Chronic Kidney Disease For the PCM

Chronic Kidney Disease For the PCM YOU Can Make a Difference! CMYuan, 2007 Goals and Objectives • Review the K/DOQI definition and classification of chronic kidney disease (CKD) • Review the prevalence and causes of CKD in the US. • Understand the primary evaluation and management of patients with CKD. Defining ―CKD‖  Kidney damage for ≥ 3 months, defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifest by either  Pathologic abnormalities, or  Markers of kidney damage, such as abnormalities of the blood or urine, or in imaging tests (but NOT HTN).  GFR < 60 mL/min/1.73 m2 for ≥ 3 months with or without kidney damage. Defining ―Kidney Damage‖  Pathologic Abnormalities?  By Radiology (US, CT, MR, etc)--e.g.  Multiple cysts consistent with PKD  Extensive scarring  Small kidneys--but be careful of the term ―medical renal disease‖.  REMEMBER: Renal masses or cysts that are not simple should be referred to a UROLOGIST!!  By Histology--ie, renal biopsy Defining ―Kidney Damage‖  Markers of Kidney Damage?  Proteinuria  Microalbuminuria  Hematuria (especially when seen with proteinuria)  Isolated hematuria has a long differential: infection, stone, malignancy, etc.  Casts (especially with cellular elements) NKF-K/DOQI Stages of ―CKD‖ Stage 1 Description GFR (mL/min/1.73m2) 2 3 4 Kidney damage with > 90 normal or  GFR Mild  GFR 60-89 Moderate  GFR Severe  GFR 30-59 15-29 Primary Care Focus is here! 5 Kidney Failure < 15 or dialysis Prevalence of GFR Categories in the USA (There is a lot of CKD!) Stage 3 CKD Prevalence of CKD by GFR in the USA (There is a lot of CKD!) Stage Description GFR (mL/min/1.73m2) > 90 Prevalence Prevalence (%) 1 Kidney damage with normal or  GFR Mild  GFR 5.9 million 3.3% 2 60-89 5.3 million 3.0% 3 4 5 Moderate  GFR Severe  GFR Kidney Failure 30-59 15-29 < 15 or dialysis 7.6 million 400,000 300,000 4.3% 0.2% 0.2% Coresh, et al, Am J Kidney Dis. 2003; 41: 1-12 Causes of ESRD in the USA: Prevalent Counts and Adjusted Rates by Primary Diagnosis 2006 ADR: USRDS U S R D S Trends in the size of the Medicare CKD population, by diabetic status Figure 1.1 700,000 600,000 500,000 400,000 300,000 200,000 100,000 0 92-93 93-94 94-95 95-96 96-97 97-98 98-99 99-00 00-01 Non-diabetic en f b num ma s E Diabetic And the numbers are increasing… Cohort defining Period Patients continuously enrolled in Medicare Part A & Part B in any two consecutive calendar years from 1992 to 2001 (entry period), & alive on the last day of the entry period. Patients enrolled in an HMO or diagnosed with ESRD any time during the entry period are excluded. Estimates of the general Medicare population are based on the 5 percent Medicare sample. CKD Patients Are More Likely to Die than to Progress to ESRD GFR 15-29 GFR 30-59 GFR 60-89; + Proteinuria GFR 60-89, No Proteinuria 0% 20 % 40 60 % % 80 100 % % Died RRT Event Free Disenrolled 5 year follow-up N=27998 Keith, et al, Arch Int Med; 2004; 164:659-663 The Patient with early stage CKD is 5 to 10 times more likely to die from a cardiovascular event than progress to ESRD. Foley RN, Murray AM, Li S, Herzog CA, McBean AM, Eggers PW, Collins AJ. Chronic kidney disease and the risk for cardiovascular disease, renal replacement, and death in the United States Medicare population, 1998 to 1999. J Am Soc Nephrol 2005; 16:489-95. So what do we do about this? Chronic Kidney Disease • In 1999, the NKF approved a proposal for K/DOQI, Kidney Disease Outcomes Quality Initiative (an evolution of the DOQI (Dialysis Outcomes Quality Initiative). • The purpose was to develop clinical practice guidelines for the spectrum of kidney diseases. • In February 2002, Clinical Practice Guidelines for Chronic Kidney Disease (CKD): Evaluation, Classification, and Stratification were published. Find the KDOQI guidelines at http://www.kidney.org/professionals/KDOQI/ Guideline 1. Definition and Stages of Chronic Kidney Disease • Adverse outcomes of CKD can often be prevented or delayed through early detection and treatment. Earlier stages of CKD can be detected through routine laboratory measurements. • The presence of CKD should be established, based on presence of kidney damage and level of kidney function (glomerular filtration rate [GFR]), irrespective of diagnosis. • Among patients with CKD, the stage of disease should be assigned based on the level of kidney function, irrespective of diagnosis, according to the K/DOQI CKD classification Who should we screen? How should we screen? Serum Creatinine, CrCl, and eGFR-Nothing is Perfect!  Serum Creatinine alone CAN NOT be used to accurately assess level of kidney function.  S. creatinine is a function of production (muscle mass) and excretion (both GFR and tubular secretion).  Age, sex, and lean body mass have to be taken into account.  Estimations of eGFR (MDRD equation) and CrCl (Cockcroft-Gault equation) were NOT developed in subjects with normal renal function or normal health. Factors Affecting Serum Creatinine Concentration Increase • Kidney Disease • Ketoacidosis • Ingestion of cooked meat • Drugs: – – – – Trimethoprim Cimetidine Flucytosine Some cephalosporins Decrease • Reduced Muscle Mass • Malnutrition Remember…. GFR normally decreases with age! Cockcroft-Gault Equation to Predict GFR • Developed to predict creatinine clearance, thus an overestimate of GFR • Prediction based on age, gender, creatinine and ideal body weight • ClCr (cc/min) = [140-age] x IBW/72 x SCr x [0.85 if female] • Used almost universally as the basis for drug dosing! MDRD Equation to Predict GFR • Prediction based on age, gender, race and serum creatinine. Developed to follow GFR as part of the Modification of Diet in Renal Disease (MDRD) study. Validated. • GFR/1.73m2 = 186 x [Pcr]-1.154 x [age]-0.203 x [0.742 if female] x [1.212 if AfAm] Get it at http://www.kidney.org/professionals/KDOQI/gfr.cfm TA-DA! (Your on-line link to the MDRD GFR calculator) http://www.kidney.org/professionals/KDOQI/gfr.cfm Cockcroft-Gault vs. MDRD  The MDRD equation estimates GFR.  eGFR is given per 1.73m2 BSA  The Cockcroft-Gault equation estimates CrCl.  CrCl is best used for drug dosing decisions--drug dosing is usually indexed to CrCl. Comparing the Cockcroft-Gault and MDRD: Do these patients have the same level of renal function? • 20 year old AfAm Washington Redskins tackle, weighing 144 kg with a SCr 1.2 mg/dl? ClCr=[140-20][144]/72 x [1.2] =200 cc/min MDRD GFR Value:99 mL/min/1.73 m2 • 93 year old Caucasian female nursing home resident, weighing 44 kg with a SCr 1.2 mg/dl. ClCr = [140-93][44]/72 x [1.2] x 0.85 = 20 cc/min MDRD GFR Value:45 mL/min/1.73 m2 Patient meets definition of Chronic Kidney Disease? YES NO Determine Stage of CKD Determine underlying cause Identify risk factors for progression Identify comorbidites Risk Factor Reduction Tools for Determining the Cause of Chronic Kidney Disease • CKD is often silent. Assessment relies on laboratory testing and imaging. • A Good History! ROS, existence of chronic diseases (DM, HTN, CHF, cirrhosis), medication review, accurate PMH and FH of kidney disease. • Helpful Physical Examination! BP, evidence of co-morbid conditions and complications of CKD. A Simple Laboratory Evaluation! Simplified Classification of CKD by Diagnosis • Diabetic Kidney Disease • Nondiabetic Kidney Disease • Glomerular disease – autoimmune, sytemic infections, drugs, neoplasia, idiopathic • Vascular disease – ischemic renal disease, hypertensive nephrosclerosis, microangiopathy • Tubulointerstitial disease – UTO, stones, UTI, drug toxicity • • Cystic disease Post-Transplant Differential Diagnosis of Chronic Kidney Disease • • • • Everyone deserves a diagnosis! This is especially true for Stage 1 or 2 CKD! When in doubt, consult a nephrologist! Initial evaluation will guide further diagnostics, decisions about renal biopsy and often decisions about treatment and prognosis. So Now What Do You Do? (There’s a lot you can do!) CKD Clinical Action Plan On-Line http://www.kidney.org/professionals/kdoqi/cap/index.html Primary Goals of CKD Care • To prevent cardiovascular events and death • • • • Heart Attacks Congestive Heart Failure Sudden Cardiac Death Stroke • To prevent the progression of CKD to Kidney Failure or ESRD • To prevent complications of CKD • To prepare for dialysis/transplantation in a timely manner Clinical Action Plan • • A Clinical Action Plan should be developed for each patient, based on the stage of CKD (see Table 33). Patients with CKD should be evaluated to determine: – Diagnosis – Comorbid Conditions – Severity, assessed by level of kidney function – Complications, related to level of kidney function – Risk for loss of kidney function – Risk for cardiovascular disease Review of medications should be performed at all visits. Self-management behaviors should be incorporated into the treatment plan at all stages of chronic kidney disease. • • Management of Patients with Chronic Kidney Disease Early Detection of CKD Interventions that delay progression Prevention of Uremic Complications (GFR < 60 cc/min/1.73 m2) Modifcation of Comorbidity Preparation for Renal Replacement Therapy (GRF < 30 cc/min/1.73m2) ACE Inhibitors Anemia Cardiovascular Disease Education An "ESRD Clinic" ARBs Osteodystrophy Kidney Transplant Evaluation Choice of Dialysis Modality BP Control Malnutrition Pre-emptive Transplantation Timely Dialysis Access Placement Blood glucose control Reduced Functioning and Well-being Timely Dialysis Initiation PROGRESSIVE RENAL DAMAGE: The Final Common Pathway RENAL INJURY Reduction in nephron mass Glomerular capillary hypertension Increased BP Increased glomerular permeability to macromolecules Increased filtration of plasma proteins Proteinuria Excessive tubular protein reabsorption Tubulointerstitial inflammation RENAL SCARRING Patient characteristics associated with increased rate of GFR decline Nonmodifiable • African American race • Male gender • Older age • Lower baseline level of kidney function Modifiable • Higher level of proteinuria • Higher BP • Poor glycemic control • Smoking GUIDELINE 13. LOSS OF KIDNEY FUNCTION IN CKD Interventions to slow the progression should be considered in all patients with CKD Interventions proven to be effective include: 1. Strict glucose control in diabetes; 2. Strict blood pressure control; 3. ACEI and ARBs Interventions that may be effective, but studies are inconclusive, include: 1. Dietary protein restriction; 2. Lipid-lowering therapy; 3. Partial correction of anemia. Attempts should be made to prevent acute renal failure: •Volume depletion; •IV contrast; •Some antibiotics (for example, aminoglycosides and amphotericin B); •NSAIDs, including COX 2 inhibitors; •Other drugs: ACEI, ARBs, calcineurin inhibitors •Obstruction. eGFR should be obtained at least yearly in CKD, and more often in patients with: •GFR <60 mL/min/1.73 m2; •Fast GFR decline in the past •Risk factors for faster progression; •Ongoing treatment to slow progression; •Exposure to risk factors for acute GFR decline. Slowing Progression The Earlier, the Better… Interventions that delay progression of CKD: ACEI and ARBs • Mechanisms – Lower systemic blood pressure – Lower glomerular capillary blood pressure and protein filtration – Reduce AT II mediated cell proliferation and fibrosis Should be employed in all proteinuric kidney diseases! Measuring Proteinuria—Get into the right spot! When you get to this point, Don’t continue to get microalbumin! PROGRESSIVE RENAL DAMAGE: The Final Common Pathway RENAL INJURY ACEI ARB Reduction in nephron mass Glomerular capillary hypertension Increased BP Increased glomerular permeability to macromolecules Increased filtration of plasma proteins Excessive tubular protein reabsorption ACEI ARB Proteinuria Tubulointerstitial inflammation RENAL SCARRING ACEI ARB Interventions that delay progression of CKD: ACEI and ARBs • Diabetic Kidney Disease – ACEI or ARB in all diabetic patients with microalbuminuria – ACEI (alt ARB) for Type 1 Diabetics with macroalbuminuria – ARB (alt. ACEI) in Type 2 Diabetics with macroalbuminuria • Nondiabetic Kidney Disease – ACEI/ARB recommended in all proteinuric (>200 mg/g Cr on spot urine) patients with CKD – May tolerate creatinine rise of 35% above baseline – <130/80 is goal – 3 or more drugs may be required! One will probably be a diuretic (thiazide first, then loop) – ACEI and ARB may be used in combination -KDOQI Guideline 8, Table 110 -JNC 7, 2003 http://www.nhlbi.nih.gov/guidelines/hypertension/express.pdf Controlling Hypertension GUIDELINE 7. ASSOCIATION OF LEVEL OF GFR WITH HYPERTENSION -HTN is both a cause and a complication of CKD. -HTN may develop early during the course of CKD and is associated with adverse outcomes—in particular, faster loss of kidney function and development of CVD. -Blood pressure should be closely monitored in all patients with chronic kidney disease. -Treatment of high blood pressure in CKD should include specification of target BP levels, nonpharmacologic therapy, and specific antihypertensive agents for the prevention of progression of kidney disease and development of cardiovascular disease. Pathogenic Mechanisms of High Blood Pressure in CKD • • • • • • • • • • Pre-existing essential hypertension Extracellular fluid volume expansion Renin-agniotensin aldosterone system stimulation Increased sympathetic activity Alteration in endothelium-derived factors(NO/endothelin) Increased body weight Erythropoietin administration PTH secretion/hypercalcemia calcified arterial tree renal vascular disease and renal artery stenosis Relationship between BP and progression of diabetic nephropathy. BP, albumin excretion rate, and GFR in patients with type 1 DMs randomly assigned to a reduction in MAP of 10 mm Hg using metoprolol at 100 to 400 mg/d, hydralazine at 50 to 200 mg/d, and furosemide at 80 to 500 mg/d versus no antihypertensive therapy. Solid circles represent the treated group. Open circles represent the control group. Vertical lines represent standard error. Study was stopped earlier in the control group because of faster decline in GFR. Reprinted with permission.253 Controls Controls Controls Controls BP vs. Time AER vs. Time GFR vs. Time Relationship between MAP and GFR decline (Non-diabetic Pts). Mean GFR decline and achieved follow-up BP in MDRD Study A (patients with baseline GFR 25 to 55 mL/min/1.73 m2). Regression lines relating the estimated mean GFR decline over 3 years to mean follow-up MAP for groups of patients defined according to baseline proteinuria. Within each group, a 3-slope model was used with break points at 92 and 98 mm Hg. Reprinted with permission.255 “Nephrotic” JNC-7 recommends a goal blood pressure of <130/80 mm Hg for individuals with high blood pressure and CKD. http://www.nhlbi.nih.gov/guidelines/hypertension/express.pdf Recommendations for Controlling HTN in Non-Diabetic CKD Population CKD + >200mg/g Prot/Cr Ratio BP Goal <130/80 Nondrug Rx Reduce salt BMI≤25 kg/m2 Mod EtOH Stop Smoking Exercise Same Drug RX ACEI/ARB Then diuretic Then BB or CCB CKD + no proteinuria <130/80 Thiazide/Loop Then ACEI/ARB Then BB or CCB KDOQI Table 118, Guideline 9 Interventions that delay progression of CKD: Strict Glycemic Control • 80% Type I DM with microalbuminuria develop DN in 10-15years, 50% to ESRD – DCCT, benefit of tight control in reducing occurrence subclinical and overt DN(40-60%) • 20-40% Type II DM with microalbuminuria develop DN, 20% to ESRD – UKPDS 33, 25% reduction in microvascular events – Kumamoto – Steno Type 2, 73% reduction in clinical proteinuria Interventions that delay progression of CKD: Strict Glycemic Control Recommended Therapy: • HgbA1c < 7% • Additional information in 2001 ADA Clinical Practice Guidelines www.diabetes.org/clinicalrecommendations/Supple ment101/S3.htm Management of Patients with Chronic Kidney Disease Early Detection of CKD Interventions that delay progression Prevention of Uremic Complications (GFR < 60 cc/min/1.73 m2) Modifcation of Comorbidity Preparation for Renal Replacement Therapy (GRF < 30 cc/min/1.73m2) ACE Inhibitors Anemia Cardiovascular Disease Education An "ESRD Clinic" ARBs Osteodystrophy Kidney Transplant Evaluation Choice of Dialysis Modality BP Control Malnutrition Pre-emptive Transplantation Timely Dialysis Access Placement Blood glucose control Reduced Functioning and Well-being Timely Dialysis Initiation When to Expect Complications… Anemia and CKD • Anemia usually develops during the course of chronic kidney disease and may be associated with adverse outcomes. • Anemia is one of the modifiable complications of CKD. • All individuals with hemoglobin (Hb) levels lower than physiologic norms are considered anemic.  Erythropoietin deficiency is the primary cause of anemia of CKD.  The NKF recommends that evaluation for anemia should occur when GFR <60 mL/min/1.73 m 2; measurement should include Hb level.  Anemia should be treated according to the K/DOQI TM guidelines for anemia of CKD. K/DOQI: Evaluation and Management of Anemia  For Adults with ≥ Stage 3 CKD:  Assess Hemoglobin level  If anemia (HgB ≤ 12)      RBC indices/CBC Reticulocyte count Iron studies Test for occult GI bleeding as indicated Medical evaluation of comorbid conditions  Erythropoetin levels are usually NOT indicated. Prevention of Uremic Complications: Anemia Therapy • Subcutaneous administration of erythropoietin once to thrice weekly (sometimes less). • Supplemental oral or IV iron to keep ferritin > 100 and iron saturation >20%. • Monthly monitoring of Hgb, iron stores. • Monthly adjustments in EPO dose and frequency to meet target Hgb 11-12 g/dl (HCT 33-36%). GUIDELINE 10. ASSOCIATION OF LEVEL OF GFR WITH BONE DISEASE AND DISORDERS OF CALCIUM AND PHOSPHORUS METABOLISM •Bone disease and disorders of calcium and phosphorus metabolism develop during the course of chronic kidney disease and are associated with adverse outcomes. -Patients with GFR <60 mL/min/1.73 m 2 should be evaluated for bone disease and disorders of calcium and phosphorus metabolism. -Patients with bone disease and disorders of bone metabolism should be evaluated and treated—see K/DOQI Clinical Practice Guidelines on Bone Metabolism and Disease in Chronic Kidney Disease (October, 2004). Prevention of Uremic Complications: Osteodystrophy • Osteitis fibrosis cystica, due to 2o HPT, is major form of bone disease. • Check indices of bone and mineral metabolism at GFR < 60 cc/min/1.73m2: – iPTH the earliest marker – Hypocalcemia, hyperphosphatemia – Phosphorus control is cornerstone of treatment Prevention of Uremic Complications: Osteodystrophy Therapy • Restrict dietary phosphorus to 8001,000 mg/d • Calcium-based phosphate binders (but not with Vit D!) to combat hypocalcemia and bind phosphorus • Assure repletion of Vitamin D 25 • Avoid acidosis, HCO3> 23 mEq/l Management of Renal Osteodystrophy is Very Complex! http://www.kidney.org/profess ionals/KDOQI/guidelines_bo ne/index.htm GUIDELINE 9. ASSOCIATION OF LEVEL OF GFR WITH NUTRITIONAL STATUS •Protein energy malnutrition develops during the course of chronic kidney disease and is associated with adverse outcomes. Low protein and calorie intake is an important cause of malnutrition in chronic kidney disease. •Patients with GFR <60 mL/min/1.73 m 2 should undergo assessment of dietary protein and energy intake and nutritional status: •Guideline 23. Panels of Nutritional Measures for Nondialyzed Patients: "For individuals with CRF (GFR <20 mL/min) protein-energy nutritional status should be evaluated by serial measurements of a panel of markers including at least one value from each of the following clusters: (1) Serum albumin; (2) Edema-free actual body weight, percent standard (NHANES II) body weight, or subjective global assessment (SGA); and (3) Normalized protein nitrogen appearance (nPNA) or dietary interviews and diaries. (Evidence and Opinion)" •Guideline 26. Intensive Nutritional Counseling for Chronic Renal Failure: "The nutritional status of individuals with CRF should be monitored at regular intervals." Prevention of Uremic Complications: Malnutrition • Contributors to protein-energy malnutrition(PEM) in CKD: – – – – low protein and calorie intake metabolic acidosis resistance to insulin, GH, IGF-1 proinflammatory cytokines • Assessment of nutritional status requires multiple markers to assess protein status, fat stores, body composition and dietary protein and energy intake. Prevention of Uremic Complications: Nutrition Guidelines • Protein intake – 0.75g/kg/d (RDA) – GFR < 25 cc/min(Stages 4-5) consider 0.6g/kg/d • Energy intake – RDA depends on energy expenditure – GFR < 25 cc/min(Stages 4-5) 30-35kcal/kg/d • Patients with less than recommended intake need frequent follow-up of nutritional status Prevention of Uremic Complications: Just a Word About Immunizations • Don’t forget to continue routine immunizations, e.g. – Tetanus – Pneumococcus – Influenza • Hepatitis B – Check for immunity first--ie, hepatitis B sAb, sAg, cAb – Those who are immune or have chronic infection do not need the vaccine. – All others should receive the vaccine. Don’t wait for dialysis! Patients with advanced chronic kidney disease are less likely to gain immunity from the vaccine. Consider for all Stage 3 or greater CKD patients! Management of Patients with Chronic Kidney Disease Early Detection of CKD Interventions that delay progression Prevention of Uremic Complications (GFR < 60 cc/min/1.73 m2) Modifcation of Comorbidity Preparation for Renal Replacement Therapy (GRF < 30 cc/min/1.73m2) ACE Inhibitors Anemia Cardiovascular Disease Education An "ESRD Clinic" ARBs Osteodystrophy Kidney Transplant Evaluation Choice of Dialysis Modality BP Control Malnutrition Pre-emptive Transplantation Timely Dialysis Access Placement Blood glucose control Reduced Functioning and Well-being Timely Dialysis Initiation GUIDELINE 15. ASSOCIATION OF CHRONIC KIDNEY DISEASE WITH CARDIOVASCULAR DISEASE Patients with CKD, irrespective of diagnosis, are at increased risk of cardiovascular disease (CVD), including coronary heart disease, cerebrovascular disease, peripheral vascular disease, and heart failure. Both ―traditional‖ and ―chronic kidney disease related (nontraditional)‖ CVD risk factors may contribute to this increased risk. -All patients with CKD should be considered in the ―highest risk‖ group for CVD, irrespective of levels of traditional CVD risk factors. -All patients with CKD should undergo assessment of CVD risk factors, including: •Measurement of ―traditional‖ CVD risk factors in all patients; •Individual decision-making regarding measurement of selected ―CKD-related‖ CVD risk factors in some patients. -Recommendations for CVD risk factor reduction should take into account the ―highest-risk‖ status of patients with chronic kidney disease . The most common cause of death among ESRD patients is CVD Fig 5. Causes of death among period prevalent patients 1997–1999, treated with hemodialysis, peritoneal dialysis, or kidney transplantation. Data are from the USRDS 2001 Annual Data Report (www.usrds.org). Abbreviations: MI, myocardial infarction; HD, heart disease. Modification of Comorbidity: Cardiovascular Disease • CVD is the cause of death in 40-50% ESRD patients • ESRD CVD mortality rates 15x higher than general population. • CVD is leading cause of death in patients with CKD, regardless of stage. – HDFP, pts with Cr> 1.7mg/dl, 58% deaths CV – British Regional Heart Study, 50% deaths CV in patients in upper decile of baseline Cr GFR and relative risk for CVD-related death. Wannamethee625: risk is for SCr  1.5 mg% vs SCr  1.3 mg%. Culleton622: risk is for SCr  1.5 mg% and  1.4 mg% vs. <1.5 and <1.4 in men and women respectively. Upper limit for SCr was 3.0 mg%. Mann637: risk is for SC  1.4 mg% vs <1.4 mg%. Ruilope634: risk is for SCr >1.5 mg% vs  1.5 mg%. Upper limit for SCr was 3.0 mg%. Fried640: risk is for SCr  1.5 mg% versus SCr  0.9 mg%. Hemmelgarn642: risk is for SCr >2.3 mg/dL vs  2.3 mg/dL. Proteinuria and relative risk for cardiovascular disease. Where possible, results presented are from multivariable analyses. Agewall650, Ljungman647: Unadjusted results shown. Data not available to calculate age or multivariable adjusted risk. Modification of Comorbidity: Cardiovascular Disease • Patients with CKD should be considered highest risk for CVD. • Aggressive intervention and management of traditional CV risk factors is indicated. • This particularly includes dyslipidemias. – All adults with Stage1-5 CKD should be evaluated for dyslipidemia. – Fasting lipid profile with total cholesterol, LDL, HDL and triglycerides, at baseline, and at least annually. Management of Dyslipidemia in CKD http://www.kidney.org/professionals/KDOQI/guidelines_lipids/index.htm Expert Panel on Detection Evaluation and Treatment of High Blood Cholesterol in Adults. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA, 2001, 285;2486-2497. Management of Patients with Chronic Kidney Disease Early Detection of CKD Interventions that delay progression Prevention of Uremic Complications (GFR < 60 cc/min/1.73 m2) Modifcation of Comorbidity Preparation for Renal Replacement Therapy (GRF < 30 cc/min/1.73m2) ACE Inhibitors Anemia Cardiovascular Disease Education An "ESRD Clinic" ARBs Osteodystrophy Kidney Transplant Evaluation Choice of Dialysis Modality BP Control Malnutrition Pre-emptive Transplantation Timely Dialysis Access Placement Blood glucose control Reduced Functioning and Well-being Timely Dialysis Initiation When to Refer! • Consider co-management with a nephrologist if the clinical action plan cannot be carried out. • Consider subspecialty referral when*: – Unexplained proteinuria (>1gm/day) or microalbumin/Cr ratio >250mg albumin/gCr – Unexplained macroscopic or microscopic hematuria – Diabetes and macroalbuminuria – Multiple and recurring kidney stones – Rapidly deteriorating kidney function – Difficult to control hypertension • Refer to a nephrologist when GFR <30 mL/min/1.73 m2 (CKD Stages 4-5)! Mandatory Referral to Nephrologist guideline, Niagara Health Quality Coalition, NY Fig 11. Level of GFR at initiation of replacement therapy (USRDS). Data from Obrador et al. 77 Most should have started Medicare Eligible Diabetics Preparation for Renal Replacement Therapy (GFR < 30cc/min/1.73m2) • Referral to a Nephrologist allows: – Early identification of RRT modality. – Evaluation for kidney transplantation with goal of pre-emptive transplantation. – REMEMBER, in eligible patients transplantation confers a survival advantage over dialysis! – Identification of social, functional or nutritional needs. Preparation for Renal Replacement Therapy (GFR < 30cc/min/1.73m2) • Close coordination between PCM and nephrologist allows: – Timely placement of dialysis access – Timely initiation of dialysis – Timely referral for transplant evaluation with preemptive transplant if possible. Conclusions • CKD is a public health problem with poor outcomes and high cost. CKD is underdiagnosed and undertreated in the U.S. • Early CKD detection and intervention may increase opportunities for the prevention of ESRD and of complications of CKD, including death. YOU, the PCM, CAN MAKE A Difference!