nefropatiada mezzo
di contrasto
Giuseppe RombolàLa Spezia
CIN (CI-AKI)
Both clinical studies and ESUR definition(Thomsen H. Curr. Opin. Urol. 2007; 17: 70)
Increase in serum creatinine (sCr) ≥ 0.5 mg/dL and/or ≥ 25% from baseline within 3 days of CM exposure
And the absence of other causes (e.g. atheromatous embolic disease, ischemia, other nephrotoxins, etc.)
CIN (CI-AKI) definition
Stage I AKIN definition
Increase in sCr ≥ 0.3 mg/dL or ≥ 15 to 20 %from baseline (Metha R. Crit.Care 2007)
CIN definition: sCr. Increase ≥0.3mg/dL• Solomon R. Clin. JASN 2009
• Mitchell A. Clin JASN 2010
• Briguori C. Circulation 2010
ApparatoJuxtaglomerulare
RAS
Mezzo di contrastoDIURESI
OSMOTICA
vasocostrizione
Riassorbimento di Na e acqua
nel TALH
Carico tubulare di Na e acqua
Consumo diossigeno
IPOSSIAMIDOLLARE
CIN
Vasodilatazione
Chronic Kidney Disease
(scr. 2-2.9 mg/dl) 7.37 (4.7-11)
Diabetes
1.61 (1.21-2.18)
Congestive heart failure
1.53 (1.12-2.10)
Periferal vascular disease
1.71 (1.23-2.37)
Age
60 years: 1-Y increment
1.02 (1.01-1.03)
CM dose (100 ml) 1,12
493 pts. following CECTMultivariate analysis RR
Lencioni R. Acta Radiol. 2010
7856 pts. after PCIMultivariate analysis RR
Rihal C. Circulation 2002
CONNECT STUDY
Mo
rtal
ity
%
% increase in serum creatinine
0 <10 10-25 25-50 > 500
10
20
30
40
Gruberg et al. JACC 2000
renal function deterioration after PCI andone year outcomes
Goldenberg I.Am. J. Nephrol. 2009
Loss of kidney function andmortality after reversible CIN
eGFR 36±7 ml/min/1.73m2
31±15ml/min/1.73m2
16±15ml/min/1.73m2
58
115
357
1774
50 45- 40 < 30
CIN incidence following CM administration
0
10
20
30
40
50
60
1 2 3
GFR mL/min
CIN
in
cid
en
ce
%
gfr ml/min
2 V. in 4 studies (2008-2010) (diabetes 29-100 %) 3 V. in 1 study (2010) (diabetes 32%)
A. in 5 RCT studies (2007-2009) (diabetes 28-100 %)
A +CKD+ diabetes
A + CKD only
studies published before 2003 Mc Cullough, J. Cardiov. Med. 2003
90 Arteria volume di mdc …… 248 ± 112 ml00 …… 122 ± 55 10 …… 117 ± 19
Infusione venosa < 100 ml
Strategie preventive Espansione VEC (salina o bicarbonato)NAC
Linee guida ESUR1-1.5 ml/Kg/h 3-12 hrs pre e 12-24 hrs dopo mdcBicarbonato isotonico 1.4%:3 ml/kg/h: 1 hr pre e 1 ml/kg/h per 6 hrs dopo mdc
Nephrotoxicity In High-Risk PatientsA Double-Blind, Randomized, Multicenter Study of Iso-Osmolar and
Low-Osmolar, Nonionic Contrast Media
The NEPHRIC Study
NEPHRIC: Primary EndpointMean Peak Increase in SCr Up to Day 3
0Iodixanol
(n=64)Iohexol(n=65)
Incr
ea
se
in S
Cr
(mg
/dL
)
P=0.001
0.13
0.55
0.1
0.2
0.3
0.4
0.5
0.6
Adapted from Aspelin P et al. N Engl J Med. 2003;348:491-499.
CIN -creat. < 0.5 mg/dl-3 % Iodixanol26 % iohexol
N pazienti RR
Birck
Lancet 2003
805 0.43 (0.21 – 0.87)
Kshirsagar
JASN 2004
1538 efficace nel 33 %
Nallamothu
Am.J. Med.2004
2195 0.73 (0.52 – 1.0)
Alonso
Am.J. Kid. Dis. 2004
885 0.55 ( 0.34 – 0.91)
Zagler
Am. Heart J. 2006
1892 0.68 (0.46 – 1.01)
efficacia della NAC nella prevenzione della CIN
119 pts
•In 20% of ptsadditional furosemide(0.5 mg/Kg) was required
MYTHOS Protocol R
enal
Gu
ard
i.v. furosemide(0.5 mg/kg)
Volume urine826±342 ml/hr
48 - 16 min
30 min
PROCEDURA
4 ore
Diuresi > 300 ml/h
250 mli.v. saline
Infusionecontinua di
sol fisiolin volumeuguale alla
diuresi
Controlloparametri
ogni30 min
CIN 157 pts.baseline GFR 39 ± 10 ml/min.
Controls
RenalGuard
0
5
10
15
20
25
30
%
All patients NSTEMI Elective procedures
16%
5% 6%
10%
25%
P=0.028
4%
P=0.03 P NS
-69%
-80%
-60%
Marenzi; TCT 2010Transcatheter Cardiovascular Therapeutics
2003
Marenzi G. Am. J. Med. 2006
PREVENZIONE CIN & EMOFILTRAZIONE
Am J Med 2001
CONCLUSIONI
1. CIN è associata con un peggioramento della funzione renale che aumentando il rischio CV può aumentare la mortalità
2.CIN sembra rappresentare un rischio indipendente di mortalità sia a breve che a lungo termine
3.I trattamenti depurativi extracorporei sembrano promettenti nel ridurre questo rischio
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