1) Contrast induced nephropathy (CIN) is a serious complication of cardiac procedures and can lead to acute renal failure, increased mortality, and long term renal dysfunction.
2) Many risk factors increase a patient's likelihood of developing CIN, including pre-existing renal insufficiency, diabetes, older age, hypotension, and the volume and osmolality of contrast agent used.
3) Preventive strategies aim to reduce renal ischemia and oxidative stress through hydration with intravenous fluids like sodium bicarbonate or sodium chloride, as well as pharmacological interventions including N-acetylcysteine. Larger clinical trials are still needed to determine the most effective prevention protocols.
SEMINAR PRESENTATION ON CONTRAST INDUCED NEPHROPATHY BY PHARM D STUDENT
IT INCLUDES COMPLETE OVERVIEW OF THE TOPIC CIN.
POST CONTRAST ACUTE KIDNEY INJURY( PC-AKI) WITH TREATMENT AND MANAGEMENT.
Contrast induced nephropathy (CIN) is agenerally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media.
Contrast Induce Nephropathy
its include information about the nephropathy thats caused by the contrast , like in patients undergo PCI or other method of imaging containing contrast
I will discuss the causes with the risk factors then explain the headline of the pathophysiology and clinical presentaion with the mangment,
SEMINAR PRESENTATION ON CONTRAST INDUCED NEPHROPATHY BY PHARM D STUDENT
IT INCLUDES COMPLETE OVERVIEW OF THE TOPIC CIN.
POST CONTRAST ACUTE KIDNEY INJURY( PC-AKI) WITH TREATMENT AND MANAGEMENT.
Contrast induced nephropathy (CIN) is agenerally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media.
Contrast Induce Nephropathy
its include information about the nephropathy thats caused by the contrast , like in patients undergo PCI or other method of imaging containing contrast
I will discuss the causes with the risk factors then explain the headline of the pathophysiology and clinical presentaion with the mangment,
Radiographic Contrast Agents And Contrast-induced Nephropathy
All contrast agents have a basic structure of a benzene ring, which is composed of 6 joined carbon atoms, each of which has an attached hydrogen atom.
Contrast media consist of triiodinated benzene rings, whereby 3 hydrogen atoms are replaced with attached iodine atoms.
Monomers contain 1 triiodinated benzene ring, and dimers contain 2 triiodinated benzene rings
A ppt about contrast nephropathy: basics, risk factors, comparison of preventive strategies.
critical review of POSEIDON trial and brief about PRESERVE trial.
How to deal with CALCIFIED CORONARY ARTERY LESIONS .Coronary artery calcification (CAC) is highly prevalent in patients with coronary heart disease (CHD) and is associated with major adverse cardiovascular events. There are two recognized type of CAC—intimal and medial calcification, and each of them have specific risk factors. Several theories about the mechanism of vascular calcification have been put forward, and we currently believe that vascular calcification is an active, regulated process. CAC can usually be found in patients with severe CHD, and this asymptomatic phenomenon make early diagnosis of CAC important. Coronary computed tomographic angiography is the main noninvasive tool to detect calcified lesions. Measurement of coronary artery calcification by scoring is a reasonable metric for cardiovascular risk assessment in asymptomatic adults at intermediate risk. To date, effective medical treatment of CAC has not been identified. Several strategies of percutaneous coronary intervention have been applied to CHD patients with CAC, but with unsatisfactory results. Prognosis of CAC is still a major problem of CHD patients. Thus, more details about the mechanisms of CAC need to be elucidated in order to improve the understanding and treatment of CAC.
COMPARES OPTIMAL MEDICAL THERAPY WITH INVASIVE THERAPY IN A PATIENT WITH STABLE ISCHEMIC HEART DISEASE WITH MODERATE TO SEVERE MYOCARDIAL ISCHEMIA ON NON INVASIVE STRESS TESTING
Radiographic Contrast Agents And Contrast-induced Nephropathy
All contrast agents have a basic structure of a benzene ring, which is composed of 6 joined carbon atoms, each of which has an attached hydrogen atom.
Contrast media consist of triiodinated benzene rings, whereby 3 hydrogen atoms are replaced with attached iodine atoms.
Monomers contain 1 triiodinated benzene ring, and dimers contain 2 triiodinated benzene rings
A ppt about contrast nephropathy: basics, risk factors, comparison of preventive strategies.
critical review of POSEIDON trial and brief about PRESERVE trial.
How to deal with CALCIFIED CORONARY ARTERY LESIONS .Coronary artery calcification (CAC) is highly prevalent in patients with coronary heart disease (CHD) and is associated with major adverse cardiovascular events. There are two recognized type of CAC—intimal and medial calcification, and each of them have specific risk factors. Several theories about the mechanism of vascular calcification have been put forward, and we currently believe that vascular calcification is an active, regulated process. CAC can usually be found in patients with severe CHD, and this asymptomatic phenomenon make early diagnosis of CAC important. Coronary computed tomographic angiography is the main noninvasive tool to detect calcified lesions. Measurement of coronary artery calcification by scoring is a reasonable metric for cardiovascular risk assessment in asymptomatic adults at intermediate risk. To date, effective medical treatment of CAC has not been identified. Several strategies of percutaneous coronary intervention have been applied to CHD patients with CAC, but with unsatisfactory results. Prognosis of CAC is still a major problem of CHD patients. Thus, more details about the mechanisms of CAC need to be elucidated in order to improve the understanding and treatment of CAC.
COMPARES OPTIMAL MEDICAL THERAPY WITH INVASIVE THERAPY IN A PATIENT WITH STABLE ISCHEMIC HEART DISEASE WITH MODERATE TO SEVERE MYOCARDIAL ISCHEMIA ON NON INVASIVE STRESS TESTING
Anemia Indian scenario In Chronic Kidney Disease Patients Dr Ashutosh Ojha
this is a comprehensive presentation in Post Doctoral Certificate in Nephrology training program. At Gauhati Medical College Hospital ,Dept Of Nephrology.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
1. Contrast Induced NephropathyContrast Induced Nephropathy
Cardiac InterventionCardiac Intervention
Department of CardiologyDepartment of Cardiology
Apollo Hospitals, HydergudaApollo Hospitals, Hyderguda
HyderabadHyderabad
Dr. R. Vishwanath MRCP(UK)
3. ControversialControversial
• Thousands of literature and papers.
• Hundreds of meta-analysis of the published papers.
DENIAL RESPONSE !!!
Experience Vs Evidence based practice
Many contradictory results
4. Topics for Consideration….Topics for Consideration….
1. Basic understanding of renal function tests
and their fallacies
2. Definition of CIN in vogue.
3. Incidence of CIN.
4. Predictors for the development of CIN.
5. Recognition of high risk patients.
6. Proposed Pathogenesis of CIN.
7. Radio Contrast Agents
8. Preventive strategies.
9. Management of CIN.
10.Long term prognostic outcomes.
5. Renal Function TestsRenal Function Tests
1. Serum Creatinine
• Calibration and Estimation
• Many variables – Age, Race, Sex .…
A normal Serum Creatinine is not indicative of
a normal renal function.
GFR
6. How to Assess Renal Function?How to Assess Renal Function?
Abbreviated Modification of Diet in Renal Disease
equations (MDRD) equation:
eGFR, ml/min/1.73 m2
= 186 x (Serum Creatinine [mg/dL]) -1.154 x
(Age-0.203x (0.742 if female) x (1.210 if African American)
(140- age) x Body Weight [kg]*
Creatinine Clearance, ml/min =
* Multiple by 0.8 in female
Cockcroft-Gault equation:
Serum Creatinine mg/dL] x 72
7. Definition of CINDefinition of CIN
CIN ↑ in Serum Creatinine
concentration
0.5 mg/dL (44 mol/L) or
25% above baseline within
48 hours after contrast
administration
8. • Non-oliguricNon-oliguric
• ↓↓ renal function post-contrast in the absencerenal function post-contrast in the absence
of other causes.of other causes.
• Recovery usually occurs within 5 to 14 days.Recovery usually occurs within 5 to 14 days.
However the long term outcome on renalHowever the long term outcome on renal
dysfunction is unclear.dysfunction is unclear.
DefinitionDefinition
9. INCIDENCE OF CININCIDENCE OF CIN ::
Marked variation in the reported incidence of CIN
0 to >50%
Causative Factors for the wide variation of CIN:
Consensus on what is Renal dysfunction .
Variability of risk factors
Various types of contrast and variable procedures.
Radiologic procedure.
10. Predictors of All-Cause MortalityPredictors of All-Cause Mortality
to 7 Years BARI Trial + Registryto 7 Years BARI Trial + Registry
Szczech L. et al.,Szczech L. et al., CirculationCirculation 2002; 105:2253-8.2002; 105:2253-8.
11. Risk Factors for CINRisk Factors for CIN
Patient-related Risk FactorsPatient-related Risk Factors
• Renal insufficiencyRenal insufficiency
• Diabetes mellitus withDiabetes mellitus with
renal insufficiencyrenal insufficiency
• AgeAge
• Volume depletionVolume depletion
• HypotensionHypotension
• Low cardiac outputLow cardiac output
• Class IV CHFClass IV CHF
• Other nephrotoxinsOther nephrotoxins
• Renal transplantRenal transplant
• Hypoalbuminemia (<35 g/l)Hypoalbuminemia (<35 g/l)
Procedure-related Risk FactorsProcedure-related Risk Factors
• Multiple contrast mediaMultiple contrast media
injection within 72 hrsinjection within 72 hrs
• Intra-arterial injection siteIntra-arterial injection site
• High volume of contrast mediaHigh volume of contrast media
• High osmolality of contrastHigh osmolality of contrast
mediamedia
12. RiskRisk
ScoreScore
RiskRisk
of CINof CIN
Risk ofRisk of
DialysisDialysis
≤≤ 55 7.5%7.5% 0.04%0.04%
6 to 106 to 10 14.0%14.0% 0.12%0.12%
11 to11 to
1616
26.1%26.1% 1.09%1.09%
≥≥ 1616 57.3%57.3% 12.6%12.6%
Mehran et al. JACC 2004;44:1393-1399.
Hypotension
IABP
CHF
Age >75 years
Anemia
Diabetes
Contrast media volume
Risk Factors
5
5
5
4
3
3
Integer Score
1 for each 100 cc3
Scheme to Define CIN Risk ScoreScheme to Define CIN Risk Score
Serum creatinine > 1.5mg/dl 4
eGFR <60ml/min/1.73 m2
2 for 40 – 60
4 for 20 – 40
6 for < 20
eGFR < 60ml/min/1.73 m2
=
186 x (SCr)-1.154
x (Age)-0.203
X (0.742 if female) x (1.210
if African American)
Calculate
OR
13. Prognostic significance of the proposed risk score for CIN extended to
prediction of 1-year mortality. (Red bars = development dataset; blue bars =
validation dataset.)
CIN Risk Score & 1-year MortalityCIN Risk Score & 1-year Mortality
31.2 33.3
15.5
5.5
1.9 2.0
5.7
13.5
0
5
10
15
20
25
30
35
Low Moderate High Very High
1-yearmortality
Risk Groups:
Risk Score: ≤5 6 to 10 11 to 15 ≥16
Mehran et al. JACC 2004;44:1393-1399.
14. Proposed PathogenesisProposed Pathogenesis
Following exposure to contrast :
• Renal GFR ↓ due to ↓ renal vasoconstriction.
• Resultant Ischemia in the deeper portion of the outer
medulla.
• High Oxygen requirement and remote from the Vasa
recta from which it’s blood supply is derived.
Exact Mechanisms of CIN – Not fully known
Present Proposed Etiology:
Direct toxic affects of renal tubular cells, causing
vacuolization, altered mitochondrial function
and apoptosis
17. Physicochemical Properties of ContrastPhysicochemical Properties of Contrast
AgentsAgents
Table 1. Properties of Commonly Used Radiocontrast Media.
18. Renal Failure in Patients Undergoing CoronaryRenal Failure in Patients Undergoing Coronary
Procedures using Iso-osmolar or Low-osmolarProcedures using Iso-osmolar or Low-osmolar
Contrast MediaContrast Media
Liss et al. Kidney International 2006
ContrastContrast
media (CM)media (CM) CM propertiesCM properties NN Time periodTime period
IodixanolIodixanol iso-osmolar, nonionic,iso-osmolar, nonionic, 45 48545 485 2000-20032000-2003
IoxaglateIoxaglate low-osmolar, nonionic,low-osmolar, nonionic, 12 44012 440 2000-20032000-2003
• Swedish Coronary Angiography and Angioplasty Registry
• Swedish Hospital Discharge Registry
20. • 0.45% Saline0.45% Saline
• ↑↑ Free water excretion & thus dilute CM in tubuleFree water excretion & thus dilute CM in tubule
• 0.9% Saline0.9% Saline
• ↑↑ Na+ at the DCT, thus ↓ stimulation of reninNa+ at the DCT, thus ↓ stimulation of renin
angiotensin system.angiotensin system.
• NaHCO3- (isotonic)NaHCO3- (isotonic)
• Protection against free radical injuryProtection against free radical injury
FluidsFluids
21. • IV infusion vs Oral hydrationIV infusion vs Oral hydration
• IV infusion vs IV bolusIV infusion vs IV bolus
FluidsFluids
25. Optimal Hydration RegimenOptimal Hydration Regimen
Mueller et alMueller et al Arch Intern MedArch Intern Med 20022002
1937 Patients Screened
317 Ineligible or
No Consent
685 for Primary End Point
Analysis
698 for Primary End Point
Analysis
1620 Randomized
809 Received 0.9% Saline
124 Excluded From Primary
End Point Analysis
Repeat Catheterization (n=78)
Incomplete Data (n=46)
811 Received 0.45%
Sodium Chloride
113 Excluded From Primary
End Point Analysis
Repeat Catheterization (n=59)
Incomplete Data (n=53)
Bypass Grafting (n=1)
26. Optimal HydrationOptimal Hydration
0.9% NS vs 0.45% NS0.9% NS vs 0.45% NS
P=.35P=.35
0
1
2
3
CN Mortality Vascular
Incidence,%
0.9% Saline
0.45% Sodium Chloride
P=.93P=.93
P=.04P=.04
Mueller et alMueller et al Arch Intern MedArch Intern Med 20022002
27. Prevention of CIN withPrevention of CIN with
Sodium BicarbonateSodium Bicarbonate
Merten GJ et al.Merten GJ et al. JAMAJAMA, 2004;291:2328-2334, 2004;291:2328-2334
Patients With Baseline Serum Creatinine >1.8 mg/dlPatients With Baseline Serum Creatinine >1.8 mg/dl
who Underwent Contrast Exposure (Iopamidol in All)who Underwent Contrast Exposure (Iopamidol in All)
N=137N=137
Sodium ChlorideSodium Chloride
Hydration (154 mEq/L ofHydration (154 mEq/L of
Sodium Chloride)Sodium Chloride)
N=68N=68
Sodium BicarbonateSodium Bicarbonate
Hydration (154 mEq/L ofHydration (154 mEq/L of
Sodium Bicarbonate)Sodium Bicarbonate)
N=69N=69
Primary endpoint: increase in serum creatinine ≥25%Primary endpoint: increase in serum creatinine ≥25%
within 2 days post-exposurewithin 2 days post-exposure
28. Prevention of CIN with SodiumPrevention of CIN with Sodium
Bicarbonate: ResultsBicarbonate: Results
EndpointsEndpoints
SodiumSodium
ChlorideChloride
N=59N=59
SodiumSodium
BicarbonateBicarbonate
N=60N=60
PP
valuevalue
Incidence of CIN (%)Incidence of CIN (%) 13.6%13.6% 1.7%1.7% 0.020.02
Incidence of CINIncidence of CIN
(↑SCr 0.5 mg/dL)(↑SCr 0.5 mg/dL)
11.9%11.9% 1.7%1.7% 0.030.03
Merten GJ et al.Merten GJ et al. JAMA,JAMA, 2004;291:2328-23342004;291:2328-2334
29. REMEDIAL TrialREMEDIAL Trial
Saline + NACSaline + NAC
N=118N=118
Bicarbonate + NACBicarbonate + NAC
N=117N=117
Saline+AA+NACSaline+AA+NAC
N=116N=116
7 excluded7 excluded
Pts with eGFR<40Pts with eGFR<40
N=393N=393
Randomized N=351Randomized N=351
Excluded N=42Excluded N=42
NAC =NAC = NN-acetylcysteine, AA = ascorbic acid-acetylcysteine, AA = ascorbic acid
9 excluded9 excluded9 excluded9 excluded
107 included107 included
into analysisinto analysis
108 included108 included
into analysisinto analysis
111 included111 included
into analysisinto analysis
Briguorio C. et al,Briguorio C. et al, CirculationCirculation 20072007
30. REMEDIAL Trial: ResultsREMEDIAL Trial: Results
Saline + NAC
Bicarbonate +
NAC
Saline +
Ascorbic Acid
+ NAC
P Value
N=111 N=108 N=107
Serum creatinine
increase by ≥25%
11 (9.9%) 2 (1.9%)* 10 (10.3%) 0.010
Serum creatinine
increase by ≥0.5 mg/dL
12 (10.8%) 1 (0.9%)† 12 (11.2%) 0.026
eGFR decrease by
≥25%
10 (9.2%) 1 (0.9%)† 10 (10.3%) 0.018
*P=0.019P=0.019, †P<0.01P<0.01 vs. saline + NAC group
Briguorio C. et al,Briguorio C. et al, CirculationCirculation 20072007
31. MEENAMEENA
DesignDesign
• DESIGN: Prospective,
randomized, parallel-group,
single-center clinical evaluation
of two hydration strategies for
patients undergoing coronary
angiography
• OBJECTIVE: To compare the
incidence of CIN between
periprocedural hydration with
sodium bicarbonate vs. sodium
chloride (0.9%, normal saline)
• PRIMARY ENDPOINT:
Decrease in estimated GFR by ≥
25% within 4 days of coronary
angiography
353 patients enrolled between January 2006
and January 2007
353 patients enrolled between January 2006
and January 2007
236 patients
assigned to sodium
chloride
236 patients
assigned to sodium
chloride
178 patients
assigned to sodium
bicarbonate
178 patients
assigned to sodium
bicarbonate
156 evaluable
patient
156 evaluable
patient
Brar, S et. al., i2/ACC 2007
147 evaluable
patient
147 evaluable
patient
22
excluded
22
excluded
28
excluded
28
excluded
Hydration ProtocolHydration Protocol
•3 mL/kg for 1 hr before the procedure
•1.5 mL/kg during and for 4hrs post-
procedure
Hydration ProtocolHydration Protocol
•3 mL/kg for 1 hr before the procedure
•1.5 mL/kg during and for 4hrs post-
procedure
35. CIN: Effect of n-AcetylcysteineCIN: Effect of n-Acetylcysteine
• Prospective, randomizedProspective, randomized
• 83 high risk patients83 high risk patients
CrCl < 50 ml/minCrCl < 50 ml/min
Diabetes 33%Diabetes 33%
• IV CONTRAST for CT (75IV CONTRAST for CT (75
ml of Low Osmolar CM)ml of Low Osmolar CM)
• n-AC 600 bid x 2 days pre-n-AC 600 bid x 2 days pre-
• CIN definition: creatinineCIN definition: creatinine
increase of 0.5 mg/dlincrease of 0.5 mg/dl
• Hydration with 0.45% @ 1Hydration with 0.45% @ 1
ml/kg/h x 24 hml/kg/h x 24 h
21%
2%
0%
5%
10%
15%
20%
25%
Control (42) AC (41)
CIM(%)
TepelTepel NEJMNEJM 20002000
p= 0.01p= 0.01
36. Zagler et al. Am Heart J 2006;151:140-145.
Relative Risk for Developing CIN after NACRelative Risk for Developing CIN after NAC
Risk Ratio (Random)Risk Ratio (Random)
95% Cl95% Cl
0.10.1 11 1010
Favors treatmentFavors treatment Favors controlFavors control
0.20.2 0.50.5 22 55
RR (Random)RR (Random)
95% Cl95% Cl
ControlControl
n/Nn/N
NACNAC
n/Nn/N
Study orStudy or
substurysubstury
Review:Review: Acetylcysteine and CINAcetylcysteine and CIN
Comparison:Comparison: 01 NAC on CIN01 NAC on CIN
Outcome:Outcome: 01 CIN01 CIN
Total events:Total events: 124 (NAC), 162 (Control)124 (NAC), 162 (Control)
Test for heterogenety:Test for heterogenety: Ch=27.54 (P0.005), 1Ch=27.54 (P0.005), 122
=56.4%=56.4%
Test for overall effect:Test for overall effect: Z=1.88 (Z=1.88 (P=0.05P=0.05))
Allaqaband et al 8/45 6/40 1.19 (0.45, 3.12)
Briguori et al 6/92 10/91 0.59 (0.23, 1.57)
Diaz-Sandoval et al 2/25 13/29 0.18 (0.04, 0.72)
Durham et al 10/38 9/41 1.20 (0.55, 2.63)
Goldenberg et al 4/41 3/39 1.27 (0.30, 5.31)
Gomes et al 8/78 8/78 1.00 (0.40, 2.53)
Kay et al 4/102 12/98 0.32 (0.11, 0.96)
Nguyen-Ho et al 9/95 19/85 0.42 (0.20, 0.89)
Oldemeyer 4/49 3/47 1.28 (0.30, 5.41)
Pate et al 57/238 50/239 1.14 (0.82, 1.60)
RAPIDO 2/41 8/39 0.24 (0.05, 1.05)
Shyu 2/60 15/61 0.14 (0.03, 0.57)
Fung et al 8/46 6/45 1.30 (0.49, 3.46)
Total: (95% Cl)Total: (95% Cl) 950950 932932 0.68 (0.46, 1.02)0.68 (0.46, 1.02)
37. Meta-analysis: High vs.Meta-analysis: High vs.
Low Osm Contrast MediaLow Osm Contrast Media
• 39 Trials - 5146 patients39 Trials - 5146 patients
• CIN > 0.5 mg/dlCIN > 0.5 mg/dl
• CIN in 7% of all patientsCIN in 7% of all patients
• CIN in 30% of CRICIN in 30% of CRI
patientspatients
• For CRI, NNT=8 (treat 8 toFor CRI, NNT=8 (treat 8 to
prevent 1 CIN case)prevent 1 CIN case)
• Low osmolal groupLow osmolal group
included Ioxaglateincluded Ioxaglate
(Hexabrix); Iodixanol(Hexabrix); Iodixanol
(Visipaque) not studied(Visipaque) not studied
Barrett and CarlisleBarrett and Carlisle J Am Soc NephrolJ Am Soc Nephrol 92;92;
1.0
0.61
0.0
0.2
0.4
0.6
0.8
1.0
1.2
High Osm Low Osm
RelativeRiskofCIN
38. The NEPHRIC StudyThe NEPHRIC Study
Nephrotoxicity in High-risk PatientsNephrotoxicity in High-risk Patients
a Double Blind Randomized Multicentrea Double Blind Randomized Multicentre
Study of Iso-osmolar and Low-osmolarStudy of Iso-osmolar and Low-osmolar
Non-ionic Contrast MediaNon-ionic Contrast Media
39. NEPHRICNEPHRIC Study: ProtocolStudy: Protocol
• Randomized, double blind, prospective, multicenterRandomized, double blind, prospective, multicenter
• Primary endpoint: peak increase in serum creatininePrimary endpoint: peak increase in serum creatinine
concentration @ 3 days after angiographyconcentration @ 3 days after angiography
Patients with diabetes and serum creatinine 1.5-3.5 mg/dl whoPatients with diabetes and serum creatinine 1.5-3.5 mg/dl who
underwent coronary or aortofemoral angiographyunderwent coronary or aortofemoral angiography
Iso-osmolar, non-ionicIso-osmolar, non-ionic
Iodixanol [Visipaque]Iodixanol [Visipaque]
N=64N=64
Mean Contrast Volume = 163 mlMean Contrast Volume = 163 ml
PTCA – 17%PTCA – 17%
Low-osmolar, non-ionicLow-osmolar, non-ionic
Iohexol [Omnipaque]Iohexol [Omnipaque]
N=65N=65
Mean Contrast Volume =Mean Contrast Volume = 162 ml162 ml
PTCA – 25%PTCA – 25%
Aspelin P et al,Aspelin P et al, NEJMNEJM, 2003; 348: 491-499, 2003; 348: 491-499
40. Primary Endpoint –Primary Endpoint –
Peak Increase in Scr from Baseline to Day 3Peak Increase in Scr from Baseline to Day 3
(µmol/l)(µmol/l) p=0.002p=0.002
IodixanolIodixanol
(Visipaque)
IohexolIohexol
(Omnipaque)
n=62n=62 n=64n=64
MeanMean 11.2 ±19.711.2 ±19.7 41.5 ± 68.641.5 ± 68.6
MinimumMinimum - 19.0- 19.0 - 21.0- 21.0
MaxMax 74.074.0 331.0331.0
41. RECOVER Trial – Renal Toxicity Evaluation and ComparisonRECOVER Trial – Renal Toxicity Evaluation and Comparison
Between Visipaque and Hexabrix in Patients With RenalBetween Visipaque and Hexabrix in Patients With Renal
Insufficiency Undergoing Coronary AngiographyInsufficiency Undergoing Coronary Angiography
Jo et al. JACC 2006; 48:924-30
Prospective, randomized trialProspective, randomized trial
300 patients
with CrCl ≤ 60 ml/min
149 pts. (135 pts. included
in primary analysis)
ioxaglate
151 pts. (140 pts. included
in primary analysis)
iodixanol
Primary endpoint – Incidence of CIN
Increase in SCr ≥ 25% or ≥ 0.5 mg/dl
42. RECOVER Trial – Incidence of CINRECOVER Trial – Incidence of CIN
Jo et al. JACC 2006; 48:924-30
17.0%
7.9%
0.0%
10.0%
20.0%
CIN
ioxaglate
iodixanol
P=0.021P=0.021
N=300
43. 24.2%
16.2%
0%
10%
20%
30%
Ioxaglate Iodixanol
ICONICON TTrialrial
PatientsPatients wwithith cchronichronic rrenalenal iinsufficiencynsufficiency
uundergondergoinging PCIPCI wwith atith at lleast 150cc ofeast 150cc of ccontrastontrast vvolumeolume
PatientsPatients wwithith cchronichronic rrenalenal iinsufficiencynsufficiency
uundergondergoinging PCIPCI wwith atith at lleast 150cc ofeast 150cc of ccontrastontrast vvolumeolume
IoxaglateIoxaglate
N=74N=74
IoxaglateIoxaglate
N=74N=74
IodixanolIodixanol
N=71N=71
IodixanolIodixanol
N=71N=71
NN=130=130
P=0.26P=0.26
Incidence of CIN
Mehran R. et al, Transcatheter Cardiovascular Therapeutics.
2006.
44. Rehospitalization with Renal Failure as aRehospitalization with Renal Failure as a
Primary DiagnosisPrimary Diagnosis
Liss et al. Kidney International 2006
0.02% 0.03%
0.10%
0.07%
0.20%
0.30%
0.00%
0.10%
0.20%
0.30%
0.40%
Within 1 week Within 1 month Within 3
months
Ioxaglate
Iodixanol P<0.001P<0.001
P<0.001P<0.001
P=0.022P=0.022
45. Start of Dialysis after CoronaryStart of Dialysis after Coronary
Angiography or PCIAngiography or PCI
Liss et al. Kidney International 2006
0.00%
0.02%
0.10%
0.02%
0.10%
0.20%
0.00%
0.05%
0.10%
0.15%
0.20%
0.25%
Within 1 week Within 1 month Within 3 months
Ioxaglate
Iodixanol
P=0.098P=0.098
P=0.010P=0.010
P=0.009P=0.009
46. 1-year Follow-up1-year Follow-up
Liss et al. Kidney International 2006
* Groups differ in
time period !
CMCM N of ptsN of pts
iodixanoliodixanol 54 61654 616
ioxaglateioxaglate 24 47924 479
** iohexoliohexol 6 8546 854
Renal failureRenal failure
Iodixanol
Iohexol
Ioxaglate
f
Time (years)
%
6
5
4
3
2
1
0
0 1 2 3 4 5 6 7 8 9 10 11 12
47. CARECARE
DesignDesign
• DESIGN: Prospective,
randomized, double-blind,
parallel-group, multi-center
clinical evaluation ipamidol-370
and iodixanol-320
• OBJECTIVE: To compare the
incidence of CIN between
iopamidol-370 and iodixanol-320
• PRIMARY ENDPOINT:
Increase in SCr ≥ 0.5 mg/dL from
baseline to 45 to 120 hours after
administration
482 patients enrolled between July 2005 and
June 2006 in 25 clinical site in North
America
482 patients enrolled between July 2005 and
June 2006 in 25 clinical site in North
America
14 patients withdrew
consent
14 patients withdrew
consent
468 assigned to a treatment arm468 assigned to a treatment arm
236 patients
assigned to
Iodixanol-320
236 patients
assigned to
Iodixanol-320
230 patients
assigned to
Iopamidol-370
230 patients
assigned to
Iopamidol-370
204 evaluable
patient
204 evaluable
patient
Solomon, RJ et. al., Circulation 115, 3189 (2007)
210 evaluable
patient
210 evaluable
patient
26
excluded
26
excluded
26
excluded
26
excluded
49. CARECARE
p = 0.11p = 0.11 p = 0.37p = 0.37 p = 0.20p = 0.20
Diabetic SubgroupDiabetic Subgroup
50. Figure. Strategy for Management of Patients With Risk Factors for Contrast-Induced
Nephropathy *See Box for listing of risk factors for contrast-induced nephropathy.
Pannu, N. et al. JAMA 2006;295:2765-2779
51. Conclusions (1)Conclusions (1)
• CRI is one of the most important independentCRI is one of the most important independent
predictors of poor outcome post PCIpredictors of poor outcome post PCI
• CIN remains a frequent source of acute renalCIN remains a frequent source of acute renal
failure and is associated with increased morbidityfailure and is associated with increased morbidity
and mortality, and higher resource utilizationand mortality, and higher resource utilization
• Several factors predispose patients to CINSeveral factors predispose patients to CIN
• Preventive measures pre procedure, as well asPreventive measures pre procedure, as well as
careful post procedure management should becareful post procedure management should be
routine in all patientsroutine in all patients
52. Conclusions (2)Conclusions (2)
• Hydration pre-PCI (12 hours recommended)Hydration pre-PCI (12 hours recommended)
• Avoid nephrotoxic drugs (NSAIDS, antibiotics, metformin etc)Avoid nephrotoxic drugs (NSAIDS, antibiotics, metformin etc)
• Role of n-acetylcysteine is disputableRole of n-acetylcysteine is disputable
• No Role for IV FenoldopamNo Role for IV Fenoldopam
• Sodium bicarbonate may be useful, but need more definitiveSodium bicarbonate may be useful, but need more definitive
datadata
• Limit contrast agent volumeLimit contrast agent volume
• Low-osmolar agents are better than high-osmolarLow-osmolar agents are better than high-osmolar
Within non-ionic contrast, the data are contradictoryWithin non-ionic contrast, the data are contradictory
Allow time before repeat procedures / staged procedures.Allow time before repeat procedures / staged procedures.
• Role of local drug delivery for prevention of CIN requiresRole of local drug delivery for prevention of CIN requires
further investigationfurther investigation
• Role of Cooling Therapy is being examined: COOL CIN StudyRole of Cooling Therapy is being examined: COOL CIN Study
53. Take home message ?Take home message ?
Perhaps testing Serum creatinine and GFR
should become a regular practice to know the
true incidence at our centre.
Editor's Notes
There is a strong bidirectional association between cardiac diseases and renal insufficiency.
In multiple clinical trials and analyses, and you see just one of them, CKD represented the most significant independent predictor of long-term mortality.
Risk factors for CIN maybe divided into patient-related and procedure-related. Patient-related factors include Renal insufficiency Diabetes mellitus with renal insufficiency Age Volume depletion Hypotension Low cardiac output Class IV CHF Other nephrotoxins Renal transplant Hypoalbuminemia (<35 g/l) And procedure-related factors include Multiple contrast media injection within 72 hrs Intra-arterial injection site High volume of contrast media High osmolality of contrast media
Recently, CIN risk score was developed and validated based on the analysis of large prospectively created database. You may see that risk of CIN may be as high as 57% and risk of dialysis maybe as high as 12% in pts with multiple risk factors.
We also found a strong relationship between 1-year mortality and risk score of CIN.
A prospective randomized trial utilizing the oxygen radical scavenger, acetylcysteine, explored the role of oxidative injury in contrast induced nephropathy. Patients undergoing a contrast CT scan were randomized to usual care or pretreatment with 600 mg bid of acetylcysteine starting 24 hours before the contrast exposure and continuing for 24 hours after the exposure. A marked decrease in the incidence of contrast induced nephropathy (CIN) was noted. Although the study is very exciting, a number of limitations are worth noting. First, the low dose of contrast and the route of administration (intravenous) make it difficult to extrapolate the positive results to patients receiving 2-3 times as much contrast intraarterially. Second, the marked reduction in the incidence of CIN was associated with an actual decrease in serum creatinine in many patient, a finding difficult to explain based on the presumed mechanism of action of acetylcysteine. Finally, a number of other experiments involving animal models of renal injury have failed to produce such dramatic results using other free oxygen radical scavengers. This may simply mean that animal models don’t mimic human pathophysiology accurately. In any case, until additional studies in other clinical situations confirm the dramatic results found here, it should not be assumed that acetylcysteine is a magic bullet.
Solomon A meta-analysis of 39 clinical trials involving more than 5000 patients found that there were no significant benefits of low osmolar media compared to high osmolar media in low risk patients. However, in high risk patients (for example, those with baseline renal insufficiency), low osmolar media reduced the risk of contrast-induced nephropathy by 39%. Based upon the expected incidence of contrast-induced nephropathy, only a small number of high risk patients would need to be treated to prevent a single case of contrast-induced nephropathy. Since contrast-induced nephropathy is associated with significant morbidity, a cost-benefit analysis favors the use of low osmolar media in high risk patients.
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