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Contrast Induced Nephropathy and Nephrogenic Systemic Fibrosis

Contrast Induced Nephropathy and Nephrogenic Systemic Fibrosis. By Dr. HP Shum Apr 2008. Overview. Contrast induced nephropathy (CIN) Definition Pathogenesis Prevalence Risk factors Adverse outcome Prevention Nephrogenic systemic fibrosis. Definition of CIN.

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Contrast Induced Nephropathy and Nephrogenic Systemic Fibrosis

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  1. Contrast Induced Nephropathy and Nephrogenic Systemic Fibrosis By Dr. HP Shum Apr 2008

  2. Overview • Contrast induced nephropathy (CIN) • Definition • Pathogenesis • Prevalence • Risk factors • Adverse outcome • Prevention • Nephrogenic systemic fibrosis

  3. Definition of CIN • Including three components • Absolute or relative increase in serum Cr compared to baseline • Temporal relationship between the rise of Cr and exposure to contrast agents • Exclusion of alternative explanations for renal impairment >25% or 44umol/l increase of Cr level from baseline Within 48-72 hrs of exposure Cholesterol embolism, hypotension, UTI etc

  4. Pathogenesis Use of adenosine antagonist Use of IVF / IOCM Use of IOCM Use of NAC Use of IVF / IOCM

  5. 4622 admitted to medical and surgical ward • 7.2% with baseline Cr >105umol/l AJKD, Vol 39, No 5 (May), 2002: pp 930-936

  6. The overall incidence of CIN among general population is around 0.6-2.3% Radiology 1997; 203:605-610

  7. Pre-existing renal disease % of CIN JSurgRes 1992; 53:317-320

  8. However… • Serum Cr varies with age, muscle mass and gender -> not reliable enough to identify patients at risk • Use Cockcroft or MDRD equation to calculate CrCl • eGFR <=60ml/min/1.73m2 is a reliable cut-off

  9. DM + CRF Nephrol Dial Transplant 2007, 22, 819-826 NB: 400 pts, baseline GFR around 50ml/min

  10. Volume of CM AmJCardiol 2004; 94:300-305 DM patients receiving PCI

  11. Anemia Kidney Int 2005; 67:706-713

  12. Type of CM: Osmolality and Viscosity

  13. Type of CM Nephrotoxicity of iso-osmolar iodixanol compared with nonionic low-osmolar contrast media: meta-analysis of randomized controlled trials. (25 RCTs) Radiology. 2009 Jan;250(1):68-86 A meta-analysis of the renal safety of isosmolar iodixanol compared with low-osmolar contrast media. (26 RCTs) J Am Coll Cardiol. 2006 Aug 15;48(4):692-9 Iso-osmolar CM have lower CIN risk c/w low osmolar CM among patients with renal impairment or DM

  14. J Am Coll Cardiol 2004, 44, 1393-99

  15. CIN and mortality Mayo Clin Proc. 2008;83(10):1095-1100

  16. CINConsensusWorkingPanelAmJCardiol 2006;98:2K-4K

  17. IV Hydration • Decrease activity of the RAAS • Reduce vasocontrictive hormones like endothelin • Increase sodium diuresis • Decrease tubulo-glomerular feedback • Prevent tubular obstruction • Protect against reactive oxygen species • Dilute contrast medium in tubules

  18. 0.45% NaCl vs 0.9% NaCl N Tx regimen baseline Cr results P NS may be better than 0.45% NaCl

  19. NaHCO3 vs NaCl • 12 RCTs, 1854 patients • Isotonic NaHCO3 decrease incidence of CIN (OR 0.39) c/w NaCl • No significant difference in needs for RRT and in-hospital mortality Am J Kidney Dis 2009 Apr; 53 (4), 617-627

  20. Oral vs IVF Inconclusive, IVF may be better than oral route

  21. NAC • Potent anti-oxidant • Scavenger of wide variety of oxygen derived free radicals • Prevent direct oxidative tissue damage

  22. NAC beneficial for CIN prevention, especially those with renal impairment Ann Intern Med 2008; 148, 284-294

  23. Adenosine antagonist (amiophylline and theophylline) • CM bind to renal adenosine receptor • Causing potent vasoconstriction • Impair renal blood flow • Adenosine antagonist may reverse renal vasoconstriction

  24. Adenosine antagonist Benefit inconclusive, may be useful Ann Intern Med 2008; 148, 284-294

  25. Dopamine and fenoldopam • Induce renal vasodilatation • Increase renal blood flow • Increase urine output

  26. Dopamine and fenoldopam Not useful for CIN prevention Ann Intern Med 2008; 148, 284-294

  27. Lasix Increase risk of CIN Ann Intern Med 2008; 148, 284-294

  28. Renal replacement therapy • CM properties • Water solubility • Low protein binding • Low intracellular penetration • “middle size” molecules, much larger than urea and creatinine • 80% removal over 4hrs time by high flux dialyzer but much lower for low flux membranes • PD also remove CM but much slower (50% removal over 16 hrs)

  29. Renal replacement therapy Int J Artif Organs 2008; 31, 515-524

  30. RRT cannot prevent CIN Int J Artif Organs 2008; 31, 515-524

  31. Conclusion • Prevent CIN by • Eliminate risk factors if possible • Use low or iso-osmolar CM • Use lower volume of CM • IV hydration (NaHCO3 > NS > 0.45 NaCl) • NAC

  32. Nephrogenic Systemic Fibrosis • Scleroderma-like systemic fibrosing disorder • Originally termed “nephrogenic fibrosing dermopathy” due to its dominant skin findings but subsequently changed to NSF because of its systemic involvement • First case description in 1997

  33. Peau d’orange skin changes Non-pitting edema with blister and bullae Contracture Cobblestoning and induration skin

  34. Collagen bundles in thickened reticular dermis Extend through subcutaneous tissue Often involve fascia and skeletal muscle

  35. NSF • No single causative agent or trigger was identified previously until 2006 • Five ESRF on HD developed NSF following exposure to Gadolinium-based contrast Nephrol Dial Transplant 21:1104-1108,2006 • Subsequently, numerous published studies and NSF registry have confirmed the link

  36. Gadolinium • Silvery white rare earth metal • Strongly paramagnetic at room temp • Solution of organic gadolinium complex are used as MRI contrast

  37. Gadolinium based contrast agents available

  38. GBCM - pharmacokinetics • Molecular mass – 500-1000Da • Distributed in ECF only (0.26-0.28l/kg) • No protein binding • Excreted unchanged by kidney, renal clearance approx GFR in normal individual • Half life 1.3-1.6hrs but prolonged with low GFR

  39. GBCM - clearance • Normal t1/2 1.3-1.6hr • CKD 3 (30-59) t1/2 5hr • CKD 4 (15-29) t1/2 9hr • CKD 5 (<15) t1/2 34hr • HD t1/2 2.1hr • PD without residual renal fx t1/2 53hr

  40. NSF - Pathogenesis • Delay in GBCM excretion due to renal impairment • Spontaneous dissociation of the Gd-chelate complex into metal-ion and ligand • Free Gd forms precipitate with anions (PO4, CO3 etc) in the tissue • Internalized macrophages • Produce cytokines • Attract circulating fibrocytes • Induce tissue fibrosis

  41. Procedure in which 10-15% of the patient's white blood cells are removed from the body by leukapheresis. White blood cells are exposed to a chemical agent that is activated by ultraviolet A (UVA) light. Activation by the UVA light induces an inhibition of the host response to foreign histocompatibility antigens. The photo-irradiated cells are washed free of the drug and re-infused into the patient. Indications: Cutaneous TCL, scleroderma

  42. End of presentationQuestions and Comments

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