1. John Morris, MD Nephrology – BMH Memphis I have the following financial relationships with commercial interests to disclose: NONE Disclosure

2. Cardiorenal Syndrome No pump, no pee, no mystery. John T. Morris, III, M.D.

3. 2004 Working Group- heart failure treatment limited by worsening renal function 2008 Working Group- 5 part classification scheme Type 1: Acute cardiorenal syndrome Type 2: Chronic cardiorenal syndrome Type 3: Acute renocardiac syndrome Type 4: Chronic renocardiac syndrome Type 5: Secondary cardiorenal syndrome Definition:

4. PRE-TEST Polling Questions

5. CASE #1: Match the clinical scenario with class of CRS A 26 yo AAF with active lupus nephritis presents with a creatinine of 2.4, albumin of 2.1, 3 plus pitting edema, UA with > 300 of protein and large blood, mild pulmonary edema on CXR, proBNP=3000, and troponin of 1.5 A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

6. CASE #2: Match the clinical scenario with class of CRS 67 yo WM presents with abdominal pain and found to have 2 blood cultures with Gram positive cocci, a creatinine of 2.9, AST= 250, lactic acid of 4, and a troponin of 4.2 A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

7. CASE #3: Match the clinical scenario with class of CRS 36 yo AA male with dilated CMP on home Milrinone presents with increased SOB and edema. He is admitted to the hospital and started on Lasix 80 mg IV q 8 hrs and 10 mg Zaroxolyn q day. His creatinine of admission was 0.9. His creatinine on hospital day 3 is 2.4 A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

8. CASE #4: Match the clinical scenario with class of CRS 58 yo WF with ESRD on maintenance dialysis for 6 years poorly compliant with phosphate binders has an intact PTH of 490, phosphorus of 8.2, and and ECHO that revealed LVH presents to the ER after she began having chest pain while on dialysis. Initial troponin in ER minimally elevated A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

9. CASE #5: Match the clinical scenario with class of CRS 26 yo WM was diagnosed 2015 with idiopathic dilated CMP initially treated with ACE, Betablocker, and diuretics has had progression of his disease and is now on continuous Milrinone. His creatinine was.9 to 1.1 for most of 2015 but has been 1.5 to 1.7 for the past several months. No protein in his UA A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

10.  Of CKD in HF: about 30-60% -ADHERE database -Systemic review by Lichtman  Of AKI in HF: about 20-30%  POSH study Prevalence

11. Impaired kidney function in heart failure is defined as a reduction in GFR …duh!  Problems with creatinine  Production  Secretion  Problems estimating GFR  Acute vs. chronic kidney disease Diagnosis

13.  Impaired kidney function is diagnosed with a decrease in GFR-duh - Problems with creatinine, problems with estimating GFR

14. Glomerulus

15.  Neurohormonal adaptations - Sympathetic nervous system -RAAS -Vasopressin -Endothelin-1  Reduced renal perfusion - ESCAPE trial  Increased renal venous pressures -Human and animal studies have shown that increased abdominal pressure and/or elevated CVP can cause a reduction in GFR Pathophysiology

16. Sympathetic nervous system  activated due to decreased stroke volume and cardiac output  causes arterial vasoconstriction and increased myocardial contractility and heart rate Pathophysiology, con’t

17. RAAS

19. GFR Maintenance

21. Pathophysiology

23. Endothelin  potent vasoconstrictor  has been implicated in progression of renal failure and glomerular hypertrophy  causes hypertrophy of cardiac myocytes  stimulates and potentiates noradrenaline, angiotensin II, and aldosterone Pathophysiology

24. Reduced renal perfusion  ESCAPE trial- 433 patients with ADHF  no correlation between C.I. and either GFR or WRF for C.I above 1.5  Improving C.I. did not improve renal fx at discharge Pathophysiology

25. Increased renal venous pressure  Mullins study in 2009- 145 patients with ADHF  40 % developed AKI. These patients had higher CVPs and admit and discharge  WRF less frequent in patients who achieved CVP less than 8  CVP was able to risk stratify for the development of WRF Pathophysiology

26. …Increased renal venous pressure (continued)  Incremental risk of WRF with higher categories of baseline CVP  75% of patients with CVP>24 developed WRF and mean baseline CVP higher (18 vs 12) in patients who had WRF…….linear relationship  2 strongest determinants for developing WRF were presence of CKD and increased CVP  Improved C.I. had no correlation with WRF Pathophysiology

27. …Increased renal venous pressure (continued) Mechanism  increased pressure transmitted back to renal vein causing increased renal interstitial pressure Pathophysiology

29. POST-TEST Polling Questions

30. CASE #1: Match the clinical scenario with class of CRS A 26 yo AAF with active lupus nephritis presents with a creatinine of 2.4, albumin of 2.1, 3 plus pitting edema, UA with > 300 of protein and large blood, mild pulmonary edema on CXR, proBNP=3000, and troponin of 1.5 A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

31. CASE #2: Match the clinical scenario with class of CRS 67 yo WM presents with abdominal pain and found to have 2 blood cultures with Gram positive cocci, a creatinine of 2.9, AST= 250, lactic acid of 4, and a troponin of 4.2 A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

32. CASE #3: Match the clinical scenario with class of CRS 36 yo AA male with dilated CMP on home Milrinone presents with increased SOB and edema. He is admitted to the hospital and started on Lasix 80 mg IV q 8 hrs and 10 mg Zaroxolyn q day. His creatinine of admission was 0.9. His creatinine on hospital day 3 is 2.4 A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

33. CASE #4: Match the clinical scenario with class of CRS 58 yo WF with ESRD on maintenance dialysis for 6 years poorly compliant with phosphate binders has an intact PTH of 490, phosphorus of 8.2, and and ECHO that revealed LVH presents to the ER after she began having chest pain while on dialysis. Initial troponin in ER minimally elevated A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20

34. CASE #5: Match the clinical scenario with class of CRS 26 yo WM was diagnosed 2015 with idiopathic dilated CMP initially treated with ACE, Betablocker, and diuretics has had progression of his disease and is now on continuous Milrinone. His creatinine was.9 to 1.1 for most of 2015 but has been 1.5 to 1.7 for the past several months. No protein in his UA A.CRS I B.CRS II C.CRS III D.CRS IV E.CRS V 20