Nefropatia de Contraste

Transcription

1 Nefropatia de Contraste H. Luz Rodrigues Serviço de Nefrologia e Transplantação Instituto de Farmacologia e Neurociências

2 Contrast-induced nephropathy Agenda Pathogenesis Clinical features Prevention

3 Postulated Pathophysiology of Contrast-Induced AKI J Am Coll Cardiol 2008;51:

4 How to explain the short duration of ATN? 1. The degree of tubular necrosis is much less severe than seen in other settings. 2. The decline in GFR is due to functional changes in tubule epithelial cells rather than necrosis per se. Similar to postischemic dysfunction in the "stunned" myocardium Due to redistribution of membrane transport proteins from the basolateral to the luminal membrane

5 Types of radiocontrast agents Sodium diatrizoate Ionic monomer Iohexol Nonionic monomer mosm/kg mosm/kg 290 mosmol/kg Iodixanol Nonionic dimer

6 Properties of Commonly Used Radiocontrast Media JAMA 2006;295:

7 Rates of Contrast-Induced AKI in a Meta-Analysis of 16 Trials of Iso-Osmolar CM (iodixanol) compared with Low Osmolar CM Iso-osm Low-osm CKD baseline = eclcr 60 ml/min J Am Coll Cardiol 2008;51:

8 We recommend using either iso-osmolar or lowosmolar iodinated contrast media, rather than high-osmolar iodinated contrast media in patients at increased risk of CI-AKI. (1B) Kidney Int 2012; Supp 2:69-88 JACC 2009; 54: In patients with chronic kidney disease undergoing angiography who are not undergoing chronic dialysis, either an isosmolar contrast medium (Level of Evidence: A) or a low-molecular-weight contrast medium other than ioxaglate or iohexol is indicated. (Level of Evidence: B) (NKF KDOQI) Am J Kidney Dis 2013; 61:649-72

9 Contrast-enhanced MRI as an alternative Major concerns with gadolinium-based chelates: In moderate and particularly severe kidney disease, the possible development of the severe syndrome of nephrogenic systemic fibrosis. The possible development of nephrotoxicity, similar to that seen with iodinated contrast agents. Patients who are already maintained on IHD: perform IHD after the exposure and the next 2 days

10 Contrast-induced nephropathy Agenda Pathogenesis Clinical features Prevention

11 Contrast-induced nephropathy Clinical features 24 to 48 (72 h) hours after contrast exposure Oliguria or Scr ( Scr 25% and/or 0.5 mg/dl) Most patients are nonoliguric 3 to 7 days Scr starts to Urinary sediment Muddy brown granular and epithelial cell casts No dysmorphic red blood cells or red blood casts (glomerular disease) No white cells or white cell casts (interstitial nephritis)

12 Risk factors for contrast nephropathy No risk factors, negligible ( 1 %) risk of contrast nephropathy Patient Related Chronic kidney disease Diabetic nephropathy with renal insufficiency (DM risk multiplier) Advanced heart failure or other cause of reduced renal perfusion (hypovolemia or hemodynamic instability) Multiple myeloma (especially with older contrast agents) Volume depletion promotes the intratubular precipitation of filtered light chains Possible interaction between light chains and the contrast agent Not Patient Related High osmolar contrast Ionic contrast Contrast viscosity Contrast volume JAMA 2006;295:

13 Risk of Contrast-Induced AKI According to Baseline Renal Function AKI = Scr 25% and/or 0.5 mg/dl J Am Coll Cardiol 2008;51:

14 Mayo Clinic 254 (3.3%) ARF /7586 pts Observed Incidence of ARF Stratified by Baseline Serum Cr and Diabetic Status Hospital Death: 22 % ARF vs 1.4 % No ARF Circulation 2002;105:

15 CI-AKI risk-scoring model for percutaneous coronary intervention Low risk: cumulative score <5 High risk: cumulative score >16 IABP, intra aortic balloon pump J Am Coll Cardiol 2004; 44:

16 CI-AKI risk-scoring model for percutaneous coronary intervention N Engl J Med 2006;354:379-86

17 Contrast Nephropathy must be distinguished from Renal Atheroemboli Presence of other embolic lesions (such as digital ischemia of the toes) or livedo reticularis Transient eosinophilia and hypocomplementemia Onset of kidney injury may be delayed for days to weeks after the procedure Protracted course with frequently little or no recovery of renal function Am J Kidney Dis 1994;24:713-27

18 Contrast-induced nephropathy Agenda Pathogenesis Clinical features Prevention

19 Preventive measures for patients at increased risk of contrast nephropathy (Scr > 1.5 mg/dl particularly Diabetes) 1. Consider alternative imaging methods in patients at increased risk for CI-AKI Ultrasonography Magnetic resonance imaging (MRI) without gadolinium contrast, Computed tomography (CT) scanning without radiocontrast agents 2. Avoid volume depletion and NSAID drugs

20 Potential effects Extracellular volume expansion Attenuate medullary hypoxia Suppression of vasopressin Inhibition of the renin angiotensin axis Increased synthesis of renal prostaglandins Reduce cellular damage by Dilution of the contrast medium Reduced fluid viscosity Sodium bicarbonate infusion Tubular ph Generation free radicals (Haber-Weiss reaction) Scavenge peroxynitrite (ONOO - )

21 Preventive measures for patients at increased risk of contrast nephropathy (Scr > 1.5 mg/dl particularly Diabetes) 3. If there are no contraindications to volume expansion, recommend isotonic intravenous fluids Optimal type of fluid and timing of administration are not well established. Isotonic bicarbonate* bolus of 3 ml/kg for 1 h prior to the procedure, continued at a rate of 1 ml/kg/h for 6 h after the procedure. Isotonic saline 1 ml/kg/h, begun > 2 h and preferably 6 to 12 h prior to the procedure continuing for 6 to 12 h after contrast administration *add 150 meq of sodium bicarbonate (three 50 ml ampules of 1 meq/ml sodium bicarbonate) to 850 ml of sterile water

22 Preventive measures for patients at increased risk of contrast nephropathy (Scr > 1.5 mg/dl particularly Diabetes) 4. Suggest using oral NAC, together with i.v. isotonic crystalloids, in patients at increased risk of CI-AKI. (2D) Substantial inconsistency in reported results. 5. No use mannitol or other diuretics prophylactically 6. No use inhibitors of renal vasoconstriction Theophylline (inhibition of adenosine) Nifedipine Prostaglandin E or I 2 Low-dose dopamine Fenoldopam ACEi (captopril) 7. No perform prophylactic hemofiltration or hemodialysis for contrast media removal (stage 3 and 4 CKD)

23 Only 15.7% Scr >1.5 mg/dl Baseline Scr obtained up to 90 days prior to the angiographic procedure acetylcysteine 1200 mg orally 2xdaily before and after angiography 2308 patients 1 risk factor: age 70 years renal failure, DM, heart failure, or hypotension Circulation 2011;124:1250-9

24 Conclusion: N-acetylcysteine 3 g in 500 ml normal saline solution as IV bolus and then 200 mg/ hour for up to 24 hours We did not find evidence of a benefit for N-acetylcysteine administration to our ED patients undergoing contrast-enhanced CT. However, we did find a significant association between volume of intravenous fluids administered and reduction in contrast-induced nephropathy. 69% RR (OR 0.41; 95% CI 0.21 to 0.80) per liter of intravenous fluids Ann Emerg Med 2013;62:511-20

25 410 pts DM2: 40% Incidence of CIAKI NAPLES II trial 80 mg within 24 h before contrast media Circulation 2012;126:

26 410 pts DM2: 40% Benefit of Atorvastatin according to severity of CKD and presence of DM NAPLES II trial 80 mg within 24 h before contrast media Circulation 2012;126:

27 2,998 patients Stage 2 or 3 CKD CI-AKI Occurrence Rosuvastatin 10 mg/day 2 days before, and 3 days after procedure The beneficial effect on CI-AKI occurred exclusively in patients with stage-2 CKD (1.5% vs. 3.3%). NNT = 62 J Am Coll Cardiol 2014;63:62 70

28 PRATO-ACS Study 504 Pts DM 2: 20% ecrcl: 70±25 ml/min Incidence of CI-AKI Rosuvastatin 40 mg on admission, followed by 20 mg/day J Am Coll Cardiol 2014;63:71-9

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