Nefropatia inducida por medio de contraste 2015
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Revisión de la evidencia vigente en nefropatía inducida por contraste
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Nefropatia inducida por medio de contraste 2015
- 1. Nefropatía Inducida por Contraste 2015 Dr. Cristhian Mauricio Bueno Lara Especialista en medicina interna – Universidad Autónoma de Bucaramanga Fellow en Nefrología – Universidad del Valle
- 2. Medios de contraste contrast-induced nephropathy: how it develops, how to prevent it. Cleveland clinic journal of medicine. volume 73, number 1. January 2006 • Antes de 1980 • Alta osmolaridad (2000 mOsm/L) • 1980 • baja osmolaridad (600 - 900 mOsm/L)
- 3. Medios de contraste contrast-induced nephropathy: how it develops, how to prevent it. Cleveland clinic journal of medicine. volume 73, number 1. January 2006 • En la actualidad • Iso-osmolar (300 mOsm/L)
- 4. Medios de contraste 2003 Iso-osmolar Vs Baja osmolaridad 3% Vs 26%Valor P = 0.002
- 5. Nefropatía Inducida de Contraste Definición Incremento en la creatinina sérica ≥ 0.5 mg/dL o un aumento del 25% en relación al valor de base 48 horas posterior al contraste. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements (2012) 2, 4
- 6. Nefropatía Inducida de Contraste Definición 2010
- 7. Nefropatía Inducida de Contraste Epidemiología • El riesgo de NIC en ausencia de enfermedad renal es 1 a 2%. • Con enfermedad renal preexistente puede aumentar hasta el 25% KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements (2012) 2, 4
- 8. Lesión renal aguda Nefropatía por contraste Muerte Hemof 33% 3% - 7% 7.1% - 35.7% Nefropatía Inducida de Contraste Epidemiología KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements (2012) 2, 4 Lesión renal aguda Nefropatía por contraste Terapia de reemplazo renal
- 9. Nefropatía Inducida de Contraste Fisiopatología Contrast Medium–induced Nephrotoxicity: Which Pathway?. Radiology 2005; 235:752–755
- 10. Nefropatía Inducida de Contraste Fisiopatología Contrast Medium–induced Nephrotoxicity: Which Pathway?. Radiology 2005; 235:752–755 • Respuesta hemodinámica “bifásica” • Hipótesis de la isquemia. • Modelos animales = Isquemia al detener el flujo sanguíneo renal por 120 minutos. Efecto hemodinámico
- 11. Nefropatía Inducida de Contraste Fisiopatología Contrast Medium–induced Nephrotoxicity: Which Pathway?. Radiology 2005; 235:752–755 • Vacuolización celular, inflamación intersticial, necrosis celular y enzimuria. Alteraciones bioquímica y Toxicidad directa
- 12. Nefropatía Inducida de Contraste Factores de riesgo contrast-induced nephropathy: how it develops, how to prevent it. Cleveland clinic journal of medicine. volume 73, number 1. January 2006 • Factor de riesgo mas importante. • 60 % de los pacientes que realizan nefropatía inducida por contraste tienen compromiso renal previo. Disfunción renal preexistente Probabilidad de NIC = Creatinina sérica (mg/dL) x 10
- 13. Nefropatía Inducida de Contraste Factores de riesgo 2010 Diabetes Mellitus 6358 Pacientes
- 14. Nefropatía Inducida de Contraste Factores de riesgo Volumen del contraste 1989 Peso: 70 Kg Creatinina: 2 mg/dL Volumen permitido: 175 ml
- 15. Nefropatía Inducida de Contraste Valoración pre-test 2004
- 16. Nefropatía Inducida de Contraste Valoración pre-test 2004 Riesgo de nefropatia inducida por contraste Riesgo de requerimiento de hemodialisis
- 17. Nefropatía Inducida de Contraste Valoración pre-test Escala de riesgo de Mehran
- 18. Nefropatía Inducida de Contraste Valoración pre-test 2014
- 19. Nefropatía Inducida de Contraste Valoración pre-test 2014 67% Sensibilidad 76% Especificidad
- 20. Nefropatía Inducida de Contraste Valoración pre-test 2015 Edad≥ 75 años: 1 punto Función ventricular < 40%: 1 punto Creatinina sérica > 1.5 mg/dL: 2 puntos Riesgo bajo 0 puntos: 0% Riesgo moderado 1 punto: 5.10% Riesgo alto ≥ 2 puntos: 19.4%
- 21. Nefropatía Inducida de Contraste Valoración pre-test 2015
- 22. Nefropatía Inducida de Contraste Prevención Trang H. Au, PharmD, Anne Bruckner, PharmD, Syed M. Mohiuddin, MD, and Daniel E. Hilleman, PharmD. The Prevention of Contrast-Induced Nephropathy. Annals of Pharmacotherapy 2014, Vol. 48(10) 1332–1342
- 23. Nefropatía Inducida de Contraste Prevención Cristaloides 2013
- 24. Nefropatía Inducida de Contraste Prevención Estatinas Efficacy of Short-Term High-Dose Statin in Preventing Contrast-Induced Nephropathy: A Meta-Analysis of Seven Randomized Controlled Trials Yongchuan Li. , Yawei Liu. , Lili Fu, Changlin Mei*, Bing Dai* Division of Nephrology, Nephrology Institute of PLA, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China Abstract Background: A few studies focused on statin therapy as specific prophylactic measures of contrast-induced nephropathy have been published with conflicting results. In this meta-analysis of randomized controlled trials, we aimed to assess the effectiveness of shor-term high-dose statin treatment for the prevention of CIN and clinical outcomes and re-evaluate of the potential benefits of statin therapy. Methods: We searched PubMed, OVID, EMBASE, Web of science and the Cochrane Central Register of Controlled Trials databases for randomized controlled trials comparing short-term high-dose statin treatment versus low-dose statin treatment or placebo for preventing CIN. Our outcome measures were the risk of CIN within 2–5 days after contrast administration and need for dialysis. Results: Seven randomized controlled trials with a total of 1,399 patients were identified and analyzed. The overall results based on fixed-effect model showed that the use of short-term high-dose statin treatment was associated with a significant reduction in risk of CIN (RR= 0.51, 95% CI 0.34–0.76, p = 0.001; I2 = 0%). The incidence of acute renal failure requiring dialysis was not significant different after the use of statin (RR= 0.33, 95% CI 0.05–2.10, p = 0.24; I2 = 0%). The use of statin was not associated with a significant decrease in the plasma C-reactive protein level (SMD 2 0.64, 95% CI: 2 1.57 to 0.29, P= 0.18, I2 = 97%). Conclusions: Although this meta-analysis supports the use of statin to reduce the incidence of CIN, it must be considered in the context of variable patient demographics. Only a limited recommendation can be made in favour of the use of statin based on current data. Considering the limitations of included studies, a large, well designed trial that incorporates the Table1.Characteristicsofincludedstudies. Author, yearPatients,n Inclusion criteria Sta pro StatinControl Sang-HoJo etal,2008 118118CAG.SCr$1.1mg/dLor CrCl#60mL/min Sim hou and AnnaToso etal,2009 152152CAGand/orPCI. CrCl,60ml/min Ato pre- pro fro pos Xinwei etal,2009 113115PCISim ad 20 ZhouXia etal,2009 5050CAGorPCIAto for afte SadikAcikel etal,2010 8080CAG.eGFR.60ml/minper 1.73m2 Ato pre- pos HakanOzhan etal,2010 6070CAG.SCr#1.5mg/dlor eGFR$70ml/minper1.73m2 Ato pre- pos NA GiuseppePatti etal,2011 120121CAGand/orPCI. SCr#3mg/dl Ato bef 40 Statin=statin-treatedgroup(high-dose);Control=controlgroup(low-dose glomerularfiltrationrate;NAC=N-acetylcysteine;NS=0.9%sodiumchlorid doi:10.1371/journal.pone.0034450.t001 PLoSONE | www.plosone.org 2 April 2012 | Volume 7 | Issue 4 | e34450 etal,20101.73m2 HakanOzhan etal,2010 6070CAG.SCr#1.5mg/ eGFR$70ml/min GiuseppePatti etal,2011 120121CAGand/orPCI. SCr#3mg/dl Statin=statin-treatedgroup(high-dose);Control=cont glomerularfiltrationrate;NAC=N-acetylcysteine;NS= doi:10.1371/journal.pone.0034450.t001 April 2012 | Volume 7 | Issue 4 | e34450 Table 1. Characteristics of included studies. Author, year Patients,n Inclusion criteria Statin protocol Control Contrast type Median contrast volume,ml Hydration procedure Statin Control Statin Control Sang-Ho Jo et al,2008 118 118 CAG.SCr$ 1.1 mg/dL or CrCl# 60 mL/min Simvastatin,40 mg every 12 hours, 1 day pre-procedure and 1 day post-procedure Placebo Iodixanol 173 191 Isotonic saline,1 mg/kg/hour for 12 h before and 12 h after procedure Anna Toso et al,2009 152 152 CAG and/or PCI. CrCl, 60 ml/min Atorvastatin,80 mg/day 2 days pre-procedure and 2 days post- procedure+NAC,1200 mg bid from 1 day before to 1 day post-procedure Placebo+NAC, 1200 mg bid from 1 day before to 1 day post-procedure Iodixanol 151 164 NS,1 ml/kg/hour for 12 h before and after the procedure Xinwei et al,2009 113 115 PCI Simvastatin, 80 mg/day from admission to the day before, 20 mg/day after procedure Simvastatin, 20 mg/ day from admission to the end Iodixanol for CKD,iohexol for others 227 240 NS, 1 ml/kg/hour for 6 to 12 hours before and 12 hours after procedure Zhou Xia et al,2009 50 50 CAG or PCI Atorvastatin,80 mg/day before for 1day,10 mg/day for 6days after procedure Atorvastatin, 10 mg/ day for 7 days Iopamidol 119 113 1000 mL saline infusion, for 12 hours before and 12 hours after intervention Sadik Acikel et al,2010 80 80 CAG.eGFR. 60 ml/min per 1.73 m2 Atorvastatin,40 mg/day,3 days pre-procedure and 2 days post-procedure Nothing Iohexol 105 103 Isotonic saline,1 ml/kg/hour starting 4 h before and continuing until 24 h after procedure Hakan Ozhan et al,2010 60 70 CAG.SCr# 1.5 mg/dl or eGFR$ 70 ml/min per 1.73 m2 Atorvastatin,80 mg 1 day pre-procedure and 2 days post-procedure+600 mg NAC bid pre-procedure 600 mg NAC bid pre- procedure Iopamidol 97 93 1000 ml saline infusion during 6 h after procedure Giuseppe Patti et al,2011 120 121 CAG and/or PCI. SCr# 3 mg/dl Atorvastatin,80 mg(12 hs before)+40 mg(2 hs before), 40 mg for 2days after procedure Placebe+40 mg atorvastatin for 2days after procedure Iobitridol 209 213 For patients CrCl, 60 ml/min,1 ml/hour/ kg for 12 h before and 24 h after intervention Statin = statin-treated group(high-dose);Contro l = control group(low-dose or non-statin);CAG = coronary angiography;PCI = percutaneous coronary intervention;CrCl = creatinine clearance;Scr = serum creatinine;eGFR= estimated glomerular filtration rate;NAC= N-acetylcysteine;NS= 0.9% sodium chloride. doi:10.1371/journal.pone.0034450.t001 StatinPreventsContra 2012
- 25. Nefropatía Inducida de Contraste Prevención Estatinas Efficacy of Short-Term High-Dose Statin in Preventing Contrast-Induced Nephropathy: A Meta-Analysis of Seven Randomized Controlled Trials Yongchuan Li. , Yawei Liu. , Lili Fu, Changlin Mei*, Bing Dai* Division of Nephrology, Nephrology Institute of PLA, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China Abstract Background: A few studies focused on statin therapy as specific prophylactic measures of contrast-induced nephropathy have been published with conflicting results. In this meta-analysis of randomized controlled trials, we aimed to assess the effectiveness of shor-term high-dose statin treatment for the prevention of CIN and clinical outcomes and re-evaluate of the potential benefits of statin therapy. Methods: We searched PubMed, OVID, EMBASE, Web of science and the Cochrane Central Register of Controlled Trials databases for randomized controlled trials comparing short-term high-dose statin treatment versus low-dose statin treatment or placebo for preventing CIN. Our outcome measures were the risk of CIN within 2–5 days after contrast administration and need for dialysis. Results: Seven randomized controlled trials with a total of 1,399 patients were identified and analyzed. The overall results based on fixed-effect model showed that the use of short-term high-dose statin treatment was associated with a significant reduction in risk of CIN (RR= 0.51, 95% CI 0.34–0.76, p = 0.001; I2 = 0%). The incidence of acute renal failure requiring dialysis was not significant different after the use of statin (RR= 0.33, 95% CI 0.05–2.10, p = 0.24; I2 = 0%). The use of statin was not associated with a significant decrease in the plasma C-reactive protein level (SMD 2 0.64, 95% CI: 2 1.57 to 0.29, P= 0.18, I2 = 97%). Conclusions: Although this meta-analysis supports the use of statin to reduce the incidence of CIN, it must be considered in the context of variable patient demographics. Only a limited recommendation can be made in favour of the use of statin based on current data. Considering the limitations of included studies, a large, well designed trial that incorporates the Table1.Characteristicsofincludedstudies. Author, yearPatients,n Inclusion criteria Sta pro StatinControl Sang-HoJo etal,2008 118118CAG.SCr$1.1mg/dLor CrCl#60mL/min Sim hou and AnnaToso etal,2009 152152CAGand/orPCI. CrCl,60ml/min Ato pre- pro fro pos Xinwei etal,2009 113115PCISim ad 20 ZhouXia etal,2009 5050CAGorPCIAto for afte SadikAcikel etal,2010 8080CAG.eGFR.60ml/minper 1.73m2 Ato pre- pos HakanOzhan etal,2010 6070CAG.SCr#1.5mg/dlor eGFR$70ml/minper1.73m2 Ato pre- pos NA GiuseppePatti etal,2011 120121CAGand/orPCI. SCr#3mg/dl Ato bef 40 Statin=statin-treatedgroup(high-dose);Control=controlgroup(low-dose glomerularfiltrationrate;NAC=N-acetylcysteine;NS=0.9%sodiumchlorid doi:10.1371/journal.pone.0034450.t001 PLoSONE | www.plosone.org 2 April 2012 | Volume 7 | Issue 4 | e34450 etal,20101.73m2 HakanOzhan etal,2010 6070CAG.SCr#1.5mg/ eGFR$70ml/min GiuseppePatti etal,2011 120121CAGand/orPCI. SCr#3mg/dl Statin=statin-treatedgroup(high-dose);Control=cont glomerularfiltrationrate;NAC=N-acetylcysteine;NS= doi:10.1371/journal.pone.0034450.t001 April 2012 | Volume 7 | Issue 4 | e34450 Statistical analysis Dichotomous data (contrast-induced nephropathy and need for dialysis) were analyzed using the risk ratio (RR) measure and its 95% confidence interval (CI). Moreover, heterogeneity across Results Selected studies and characteristics We identified 322 potentially relevant citations from the initial Figure 2. Forest plot of risk ratios and 95% confidence intervals (CI) for the incidence of contrast induced nephropathy among patients assigned to statin therapy versus control. doi:10.1371/journal.pone.0034450.g002 Statin Prevents Contrast-Induced Nephropathy 2012
- 26. Nefropatía Inducida de Contraste Prevención Bicarbonato 2004 Protocolo bicarbonato: 154 meq de Bicarbonato + 846 cc de DAD al 5% 3 ml/Kg/hora 1 hora antes del medio de contraste 1 ml/Kg/hora 6 horas después del medio de contraste
- 27. Nefropatía Inducida de Contraste Prevención Bicarbonato 2004
- 28. Nefropatía Inducida de Contraste Prevención Bicarbonato 2010
- 29. Nefropatía Inducida de Contraste Prevención N acetilcisteina ACTInvestigators RandomizedAcetylcysteine for Contrast-InducedNephropathyTrial(ACT) CoronaryandPeripheralVascular Angiography: MainResults Fromthe Acetylcysteine for Preventionof RenalOutcomes inPatients Undergoing ISSN: 1524-4539 Copyright © 2011 American Heart Association. All rightsreserved. Print ISSN: 0009-7322. Online 72514 Circulation ispublished by the American Heart Association. 7272 Greenville Avenue, Dallas, TX doi:10.1161/CIRCULATIONAHA.111.038943 2011,124:1250-1259:originallypublishedonline August22,2011Circulation 2011 RR: 1.0 IC 0.81 – 1.25
- 30. Nefropatía Inducida de Contraste Prevención N acetilcisteina 2013
- 31. Nefropatía Inducida de Contraste Prevención Terapias sin evidencia o contraindicadas Manitol Furosemida Dopamina Fenoldopam Hemodiálisis o Hemofiltración Prostaglandinas Calcio-antagonistas Teofilina Acido ascórbico Sulfato de magnesio N acetil cisteína
- 32. Nefropatía Inducida de Contraste Pronóstico Mortalidad William F. Finn. The clinical and renal consequences of contrast-induced nephropathy. Nephrol Dial Transplant (2006) 21 [Suppl 1]: i2–i10
- 33. Gracias
Hinweis der Redaktion
- Los primeros agentes fueron iónicos, Cada 2 moleculas tenia un atomo de sodio disociado en un medio acuoso y 3 atomos de yodo cada uno Ya en 1980 se introcen agentes con solo una molecula con la misma cantidad de atomos de yodo lo cual representa una menor osmolaridad, a estos agentes se les llamo no ionicos o de baja osmolaridad.
- - Actualmente contamos con agentes como el iodixanol, que es un dimero no ionico, e la union de 6 atomos unidos por una particula activa osmoticamente qu finalmente e traduce
- In most cases of contrast-induced nephropa- thy, serum creatinine begins to rise within 24 to 48 hours after exposure, reaches a peak within 3 to 5 days, and then returns to base- line levels within 7 to 10 days.8 In more severe cases, the creatinine concentration may not peak until 5 to 10 days, and the increase may be associated with oliguria
- La nefropatia inducida por contraste es considerada las 3era causa de LRA en pacientes hospitalizados despues de la hipoperfusion renal y la toxicidad por medicamentos.
- 25 – 30 % prevalencia de LRA en pacientes en UCI.
- Bifasica, con un incremento inicial seguido por un descenso. Aunque la disminución en el flujo sanguineo es solo del 30% en comparacion con el flujo de base, durando por solo minutos, se considera que la isquemia medular pudiese ser la causa de la LRA en relacion a los cambios hemodinamicos. Los cambios bifasicos durante la inyeccion directa de medio de contraste son considerados minimos para producir el daño isquemico.
- Estudios experimentales también han sugerido que los agentes de contraste tienen acción toxica directa sobre las células renales, principalemente sobre el epitelio tubular, documentando Vacuolización celular, inflamación intersticial y necrosis celular en estudios histopatológicos. El catabolismo de la adenosina por la xantin oxidasa conlleva a la formación de radicales libres, a mayores concentraciones mayor efecto deleterio causando estes oxidativo y daño proteico.
- - Y sin ninguna duda, entre mas severo sea el grado de enfermedad renal, mayor sera el riesgo de nefropatia inducida por contraste.
- Teoricamente la hidratacion debe dimisminuir la actividad del eje RAA, reduciendo asi niveles de otras hormonas vasoconstrictoras como la endotelina, incrementando la diuresis de Na, previniento la obstruccion tubular y finalmente diluyendo el medio de contraste en los tubulos disminuyendo cualquier efecto nefrotoxico directo sobre el epitelio tubular.