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Nephrology Mini-Symposium: Acute Cardiorenal Syndrome

Nephrology Mini-Symposium: Acute Cardiorenal Syndrome. R3 潘思宇 ,R3 李宗育 ,R3 張凱迪 ,R3 柯雅琳 R5 王介立 /VS 林水龍 Nov. 24 th , 2010. “Cardiorenal” for 100 Years. Sir Thomas Lewis (1881-1945). Lewis T., Br Med J 1913;2:1417-20. PubMed Trend. NIH Definition. Ronco Classification.

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Nephrology Mini-Symposium: Acute Cardiorenal Syndrome

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  1. Nephrology Mini-Symposium:Acute Cardiorenal Syndrome R3潘思宇,R3李宗育,R3張凱迪,R3柯雅琳 R5王介立/VS林水龍 Nov. 24th, 2010

  2. “Cardiorenal” for 100 Years • Sir Thomas Lewis (1881-1945) Lewis T., Br Med J 1913;2:1417-20

  3. PubMed Trend NIHDefinition Ronco Classification

  4. Working Definition (2004) At its extreme, cardio-renal dysregulation leads to what is termed “cardio-renal syndrome” in whichtherapy to relieve congestive symptoms of heart failure is limited by further decline in renal function. It is clear that our current understanding of cardio-renal connections is inadequate to explain many of the clinical observations in heart failure or to direct its therapy. NHLBI Working Group. http://www.nhlbi.nih.gov/meetings/workshops/cardiorenal-hf-hd.htm

  5. Proposed Classification (2008) Acute Chronic HeartKidney (cardiorenal) KidneyHeart (renocardiac) Ronco C. et al. J Am CollCardiol 2008;52:1527-39.

  6. Cardiorenal Syndrome is Always There Type 2 and 4 Type 3

  7. This year, 2010, we present you the… Type 1 Cardiorenal Syndrome Acute decompensated heart failure Acute myocardial infarction Low cardiac output syndrome post cardiac surgery

  8. CASE PRESENTATION There’s Always a Problem…

  9. Acute Cardiorenal Syndrome Epidemiology & Pathophysiology. R3 潘思宇 Diagnosis & Management......…... R3 李宗育 Volume & Diuretics………………. R3 張凱迪 Ultrafiltration………………………. R3 柯雅琳 R5 王介立 VS 林水龍

  10. Cardiorenal Syndrome Type I • Acute heart disorder leading to acute kidney injury • Acute heart disorder ? • Acute decompensated heart failure • Acute coronary syndrome • (Low cardiac output syndrome after open heart surgery) • Acute kidney injury ? • ARF, Worsening renal function • AKI: RIFLE, AKIN, K-DIGO • Biomarkers: NGAL, cystatin C

  11. Epidemiology Acute decompensated heart failure Acute coronary syndrome

  12. Acute decompensated heart failure

  13. Observational, 2002/10~2004/10, France WRF:↑Cre > 0.3 mg/dL, Total: 416 with AHF WRF: 37% D. Logeart et al, Int J Cardiol2008; 127: 228–232

  14. Event: death or unscheduled readmission for HF P = 0.01 D. Logeart et al, Int J Cardiol2008; 127: 228–232

  15. Acute coronary syndrome

  16. Observational, 1994/1~1996/2, Total: 147007 with AMI Mild: ↑0.3~0.4, Mod: ↑0.5~0.9, Severe: ↑≧1.0 mg/dL 7.1% 7.1% 5.2% CR Parikh et al, Arch Intern Med. 2008;168(9):987-995

  17. Observational, 1994/1~1996/2, Total: 147007 with AMI Mild: ↑0.3~0.4, Mod: ↑0.5~0.9, Severe: ↑≧1.0 mg/dL P < 0.01 At all time points 1 yr 3 yr 10 yr 5 yr CR Parikh et al, Arch Intern Med. 2008;168(9):987-995

  18. Pathophysiology The low flow state hypothesis Venous congestion: IAP & CVP Others: Neurohormonal activation

  19. Pgc: Glomerular pressure, PT : Tubular pressure πgc: Glomerular colloid p, πT: Tubular colloid p △π Pgc PT GFR α( Pgc- PT -△π) JG Abuelo et al, N Engl J Med 2007; 357(8): 797-805

  20. Pgc • MAP? • Intra-Abdominal hypertension? • Change of Resistance at A or E arteriole? • PT • Intra-Abdominal hypertension? • Tubular obstruction? Pgcα (MAP – IAP) MAPαPgc αGRF Factors affect GFR

  21. Franklin H. Epstein et al, N Engl J Med1999; 341(8): 577-585

  22. If this low output theory holds true, then … ? ↓LVEF / CI ↓GFR ↓Renal perfusion 灌水 Dopamine!!! 這病人 Kidney 不好

  23. Prospective, 1990, USA, CHF, Total: 34 A: CI>2 ; B: CI 1.5~2 ; C: CI <1.5 L/min/m2 Autoregulation Ljungman et al. Drugs 1990; 39(Suppl. 4): 10-21

  24. Renal auto-regulation Brenner and Rector’s The Kidney, 8th ed http://www2.kumc.edu/ki/physiology/course/two/2_4.htm

  25. Pgc • MAP? • Intra-Abdominal hypertension? • Change of Resistance at A or E arteriole? • PT • Intra-Abdominal hypertension? • Tubular obstruction? Pgcα (MAP – IAP) Factors affect GFR PTαIAP

  26. IAP range in critical care • Normal: 5-7 mmHg • Elevated: ≥8 mmHg • IAH: ≥ 12mmHg Wilfried Mullens et at, Intensive Care Med (2006) 32:1722–1732

  27. Prospective cohort, 2006/11~2007/5, CCU, USA AHF: LVEF<30%, PCWP>18 or CVP>8, Total: 40 Goal: PCWP<18, CVP<8, CI>2.2 Wilfried Mullens et at, Intensive Care Med (2006) 32:1722–1732

  28. Retrospective cohort, 1989/1~2006/12, CCU, Netherland Patient s/p Rt heart catheterization, Total: 2557 Baseline CVP vs. GFR Kevin Damman et al., J Am Coll Cardiol 2009; 53(7): 582–8

  29. Prospective, 2006/1~2007/6, USA, CCU, Total: 145 Inclusion: LVEF<30%, CI<2.4, PCWP>18 or CVP>8 PA catheter goal: PCWP<18, CVP<8, & CI>2.4 CVP rather than CI ? WilfriedMullens et al, J Am CollCardiol 2009; 53(7)589–96

  30. Animal study, Dog, 1931, Renal a & v cannulation F. R. Winton et al, J Physiol 1931; 72: 49–61.

  31. Fluid status evaluation in CRS ? Venous congestion may be more important than hypovolemia 灌水 脫水

  32. Other postulated mechanisms of CRS • Low evidence & inconclusive • Sympathetic overactivity • Adenosine • Vasopressin • Natriuretic peptide • Oxidative injury & endothelial dysfunction Jeremy S. Bock et al, Circulation. 2010;121:2592-2600.

  33. Sympathetic Overactivity

  34. Animal study, Rat, 1980, Renal sympathetic stimulate, Total: 10 Gerald F. Dibona et al, Physiol Rev, 1997; 77(1): 75-197

  35. Prospective cohort, 2007/6~2008/11, Australia & European Hypertension s/p renal sympathetic denervation, Total: 45 ? Improvement of hypertension Improvement of renal function Henry Krum et al, Lancet 2009; 373: 1275–81

  36. Pathology

  37. 老師, 第三床 ARF咧 要不要作 Renal biopsy看一看? 第三床不是 Heart failure嗎? 阿就是Pre-renal ARF阿, Biopsy做什麼?

  38. Pathology • Acute heart failure not a traditional indication for renal biopsy • Case report • The characteristics of acute renal failure in cardiogenic shock in the elderly • 4 patients with cardiogenic shock and ARF • 1 patient with ATN • 3 patients without pathological change Durakovi et al, ZFA 1986; 41(5): 301-5

  39. Can we predict who will developed CRS in patients presented with acute cardiac dysfunction?

  40. Known Predictors from Past Observations (I) WH Tang & W. Mullens. Heart. 2010; 96(4):255-60

  41. Known Predictors from Past Observations (II) WH Tang & W. Mullens. Heart. 2010; 96(4):255-60

  42. Summary • AKI occurs frequently in AHF (type 1 CRS) • It is an independent risk factor of worse outcome • However, only very limited prospective observational studies have addressed the issues • The mechanism of type 1 CRS remained largely speculative • We have no ideas why his (her) kidney failed • Venous congestion should be kept in mind other than arterial underfilling

  43. Acute Cardiorenal Syndrome Epidemiology & Pathophysiology. R3 潘思宇 Diagnosis & Management......…... R3 李宗育 Volume & Diuretics………………. R3 張凱迪 Ultrafiltration………………………. R3 柯雅琳 R5 王介立 VS 林水龍

  44. DIAGNOSIS

  45. CASE PRESENTATION Back to the Problem… How do we know the sequence?

  46. CASE PRESENTATION Time Course of the eGFR CKD stage 3 AKI Acute (type 1,3) rather than chronic (type 2,4)…

  47. CASE PRESENTATION Cause of CKD? 12 cm (Long-standing; microscopicovert) Other non-DM cause of CKD related to CVD: - Ischemic nephropathy (renovascular disease) - Malignant hypertension

  48. CASE PRESENTATION AKIfrom Heart? Hypotensive episode? “No diagnostic criteria = by exclusion”

  49. Typical Acute CRS • Acute heart failure syndrome • Acute kidney injury • No evidence of intrinsic kidney disease other than the baseline CKD So far, has the diagnosis of type 1 cardiorenal syndrome been secured?

  50. Mimickers of Type 1 CRS • NSAIDs causing concurrent heart failure and vasomotor nephropathy • Flash pulmonary edema (bilateral renal artery stenosis) • Hypertensive crisis from identifiable causes (e.g. pheochromocytoma) (the primary cause is outside the heart) (potentially treatable)

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