Crs

Cardio renal syndrome amirtha

1. CARDIORENAL SYNDROMEs By Dr.R.AMIRTHA LAKSHMI

2. Introduction Cardiac and renal diseases are common and frequently coexist to significantly increase mortality, morbidity, and the complexity and cost of care . Primary disorders of 1 of these 2 organs often result in secondary dysfunction or injury to the other. Such interactions represent the pathophysiological basis for a clinical entity called cardiorenal syndrome (CRS) .

3. Definition CRS can be generally defined as a patho physiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of one organ may induce acute or chronic dysfunction of the other. - European Heart Journal (2010)

4. CLASSIFICATION World congress of nephrology classified cardiorenal syndromes into 5 subtypes based on patho -physiology : CRS type 1 : acute cardio-renal syndrome CRS type 2 : chronic cardio-renal syndrome CRS type 3 : acute reno -cardiac syndrome CRS type 4 : chronic reno -cardiac syndrome CRS type 5 : secondary cardio-renal syndrome

5. Epidemiology and Outcomes in Combined Cardiorenal Disease Prevalence of Renal Disease in Patients With HF In the Acute Decompensated Heart Failure National Registry (ADHERE ) of 1,05,000 individuals admitted for acute decompensated HF, 30% had a history of renal insufficiency, 21 % had serum creatinine concentrations >2.0 mg/ dL , and 9 % had creatinine concentrations >3.0 mg/ dL .

6. Impact of Renal Disease on Clinical Outcomes in Patients With HF Renal dysfunction is one of the most important independent risk factors for poor outcomes and all-cause mortality in patients with HF. Baseline glomerular filtration rate ( GFR) appears to be a stronger predictor of mortality in patients with HF than left ventricular ejection fraction or NYHA functional class. Both elevated serum creatinine on admission and worsening creatinine during hospitalization predict prolonged hospitalization , rehospitalization , and death.

7. HF Outcomes in Patients With Renal Disease Patients with chronic renal insufficiency are at strikingly higher risk for myocardial infarction, HF with systolic dysfunction, HF with preserved left ventric ular ejection fraction, and death resulting from cardiac causes compared with individuals with normal GFR.

8. Age adjusted CVD mortality is about 30 times higher in CKD than in general population. Risk of dying because of cardiovascular causes in patients with ESRD – 65 times higher in pts with 45-54 yrs, 500 times higher than general population in young cohort. 1/3 of patients with mild renal impairment –h/o overt CVD.

9. Mechanisms in CRS RAAS INCREASED SNA REACTIVE OXYGEN SPECIES INFLAMMATION ENDOTHELIN EFFECT ARGININE VASOPRESSIN EFFECTS BNP EFFECTS

10. Biomarkers in the diagnosis of AKI Biomarker Assosciated injury Cystatin C Proximal tubule injury KIM 1 Ischemia and nephrotoxins NGAL Ischemia and nephrotoxins NHE3 Ischemia,prerenal , postrenal AKI  GST Proximal tubule injury ,acute rejection  GST Distal tubule injury,acute rejection L-FABP Ischemia and nephrotoxins Cyr 6 1 Ischemic ATN NETRIN 1 Ischemia and nephrotoxins,sepsis

11. CRS type 1 CRS type 1 (acute CRS)-- is characterized by a rapid worsening of cardiac function, leading to acute kidney injury ( AKI). Acute heart failure (HF) may be divided into 4 subtypes: H ypertensive pulmonary edema with preserved left ventricular (LV) systolic function , Acutely decompensated chronic HF , Cardiogenic shock, and Predominant right ventricular failure.

12. CRS Type 1

13. Management of CRS 1 Diuretics –useful in volume overloaded non hypotensive patients. Loop diuretics ,thiazides--Overzealous use → worsening renal function Exacerbates neuro hormonal activity , activates RAAS , Increase SVR ,worsens LVF . Inotropes -- dopamine,dobutamine,milirinone Vasodialtors – nesiritide Ultrafiltration( aquapheresis ) Arginine vasopressin receptor antagonists— tolvaptan

14. CRS type 2 CRS type 2 (chronic CRS) is characterized by chronic abnormalities in cardiac function (e.g., chronic congestive HF) causing progressive CKD. Worsening renal function in the context of HF is associated with adverse outcomes and prolonged hospitalizations. The prevalence of renal dysfunction in chronic HF has been reported to be approximately 25 %. Even slight decreases in estimated glomerular filtration rate (GFR) significantly increase mortality risk and are considered a marker of severity of vascular disease.

15. Pathophysiology Low cardiac output--- activation of RAAS –SNS ---subclinical inflammation ---endothelial dysfunction—increased renal vascular resistance—accelerated atherosclerosis. Relative or absolute erythropoietin deficiency. Activation of the receptor of erythropoietin in heart may protect it from apoptosis , inflammation and fibrosis.

16. Ronco, C. et al. J Am Coll Cardiol 2008;52:1527-1539 CRS Type 2

17. Management Diuretics – volume expanded state ACEI ARBs block RAAS ---decrease LVH, proteinuria, decrease progression of CKD . Vasodilators may also be useful.

18. CRS TYPE 3 CRS type 3 (acute renocardiac syndrome )- is characterized by an abrupt and primary worsening of kidney function (e.g., AKI, ischemia, or glomerulonephritis), leading to acute cardiac dysfunction (e.g., HF, arrhythmia, ischemia). Type 3 CRS appears less common than type 1 CRS , but this may only be due to the fact that, unlike type 1 CRS, it has not been systematically studied.

19. Ronco, C. et al. J Am Coll Cardiol 2008;52:1527-1539 CRS Type 3

20. Management Rx of accelerated HTN, hyperkalemia, metabolic acidosis. Hemodialysis . CRRT

21. CRS TYPE 4 CRS type 4 (chronic renocardiac syndrome )- is characterized by a condition of primary CKD (e.g ., chronic glomerular disease) contributing to decreased cardiac function , ventricular hypertrophy, diastolic dysfunction, and/or increased risk of adverse cardiovascular events.

22. Copyright ©2008 American College of Cardiology Foundation. Restrictions may apply. Ronco, C. et al. J Am Coll Cardiol 2008;52:1527-1539 CRS Type 4

23. Management Cessation of smoking, control of diabetes, HTN. Correction of anemia –iron supplements and erythropoietin Hb 11-12 gm % hct >36% Loop diuretics ,ACEI, ARB s, Beta blockers Calcium-phosphate ionic product to be kept below 50 mg2/m2 Sevelamer . Statins Vitamin E

24. CRS TYPE 5 CRS type 5 (secondary CRS )- is characterized by the presence of combined cardiac and renal dysfunction due to acute or chronic systemic disorders. S everal acute and chronic diseases can affect both organs simultaneously and that the disease induced in one can affect the other and vice versa. Examples include sepsis, diabetes, amyloidosis, systemic lupus erythematosus , and sarcoidosis . Several chronic conditions such as diabetes and hypertension may contribute to type 2 and 4 CRS.

25. CRS Type 5

26. Management Treatment of underlying cause. Vasopressors Inotropes Diuretics Intensive renal replacement therapy in sepsis.

27. Take home message CRS is a pathophysiological condition. Treatment is to be individualized based on the etiology. Early diagnosis is important for better survival. Early novel biomarkers are to be used in diagnosis. Each patient with either CKD,CVD to be assessed with risk factors and followed up.

28. Thank you