A -B)

http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-HF-FT.pdf

Significato prognostico dell’incremento dei peptidi

natriuretici

Logeart et at, JACC 2004

Prognostic stratification

Serial evaluation

Guide to treatment

Proper diagnosis

Proper treatment

Earlier diagnosis

Earlier treatment

Earlier diagnosis

Earlier treatment

From risky conditions, through acute damage and ventricular silent dysfunction, up to overt heart failure: NPs as the optimal biomarker

D

BNP, CRP and TnI: a multimarker strategy for prediction of remodeling

At baseline, BNP, CRP and TnI may help predicting the occurrence of LV remodeling

During follow-up, only BNP and TnI may maintain their independent predictive value

Fertin M et al, Am J Cardiol. 2010

Differenze significative fra tutti i gruppi

Controls LVD

crea <1.3

LVD crea >1.3

HD

Controls LVD crea <1.3

LVD crea >1.3

HD

LVEF 30+- 1

LVEF 56 +- 1

LVEF 29 +- 1

LVEF 62 +- 1

LVEF 30+- 1

LVEF 56 +- 1

LVEF 29 +- 1

LVEF 62 +- 1


Caro Collega, e gli indicatori renali?

Kidney Disease Outcome Quality Initiative (K/DOQI), 2002

CKD - stadiazione

Rischio relativo combinato in base ai valori di GFR ed albuminuria Clinical Practical Guidelines for the Evaluation and Management of Chronic

Kidney Disease - KDIGO, 2012

Poletti R et al, 2013

eGFR<60 mL/min/1.73 m2

eGFR>60 mL/min/1.73 m2

p<0.0001

eGFR by the Cockroft-Gault formula predict cardiac mortality in HF patients

Prognostic significance of renal function in HF patients

Severe systolic dysfunction (EF <35%; # 627)

p<0.0001

Prognostic significance of renal function in HF patients

Mild systolic dysfunction (EF <50, >35%; # 381)

p<0.01

Neurohormones levels according to CrClest

* p<0.05; ** p<0.01; *** p<0.001

Neurohormonal activation is more and more pronounced with lower estimated creatinine clearance

(ml/min) (ml/min)

Neurohormones levels according to CrClest

* p<0.05; ** p<0.01; *** p<0.001

(ml/min) (ml/min) (ml/min)

#627 pts with severe systolic dysfunction (EF<35%)

estCrCl

by Cockroft-Gault formula

http://www.kidney.org/kidneydisease/ckd/knowGFR.cfm

http://www.kidney.org/kidneydisease/ckd/knowGFR.cfm

Neurohormonal activation in patients with HF and CKD


NT-proBNP and PRA hold additional prognostic

value in HF patients with reduced renal function (eGFR<60 mL/min/1.73

m2)



Plasma renin activity (PRA) P-spline hazard ratio plot for cardiac mortality. The curve shows an exponential behaviour with risk increasing for higher PRA. The vertical line indicates PRA value corresponding to the 3.29 ng/mL/h cut-point.



Zoccali C et al., Cardiac natriuretic peptides relate with LVM and function and predict mortality in dialysis pts. J Am Soc Nephrol, 2001

Vergaro G, Emdin M, Iervasi A, Zyw L, Gabutti A, Poletti R, Mammini C, Giannoni A, Fontana M, Passino C. Prognostic value of plasma renin activity in heart failure. Am J Cardiol. 2011 15;108:246-51.

PRA resulted an independent prognostic marker additive to NT-proBNP level and ejection fraction. PRA might help to select those patients needing an enhanced therapeutic effort, possibly targeting incomplete renin-angiotensin-aldosterone system blockade. 996 subjects with systolic heart failure – 36 mos, 0-72 f-up - 170 died, 27


Caro Collega, ci sono markers nuovi di funzione renale che il cardiologo deve

conoscere? Come usare i vecchi?

(micro)Albuminuria in prognostic evaluation of CKD and HF

Jackson CE et al, 2009

Albuminuria is a powerful prognostic factor in patients with CKD and predicts HF related events in patients with systolic dysfunction

Krumholtz HM et al, 2010

«Classical» indices of kidney damage in HF: the value of creatinine

Serum creatinine: a limited value for detection of renal dysfunction

Creatinine generation is dependent on diet and muscle mass

Creatinine is secreted by proxymal tubular cells Extrarenal degradation

Exponential relation with renal function

Variable relationship with GFR

Not sensitive to early renal damage Overestimates renal damage in advanced renal

dysfunction

Not sensitive to tubular damage

Sensitive to changes in volume status

Metra M et al, 2012

Clinical value of biomarkers of renal damage

Taub PR et al, 2012

Tubular damage markers in HF: does it make the difference?

End-point: all cause mortality+HF hosp

CKD vs CHF: perspectives…

•Towards an AB-CD classification of CKD?

•Towards a neurohormonal model of CKD?

•Biomarkers use: be more confident w ith «cardiac biomarkers» in CKD!

•RAAS activation is a prognosticator in CKD/ CHF:

•More RAAS inhibitors…

•More «NP enhancement»

•

Trattare i FR per CKD

Trattare le complicanze

Identificare le fasi iniziali di riduzione GFR

Identificare il danno renale

precoce

CKD CHF

Prevenire la progressione della malattia cardio-renale

Approccio integrato nell’end-stage CKD/ CHF

Screening paz CHF in stadio A e B

Identificare precocemente paz

in stadio C

Artwork by Ursula ferrara

Michele Emdin, [email protected]