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Recent Advances in Management of CRF
 

Recent Advances in Management of CRF

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  • I'd like to consider how are we going to do this if the estimates of the prevalence of CKD are anywhere near true, as extrapolated from NHANES. We're talking about 20 million people with CKD, and possibly 20 million more at risk, which is many more than the nephrologists can care for. And yet there is a tremendous opportunity for a collaborative approach, a team approach with the primary care physicians (PCPs) and the nephrology teams. The PCPs are the ones who are going to identify and screen patients who are at risk for CKD, including diabetes, cardiovascular disease, and anemia. They will still remain very active and provide ongoing management of the patients, and will contribute to the education that is so essential if patients are going to take charge of their disease, which is the only way this is going to be effective. But the nephrologists and the nephrology teams have a major opportunity now. They need to help with diagnosis and assessment of these patients. I like to use the term "strategic guidance," and their main opportunity is to provide a pathway, a roadmap, for assisting the primary care team in dealing with the patients. They also have a tremendous opportunity in that they often have educational resources that the PCP does not have at his or her disposal, such as a formal education process. And many of us have, in CKD clinics, the ability to provide epoetin alfa to patients. And this is critically important. I think together this can be done. We don't want to see the example of the nephrologist who sends the patient back. It's analogous to the old time physician who saw a patient with an upper respiratory tract infection (URI) and said, "I can't help you, but come back when you have pneumonia and I can give you an antibiotic." We want to try to prevent that pneumonia. We want to try to prevent end-stage renal disease by participating aggressively with the PCPs
  • The second task is to slow the rate of progression. here we are following the natural history curve with a rapid rate of progression. Here is the hare. if we can initiate non- specific treatment that slow the rate of progression, then we can change the slope of this line and make it more like the tortoise. So you can see that, for example, if the patient presents here, they have two years according to the natural history before they end up with ESRD. But if we could change the slope of the line, they might have four years or six years before they ever face end-stage renal failure.
  • Benefits of BP Control in CKD The benefits of blood pressure control in CKD are clearly shown from a number of studies in blood pressure control. -- We're talking now about using the sixth report of the Joint National Committee on Prevention, Detection, and Treatment of High Blood Pressure (JNC VI) recommendation -- that a blood pressure below 130/85 mm Hg is recommended for people with CKD. If people have proteinuria, an even lower blood pressure level of 125/75 mm Hg is recommended. And in both diabetic and nondiabetic kidney disease, this has been shown to reduce the rate of progression.
  • These are data from Parfrey, where he looked at over 400 incident patients beginning dialysis and results of echocardiograms performed on these patients. Only 16% of these individuals had normal hearts as judged by echocardiography. There were a variety of abnormalities but concentric left ventricular hypertrophy (LVH) was the most common, followed by left ventricular (LV) dilation, and 16% had systolic dysfunction. So this is a problem. We know that patients on dialysis have about the same prevalence of LVH. United States Renal Data System (USRDS) data show that about 75% of CKD patients have LVH.
  • LVH has been shown to be an independent predictor of cardiac death in dialysis patients. There's no reason to believe that this is something that starts the day a patient starts on dialysis. Parfrey's data confirm, as do data by Levin and others, that the prevalence of LVH is not low in patients with CKD. Levin's data showed a 39% prevalence of LVH, and there was a range of CKD probably averaging about stage 3. We can use 39% to say a couple of things. One, there's an opportunity. Thirty-nine percent is not as bad as 75%. Perhaps reducing that is something that we could strive for. On the other hand, 39% is still very high and it's a major problem. Some of the studies are showing that it's not just hypertension, but other factors seem to be important and modifiable predictors of LVH. Statistically, diabetics seem to have an increased risk of LVH, but anemia is also known to be an independent predictor of LVH and can contribute to cardiovascular morbidity and mortality. There is, at least in this study, a predictable increased incidence of LVH depending upon drop in the creatinine clearance. For every 25 mL/min drop, there was a 3% increased risk of LVH. As the blood pressure rose by 5 mm Hg, another 3% increase. But look at what happens with a drop in hemoglobin level. There was a 6% increased risk of LVH as the hemoglobin dropped 1 g/dL. This is very common in patients with CKD.
  • Let's start with blood pressure. These data are summarized from the National Health and Nutrition Examination Survey (NHANES) III by Coresh and colleagues. This study is a cross-sectional study performed periodically by the US government, and it is thought to be representative of the population at large so that extrapolations are made from these data. What the NHANES III data showed as reported by Coresh and colleagues is that increased serum creatinine levels were fairly common. If one looked at the individuals who had increased serum creatinine levels, and we'll use that as our jumping off point to say they have chronic kidney disease and high blood pressure was very common. In fact, most of those who had an elevated serum creatinine were hypertensive. And of those who were hypertensive, three quarters were under treatment. But the sad point is that only 11% of those individuals had blood pressure control that we would consider adequate by today's standard. Most of them had blood pressures that were above 140/90 mm Hg, almost two thirds, and about a quarter had blood pressures that, if you didn't have any target organ damage such as kidney disease, might have been considered all right in the past. This is a sad state of events and continues to emphasize that we have a long way to go, not only in speaking to our colleagues in other disciplines in medicine, but in our own profession, our own specialty.
  • High blood pressure is very prevalent then, but inadequately controlled, even today. In the NHANES study about half of the patients were taking only 1 blood pressure medication. And for those of you who will care for patients with chronic kidney disease (CKD), we know that usually does not do the trick. Several classes of drugs are available. Angiotensin-converting enzyme inhibitors and possibly angiotensin receptor blockers are now considered first-line treatment, and can be used very effectively in combination with diuretics. Or diuretics could be a second-line agent. That point we still need to get across, and there's still a great reluctance by primary care physicians to use these agents for fear that they will damage the kidneys rather than preserve function. So this is an area where we still have a lot of work to do.
  • Slide 14: RENAAL: Components of the Primary Composite Endpoint This slide shows the individual Kaplan-Meier plots for the components of the composite primary endpoint. Doubling of serum creatinine and ESRD are both important renal endpoints. Once-daily losartan + CT significantly reduced the risk of the development of doubling serum creatinine (25%; p=0.006) and ESRD (28%; p=0.002). 2 The composite endpoint of ESRD or death also showed a significant risk reduction (20%; p=0.010). There was no significant risk reduction of death alone with losartan + CT. 2 REF2 pp 865 A REF2 pp 865 C
  • These studies from Foley and others show that for every 1 g/dL fall in hemoglobin in dialysis patients, the odds ratio of left ventricular dilation is increased by 42%. Heart failure as a risk is increased. You get increased risk for de novo heart failure, first, second, or recurrent attacks, and you get an increase in death. And this is an independent risk factor.
  • In conclusion, the data suggest that epoetin alfa and IV iron in patients with heart failure improves anemia, heart failure status, ejection fraction, and New York Heart Association class. It decreases hospitalization, lowers diuretic doses, and slows the deterioration of renal function. This is a triangle. I want to put 3 things on that triangle. On the top I want to put heart failure, on one side chronic kidney disease, and on the other side anemia. There are 3 new concepts here. The first concept is that heart failure is a cause of anemia. We didn't know that. The second thing is that anemia may be an important cause of heart failure. We may have known it but the cardiologist didn't. And the third thing is that anemia may actually cause progressive renal failure.. Hopefully we can destroy this vicious circle of destruction by active treatment of the congestive heart failure, and control of the anemia.
  • The fate of the dialysis patient is cast in the predialysis period. Patients come to end-stage renal failure with end-stage heart failure, and that isn't good. Congestive heart failure is a common and crucial contributor to the progression of chronic renal disease. That is a new concept. The treatment of anemia in patients with heart failure may improve both the cardiac and the renal function. To save the heart and the kidney, treat the anemia

Recent Advances in Management of CRF Recent Advances in Management of CRF Presentation Transcript

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  • Recent Advances in Management of CRF Yousef Boobess, M.D. Head, Nephrology Division Tawam Hospital
  • What is chronic renal failure ? Definitions
    • Azotemia:
      • Elevated blood urea and creatinine
    • Chronic renal failure:
      • The irreversible , substantial, and usually long-standing (>3 months) loss of renal function .
    • Uremia:
      • Azotemia with symptoms or signs of renal failure
    • End-stage renal disease (ESRD):
      • The degree of CRF that without renal replacement treatment would result in death.
  • Urinary abnormalities (GFR  90 ml/min) Mildly impaired (GFR 60 - 89 ml/min) Moderate CRF (GFR 30 - 59 ml/min) Severe CRF (GFR 15 - 29 ml/min) ESRD (GFR < 15 ml/min) STAGES OF Chronic Kidney Disease (CKD)
  • Epidemiology
    • The number of ESRD patients is increasing rapidly, with very costly treatment
    • Early recognition of renal disease and appropriate interventions may decrease
      • Human suffering
      • Financial costs associated with ESRD
  • Dialysis Sessions in Tawam
  • Incidence Rates of ESRD Therapy U.S. Renal Data System, (1997) 1982 1984 1986 1988 1990 1992 1994 1995 Years Rate per Million Population 300 250 200 150 100 50
  • Causes of ESRD in USA 1999 USRDS Report
  • Team Approach: Primary Helth Care (PHC) Physician and Nephrologist in CKD
    • PHC Physician
    • Early recognition of renal disease
      • PHC Physicians treat patients with DM, HTN
    • Timely referral to a Nephrologist
    • Collaboration with a Nephrologist to provide long term care
    • Patient education
    • Nephrologist
    • Diagnose and assess patients
    • Assist in developing strategic guidance
    • Recommend and implement patient care
    • Provide role-specific patient education
  • Principles of Management of CKD Patients
    • Early recognition of CKD
      • Estimate the severity of CKD
      • What is the cause of CKD?
    • Detection and correction of any reversible cause. Avoidance of additional renal injury
    • Institution of interventions to delay progression
    • Treatment of complications
    • Planning for renal replacement therapy
  • Principles of Management of CKD Patients
    • Early recognition of CKD
      • Estimate the severity of CKD
      • What is the cause of CKD?
    • Detection and correction of any reversible cause. Avoidance of additional renal injury
    • Institution of interventions to delay progression
    • Treatment of complications
    • Planning for renal replacement therapy
  • Recognizing Renal Failure, Clinical Features
    • Mild to Moderate renal failure:
      • Usually no symptoms
    • Severe renal failure: non specific
      • Pale, fatigueability & shortness of breath
      • Hypertension, headaches
      • Polyuria/nocturia
      • Body itch
      • Poor appetite, nausea, vomiting
      • Hyperventilation
      • Swelling of the face and legs
  • Recognizing Renal Failure, Clinical Features
    • Mild to Moderate renal failure:
      • Usually no symptoms
    • Severe renal failure: non specific
      • Pale, fatigueability & shortness of breath
      • Hypertension, headaches
      • Polyuria/nocturia
      • Body itch
      • Poor appetite, nausea, vomiting
      • Hyperventilation
      • Swelling of the face and legs
  • Hyperventilation
    • 13 y-o-f, came to ER with hyperventilation
    • ER physician examined her  psychosis  valium, reassured the family & DC
    • No improvement  taken to another hospital  Blood Chemistry & ABGs
    •  ESRD with very severe metabolic acidosis (Bicarbonate ~ 2.7 mmol/l)
  • Recognizing Renal Failure, Investigations
    • Urinalysis:
      • Urine dipstick & microscopic exam
      • => Ptu, Htu, pyuria, glycosuria
    • Blood chemistry:
      • s.Creatinine, urea (or BUN)
      • Electrolytes (Na + , K + , CO 2 , Ca ++ , Ph -- )
    • GFR:
      • Estimated or measured
    • Ultrasound
      • Morphologic evaluation
  • s.Creatinine Concentration
    • Normal values:
      • <115 umol/L in males (1.3 mg/dL)
      • <90 umol/L in females (1 mg/dL)
    • Changes in its level are more important:
      • an increase from 55 to 110 umol/L represents a 50% decline in renal function
    • Limitations
  • High s.Creatinine with Normal GFR
    • Spurious elevation:
      • Cephalosporin
      • DKA
      • Alcohol intoxication
    • Blocking tubular secretion:
      • Cimetidine or trimethoprim
    • Increased creatinine production:
      • Exogenous: ingestion of large quantities of cooked meat
      • Endogenous: Muscular disorders, or increases in muscular mass
  • Normal s.Creatinine with CRF
    • Poor production of creatinine:
      • Severely malnourished patients
      • Elderly
      • Small children
      • Ladies of small size
  • Glomerular Filtration Rate “GFR”
    • Normal values:
        • In males 120  20 mL/minute
        • In females 115  20 mL/minute.
    • Creatinine Clearance (24-h urine collection)
    • Creatinine Clearance in Severe CKD:
      • Overestimate GFR due to the tubular secretion
      • To correct this overestimation:
        • Take the average of urea and creatinine clearances
        • Or give oral cimetidine 1200 mg, 3h before collection
  • Estimation of Creatinine Clearance Creat. Cl =1.23 x weight x(140-age)/(s.creat) In Male: In Female Cockcroft, Nephron, 1976; 16: 31-41 1.03
  • Determine the cause of CKD
    • A specific diagnosis is needed:
      • To consider specific TRT:
        • obstructive uropathy, analgesic NP, drug-related IN, RPGN, SLE, vasculitis, accelerated HTN, tuberculosis, myeloma, amyloid, ..
      • To be aware of potential complications:
        • SLE, DM..
      • To advise the family:
        • PKD or other familial renal disease.
  • Principles of Management of CKD Patients
    • Early recognition of CKD
      • Estimate the severity of CKD
      • What is the cause of CKD?
    • Detection and correction of any reversible cause. Avoidance of additional renal injury
    • Institution of interventions to delay progression
    • Treatment of complications
    • Planning for renal replacement therapy
  • Correcting any Reversible Cause
  • Correction a Reversible Cause “Sarcoidosis”
  • Volume Depletion
    • Causes:
      • Diarrhea, vomiting, iatrogenic (surgery, overzealous use of diuretics)
      • Renal loss
      • Worsening renal arterial stenosis, cholesterol emboli
    • Volume repletion
      • Restores renal function promptly
      • Some degree of transient or permanent damage may occur
  • Principles of Management of CKD Patients
    • Early recognition of CKD
      • Estimate the severity of CKD
      • What is the cause of CKD?
    • Detection and correction of any reversible cause. Avoidance of additional renal injury
    • Institution of interventions to delay progression
    • Treatment of complications
    • Planning for renal replacement therapy
  • Slowing the Rate of Progression
      • The earlier we alter factors that damage the kidneys, the better
  • Successful Intervention 0 0 . 0 0 1 0 . 0 0 2 0 . 0 0 3 0 . 0 0 4 0 . 0 0 5 0 . 0 0 6 0 . 0 0 7 0 5 1 0 1 5 2 0 1/s.cretinine Therapeutic Intervention Months, follow-up Rashed M., Tawam #125991
  • Intervention Renal Diet
    • Protein Restriction
    • High calories
    • Law potassium
    • Law salt
    • Law phosphate
  • Intervention: Controlling BP in CKD
    • Target BP:
      • CKD: <130/85 mm Hg
      • If proteinuria: <125/75 mm Hg
    • Benefits
      • Slows the progression of CKD , especially if proteinuria
      • Reduces the cardiovascular complications
    Zabetakis PM, Nissenson AR. Am J Kid Dis . 2000;36(suppl):S31-S38.
  • BP Control and GFR Decline
    • Parving HH et al. Br Med J 1989 Moschio G et al. NEJM 1996
    • Viberti GC et al. JAMA 1993
  •  
  • Prevalence of LV Disorders at Start of Dialysis Parfrey PS, et al.. Nephrol Dial Transplant . 1996;11:1277-1285 Echocardiograms of 413 incident hemodialysis patients
  • Consequences of CKD: (LVH)
    • LVH is an independent predictor of cardiac death in dialysis patients.
    • Hypertension, anemia and diabetics are modifiable predictors of LVH
    • Increase in LVH risk: For each:
      •  C cr of 25 mL/min => 3% increased risk of LVH.
      •  Systolic BP by 5 mm Hg => 3% increased risk.
      •  Hemoglobin by 1 g/dl => 6% increased risk of LVH
    Levin A, et al. Am J Kid Dis . 1996;27:347-354.
  • BP is Poorly Controlled in CKD Coresh J, et al. Arch Intern Med . 2001;161:1207-1216.
  • Blood Pressure Control
    • Several classes of drugs are available
    • Some can slow the decline of GFR:
      • First-line treatment:
        • ACE inhibitors & angiotensin receptor blockers
          • There's still a great reluctance by PHC physicians to use them for fear that they will damage the kidneys rather than preserve function.
        • Diuretics in combination with ACE inhibitors.
    JNC VI. Arch Intern Med . 1997;157:2413-2446.
  •  
  • Reno-protective Effect of ACEis
    • ACEis (independent of their antihypertensive action):
      • Decrease proteinuria
      • Delay the progression of renal disease
    • Mechanisms:
      • Dilatation of EA =>reducing intra-glomerular pressure
      • Restoration of glomerular perm-selectivity in proteinuric NPs
      • ? Effect on the GH like of AII
  • Adverse Effects of ACEis
    • Acute worsening of renal function
      • if bilateral renal artery stenosis or if decreased effective circulating volume
      • advices:
        • monitor renal function after initiation of ACEi
        • in high risk patients: renal scan with captopril test
        • adjust the dose according to the renal function
    • Hyperkalemia
      • same considerations apply
  • Glycemic Control in Diabetics
    • Tight control of blood glucose: Hb A1C <7%
      • Delay the onset of microalbuminuria
      • Decrease or stabilize protein excretion in patients who already had microalbuminuria
    • ACE inhibitors, and ARBs:
      • Delay the progression of kidney dysfunction.
    Zabetakis PM, Nissenson AR. Am J Kid Dis . 2000;36(suppl):S31-S38. The Diabetes Control and Complications Trial, long-term Sweden study, Japanese study
  • RENAAL Primary Components ESRD Months % with event p=0.002 Risk Reduction: 28% P L ESRD or Death P (+ CT) L (+ CT) Months % with event 751 714 625 375 69 762 715 610 347 42 P L p=0.010 Risk Reduction: 20% Doubling of Serum Creatinine Months % with event p=0.006 Risk Reduction: 25% 751 692 583 329 52 762 689 554 295 36 P (+ CT) L (+ CT) P (+ CT) L (+ CT) 751 714 625 375 69 762 715 610 347 42 Brenner BM et al New Engl J Med 2001;345(12):861-869. 0 12 24 36 48 0 10 20 30 0 12 24 36 48 0 10 20 30 40 50 0 12 24 36 48 0 10 20 30 P L
  • Hyperlipidemia
    • In CRF:
      • Mainly hypertriglyceridemia
    • => Increases glomerulosclerosis by:
      • Increasing mesangial proliferation and matrix production
      • Altering glomerular hemodynamics
      • Increasing local inflammation
  • Smoking Cessation
    • All patients with renal disease should be encouraged to quit smoking
      • DM is 3 to 4 times more common in smokers than in nonsmokers
      • Smoking increases the relative risk for progression of CRF in nondiabetics
    • Former smokers have an intermediate risk
  • Principles of Management of CKD Patients
    • Early recognition of CKD
      • Estimate the severity of CKD
      • What is the cause of CKD?
    • Detection and correction of any reversible causes. Avoidance of additional renal injury
    • Institution of interventions to delay progression
    • Treatment of complications
    • Planning for renal replacement therapy
  • Fluid and electrolyte disorders Sodium and Water
    • Most often:
      • Impaired Na excretion => Edema, HTN, CHF
      • TRT:
        • Moderate Na + restriction
        • Loop diuretics
    • In some patients:
      • Salt wasting => volume depletion => worsening of CRF
      • TRT:
        • Na + replacement
  • Fluid and Electrolyte Disorders Potassium Balance
    • Hyperkalemia
      • Develops in advanced CRF
      • Can occur earlier in patients with:
        • Tubulointerstitial disease
        • Diabetic NP and hyporeninemic hypoaldosteronism
        • Drugs: as ACEis, A2 antagonist, b- blockers, NSAIDs, K + sparing diuretics, trimethoprim, salt substitutes..
      • TRT:
        • Dietary K + restriction,
        • loop diuretics,
        • K + exchange resins..
  • Fluid and Electrolyte Disorders Acid-Base Disorders
    • Metabolic acidosis:
      • Occurs relatively early
    • Treatment:
      • Decrease protein intake
      • Alkali supplementation if bicarbonate < 17mEq/L
        • Na bicarbonate or Na citrate, 1 mEq/kg/day
        • This will prevent:
          • Excessive bone loss
          • Muscle breakdown
          • Tubulointerstitial inflammation
  • Hypocalcemia & Hyperphosphatemia
    • Hypocalcemia
      • Deficiency in Vit.D, Hyperphosphatemia
    • Hyperphosphatemia
      • Early in renal failure: Ph -- clearance => Ph -- => PTH => Ph -- clearance
        • Frank hyperphosphatemia occur if GFR < 30 mL/min
    • Management:
      • Dietary phosphate restriction
      • Phosphate binders: Ca carbonate, Renalgel,..
      • Vit D: Rocaltrol, One Alpha,..
  • Anemia
    • Present when GFR < 30-35 mL/min
    • Causes:
      • Reduced EPO production
      • Others: iron deficiency, rapid destruction of RBC,..
    • Anemia is an independent risk factor for death in CHF
      • Studies of Left Ventricular Dysfunction (SOLVD) 7000 patients
        • 1% lower Hct was associated with 1% higher risk of mortality
    Al Ahmad. et al. J Am Coll Cardiol . 2001;38:955-962.
  • Independent Risk of a Fall in Mean Hb of 1 g/dL in Dialysis Patients Foley PS, et al. Am J Kidney Dis . 1996;28:53-61.
    • Death
    • IHD
    • Recurrent cardiac failure
    • De novo cardiac failure
    • LV Dilation
    0.02 0.05 0.02 0.02 P NA 1.14 1.20 1.28 1.42 Odds ratio
  • Cardio - Renal - Anemia Syndrome CKD CHF Anemia Vicious Circle of Destruction
  • Cardio - Renal - Anemia Syndrome
    • CHF is a common and crucial contributor to the progression of CKD. (new concept)
    • Treatment of anemia in patients with CHF may improve both the cardiac and the renal function
    • => To save the heart and the kidney, treat the anemia
  • Treatment of Anemia
    • Target Hgb 11 to 12 g/dL
    • Epoetin:
      • Dose: 50 U/kg/inj, iv or sc
      • 1-3 times/week
    • IV Iron Sucrose:
      • Target:
        • Serum ferritin: 100 - 500 ng/mL
        • Transferrin saturation: 20 – 50%.
      • Dose: 100 mg/session X 10, then reevaluate
  • Principles of Management of CRF Patients
    • Early recognition of CRF
      • Estimate the severity of CKD
      • What is the cause of CRF?
    • Detection and correction of any reversible cause. Avoidance of additional renal injury
    • Institution of interventions to delay progression
    • Treatment of complications
    • Planning for renal replacement therapy
  • Planning for Renal Replacement Therapy
    • Options of RRT should be discussed:
      • Difference modalities of dialysis
        • HD, PD
      • Transplantation
        • Possibility of preemptive Tx
    • Outcomes are optimal when RRT is initiated in a planned manner
      • HD => need for A-V fistula (4-6 months)
      • Tx: work-up
  • TRADITIONAL DIALYSIS START
  • Timely Dialysis Start
  • EARLY DIALYSIS START
    • Early dialysis start (CrCl > 10 ml/min) vs late dialysis start (CrCl < 4 ml/min):
      • => higher 12 yr survival (85% vs 51%)
          • [Bonomini et al Kidney Int 17:S57 1985]
      • => improved quality of life at 6 months post initiation of RRT
          • [Korevaar et al AJKD Jan 2002]
  • Conclusion, 1
    • Early recognition of renal disease
    • Early referral to Nephrologist
    • Detect and correct any reversible cause
    • Avoid any additional renal injury
    • Use ACE inhibitors whenever it is indicated
    • Lipid-lowering drugs
  • Conclusion, 2
    • Avoid:
      • Nephrotoxic drugs:
        • NSAIDs, aminoglycosides, radiocontrast
    • In moderate to severe CRF:
      • Diuretic therapy: often necessary
      • Dietary potassium restriction
      • Potassium exchange resins if hyperkalemia
      • Alkali supplementation: if CO 2 < 16-17 mEq/L
      • Phosphate binders, Vit D
      • EPO, Iron