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RENAL AND CARDIOVASCULAR INTERACTION

RENAL AND CARDIOVASCULAR INTERACTION. Renal blood flow. Each kidney weights about 150 grs Blood flow is 400 ml /100gr /min (20-25 % of cardiac output) low oxygen extraction (about 8 %of the total body oxygen consumption). CARDIOVASCULAR DISEASE. Renal hypoperfusion

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RENAL AND CARDIOVASCULAR INTERACTION

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  1. RENAL AND CARDIOVASCULAR INTERACTION

  2. Renal blood flow • Each kidney weights about 150 grs • Blood flow is 400 ml /100gr /min (20-25 % of cardiac output) low oxygen extraction (about 8 %of the total body oxygen consumption)

  3. CARDIOVASCULAR DISEASE • Renal hypoperfusion • Prerenal azotemia • Atheroembolism • Septic embolism • Immunologic phenomena • Side effect of drugs

  4. CHRONIC KIDNEY DISEASE • Accelerates atherosclerosis • Hypertension • Heart failure • Pericardial effusion • Myocardial disease • Valvular disease • Cardiac arrhythmias • Sudden death • Dialysis related problems

  5. CHRONIC KIDNEY DISEASE • eGFR of less than 60 ml/min/1.73 m2 for more than 3 months • serum creatinine (Cr) greater than 1.5 mg/dl • presence of kidney damage • microalbuminuria at any level of eGFR (random urine albumin-to-Cr ratio (ACR) of 30 to 300 mg/gm )

  6. CHRONIC KIDNEY DISEASE • JNC 7 has recognized CKD as an independent cardiovascular risk state Decreasing levels of renal function act as a major adverse prognostic factor after a variety of cardiac events

  7. Anemia and CKD • WHO definition :Hb level less than 13 g/dl in men and less than 12 g/dl in women • Anemia caused by CKD in 20 %of patients with stable CAD and 30 to 60 % of patients with HF

  8. Anemia and CKD • Relative deficiency of EPO causes: impaired vascular repair, progression of atherosclerosis

  9. Anemia and CKD • Increased levels of: • TNF-alpha • ILs 1 and 6 • Endothelin • Matrix metalloproteinases directly reduce RBC production at the level of the bone marrow and further worsen the anemia

  10. Anemia and CKD • 28 of 29 large prospective studies of HF have found anemia to be an independent predictor of mortality. • Among HF patients for each 1 g/dl decrement in Hb, there is a 13 % increase in risk for all-cause mortality • Patients with anemia and CKD are more likely to progress to ESRD irrespective of their baseline level of renal function. • As Hb drops over time, there is a graded increase in HF hospitalizations and death

  11. EPO • Increase in coronary flow reserve. • Preventing endothelial cell apoptosis. • Enhancing myocardial repair in myocardial injury that could minimize LV dysfunction by recruiting vascular progenitor cells, which can become functional myocardial cells, thereby increasing the contractile function of the injured ventricle.

  12. Treatment of anemia with EPO • Reducing morbidity, particularly that of cardiovascular origin • Improving quality of life • Favorable changes in left ventricular remodeling • Improved ejection fraction • Improved functional classification • Higher levels of peak O2 consumption with exercise testing.

  13. Treatment of anemia with EPO • Increased platelet activity, thrombin generation, and resultant increased risk of thrombosis • Increased endothelin levels, increased asymmetric dimethylarginine, which theoretically reduces nitric oxide availability and results in HTN • Worsened measures of oxidative stress.

  14. Treatment of anemia with EPO • Two RCTs in CKD indicate that treatment with EPO to higher Hb targets resulted in higher CVD events. • Until there is clear evidence that the partial correction of anemia has favorable outcomes in CVD, this form of treatment is not recommended for the primary purpose of improving the natural history of CVD.

  15. ACCELERATION OF VASCULAR CALCIFICATION • Coronary artery calcification (CAC) seems to occur exclusively in atherosclerotic arteries and is absent in normal vessel walls. • Patients with ESRD have the greatest absolute values and rates of accumulation of CAC. • using CAC as a diagnostic or therapeutic target in patients with CKD or ESRD is not recommended.

  16. RENAL DISEASE AND HYPERTENSION • An optimal BP can be defined as less than 120/80 (SBP being more important). • Most patients with CKD and HTN require 3 or more antihypertensive agents to achieve a goal BP of less than 130/80 .

  17. RENAL DISEASE AND HYPERTENSION • Pharmacological therapy : RAAS antagonist often in combination with a thiazide-type diuretic. • Dihydropyridine CCBs alone, cause relative afferent arteriolar dilation, increase intraglomerular pressure and worsen glomerular injury and thus should be avoided as singular agents for BP control.

  18. Antihypertensive Agents in CKD

  19. ACEI/ARB in CKD • Elevation in Cr and ARF that are more likely when the patient is volume depleted or in the presence of occult bilateral renal artery stenosis or equivalent. • Have SBP stable and greater than 90 mm Hg, euvolemia, and a drug regimen without concurrent renal toxic agents

  20. ACEI/ARB in CKD • CKD patients enjoy an improved survival and reduced rates of ESRD on ACEI/ARB agents even though the serum Cr is chronically elevated on these agents because of reductions in intraglomerular pressure. • Discontinuation of ACEI/ARB drugs because of moderate, asymptomatic rises in Cr is a common management error.

  21. ACEI/ARB in CKD • Use ACEI or ARB in patients down to an eGFR of 15 ml/min/1.73 m2 • Below this level, case reports suggest a high rate of hyperkalemia and the concern of accelerating the course to ESRD and dialysis .

  22. CONTRAST-INDUCEDNEPHROPATHY

  23. CONTRAST-INDUCEDNEPHROPATHY • A form of acute kidney injury • definition: rise in serum Cr greater than 25 % or greater than 0.5 mg/dl from baseline after IV contrast administration • frequency :13 % in nondiabetics and 20 % in diabetics undergoing PCI is related in a curvilinear fashion to the eGFR

  24. Definition New onset or exacerbation of renal dysfunction after contrast administration in the absence of other causes: increase by > 25% or absolute  of > 0.5 mg/dL Contrast-Induced Nephropathy from baseline serum creatinine Occurs 24 to 48 hrs post–contrast exposure, with creatinine peaking 5 to 7 days later and normalizing within 7 to 10 days in most cases

  25. Epidemiology • Incidence varies according to the population and risk factor profile. • Reports of incidence subject to under-reporting, due to lack of appropriate follow-up. • Incidence of 7% reported in the overall population exposed to radio-contrast agents. Incidence declining. • Incidence ≥50% in patients with multiple risk factors.

  26. Prognostic Implications • 3rd most common cause of hospital acquired renal insufficiency (11% of all cases). Behind pre-renal causes and nephrotoxic medications. • 5.5 fold increase in mortality (in-hospital). • < 1% risk of Hemodialysis. (19 % 2 yr survival) • Associated with MI, TVR at 1 year; longer hospital stay. • Post-procedural creatinine more powerful predictor of late events than CK-MB.

  27. Prognostic Implications- Increased In-Hospital mortality. • Retrospective, 16,248 inpatients • Cases with CIN(n=183) matched with controls (n = 174). Adjusted co-morbidity • CIN: > 25% increase in baseline creatinine. OR 5.5 Levy EM, et al; JAMA 1996;275(19):1489-94

  28. PATHOPHYSIOLOGY

  29. Pathophysiology of CIN • (1) direct toxicity of iodinated contrast material to nephrons related to the ionicity and osmolality of the contrast media. • (2) microshowers of atheroemboli to the kidneys • (3) contrast material– and atheroemboli-induced intrarenal vasoconstriction.

  30. Pathophysiology of CIN • The most important predictor of CIN is underlying renal dysfunction.

  31. Risk Stratification • Pre-existing renal impairment • Age • Diabetes • Heart failure • Acute MI • Cardiogenic shock • Nephrotoxins • Hypoalbuminemia • Anemia • Volume depletion Patient related Procedural related • Procedural hypotension • Intra-aortic balloon pump • Cholesterol embolization • Contrast volume and type

  32. Risk Stratification- Risk score • 9639 patients • Multivariate predictors chosen by backward logistic regression with a entry/leave criteria of 0.1 Mehran et al, JACC 2004

  33. CIN PREVENTION

  34. PREVENTION OF CONTRAST-INDUCED NEPHROPATHY • CIN must be discussed in detail during the informed consent process of high-risk patients before use of intravascular iodinated contrast.

  35. Basic concepts in CIN prevention • (1) hydration and volume expansion • (2) choice and quantity of contrast material • (3) pre-, intra-, and postprocedural end-organ protection with pharmacotherapy • (4) postprocedural monitoring and expectant care.

  36. CIN Prevention Trials

  37. HYDRATION

  38. Hydration

  39. Hydration • Normal saline or isotonic sodium bicarbonate is reasonable • Starting 3 to 12 hours before the procedure at a rate of 1 to 2 ml/kg/hr • In those at risk, at least 300 to 500 ml of IV hydration before the contrast material is administered • The postprocedural hydration target is a urine output of 150 ml/hr.

  40. Sodium Chloride Hydration (154 mEq/L of Sodium Chloride) N=68 Sodium Bicarbonate Hydration (154 mEq/L of Sodium Bicarbonate) N=69 Prevention of CIN with Sodium Bicarbonate Patients With Baseline Serum Creatinine 1 to 8 mg/dl who Underwent Contrast Exposure (Iopamidol in All) N=137 Primary endpoint: increase in serum creatinine ≥25% within 2 days post-exposure Merten GJ et al. JAMA, 2004;291:2328-2334

  41. Prevention of CIN with Sodium Bicarbonate: Results Merten GJ et al. JAMA, 2004;291:2328-2334

  42. Iodinated contrast agents

  43. Iodinated contrast agents • lowest rates of CIN with nonionic, iso-osmolar iodixanol (visipaque) • Iodixanol(290 mOsm/kg) is less nephrotoxic than LOCM agents with osmolalities ranging from 600 to 800 mOsm/kg in the volumes of contrast used in trials. • Iodixanol is the contrast agent of choice in patients at high renal risk undergoing PCI

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