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Recent Advances in Management of CRF

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:

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Recent Advances in Management of CRF

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  1. Recent Advances in Management of CRF Yousef Boobess, M.D. Head, Nephrology Division Tawam Hospital

  2. 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.

  3. STAGES OF Chronic Kidney Disease (CKD) 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)

  4. 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

  5. Dialysis Sessions in Tawam

  6. Incidence Rates of ESRD Therapy 300 250 200 150 100 50 Rate per Million Population 1982 1984 1986 1988 1990 1992 1994 1995 Years U.S. Renal Data System, (1997)

  7. Causes of ESRD in USA 1999 USRDS Report

  8. 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 Team Approach: Primary Helth Care (PHC) Physician and Nephrologist in CKD

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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)

  14. Recognizing Renal Failure,Investigations • Urinalysis: • Urine dipstick & microscopic exam • => Ptu, Htu, pyuria, glycosuria • Blood chemistry: • s.Creatinine, urea (or BUN) • Electrolytes (Na+, K+, CO2, Ca++, Ph--) • GFR: • Estimated or measured • Ultrasound • Morphologic evaluation

  15. 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

  16. 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

  17. Normal s.Creatinine with CRF • Poor production of creatinine: • Severely malnourished patients • Elderly • Small children • Ladies of small size

  18. 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

  19. Estimation of Creatinine Clearance Creat. Cl =1.23 x weight x(140-age)/(s.creat) In Male: In Female 1.03 Cockcroft, Nephron, 1976; 16: 31-41

  20. 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.

  21. 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

  22. Correcting any Reversible Cause

  23. Correction a Reversible Cause“Sarcoidosis”

  24. 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

  25. 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

  26. Slowing the Rate of Progression The earlier we alter factors that damage the kidneys, the better

  27. Successful Intervention Therapeutic Intervention 0 . 0 0 7 0 . 0 0 6 0 . 0 0 5 0 . 0 0 4 0 . 0 0 3 0 . 0 0 2 1/s.cretinine 0 . 0 0 1 0 0 5 1 0 1 5 2 0 Months, follow-up Rashed M., Tawam #125991

  28. InterventionRenal Diet • Protein Restriction • High calories • Law potassium • Law salt • Law phosphate

  29. 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.

  30. 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

  31. Prevalence of LV Disorders at Start of Dialysis Echocardiograms of 413 incident hemodialysis patients Parfrey PS, et al.. Nephrol Dial Transplant. 1996;11:1277-1285

  32. 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: •  Ccr 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.

  33. BP is Poorly Controlled in CKD Coresh J, et al. Arch Intern Med. 2001;161:1207-1216.

  34. 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.

  35. 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

  36. 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

  37. Glycemic Control in Diabetics • Tight control of blood glucose: HbA1C <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

  38. 30 20 10 30 0 0 12 24 36 48 P 20 L 10 50 0 40 0 12 24 36 48 30 20 10 0 0 12 24 36 48 RENAAL Primary Components ESRD Risk Reduction: 28% P p=0.002 % with event L Doubling of Serum Creatinine Risk Reduction: 25% p=0.006 Months P (+ CT) 762 715 610 347 42 L (+ CT) 751 714 625 375 69 % with event ESRD or Death Risk Reduction: 20% p=0.010 P % with event L Months P (+ CT) 295 762 689 554 36 L (+ CT) 52 751 692 583 329 Brenner BM et al New Engl J Med2001;345(12):861-869. Months P (+ CT) 762 715 610 347 42 L (+ CT) 751 714 625 375 69

  39. Hyperlipidemia • In CRF: • Mainly hypertriglyceridemia • => Increases glomerulosclerosis by: • Increasing mesangial proliferation and matrix production • Altering glomerular hemodynamics • Increasing local inflammation

  40. 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

  41. 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

  42. 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

  43. Fluid and Electrolyte DisordersPotassium 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..

  44. Fluid and Electrolyte DisordersAcid-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

  45. 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,..

  46. 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.

  47. 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.

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