Chronic renal failure secondary prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]

Secondary Prevention

Reduce Progression

• Protective therapy most effective if initiated early, before Creatinine > 1.5-2.0 mg/dL
  • Treat Hypertension
    • Systemic hypertension--elevated intraglomerular pressure +/or glom hypertrophy
    • Blood Pressure (BP) control shown in multiple trials to slow progression of renal disease
    • Goal Blood pressure < 130/80-85; < 125/75 in patients with proteinuria > 1-2 g/d
    • ACE inhibitors (ACEI) and Angiotensin II receptor blockers (ARB) preferred 1st line agents due to reno-protective effects
    • Additional agents as needed, including diuretics if volume overload
  • Restrict Dietary Protein
    • Controversial – may decrease intraglomerular pressure
    • Conflicting studies – some show benefit, others do not
    • No significant adverse effects shown in large trial
    • Recommendations
      • No restriction (> 0.8 g/kg/d) if GFR 25-55 mL/min
      • Limit protein to 0.8 g/kg/d if progression or uremic symptoms
      • Limit to 0.6 g/kg/d if severe renal insufficiency (GFR 13-25 mL/min)
    • Close follow-up by dietician given risk of malnutrition in this population
  • Control Blood sugar:
    • Tight control (HbA1c < 7.0, [[Fasting blood sugar 70-120) reduces progression in DM I
    • Unclear if as beneficial in DM II, but potentially helpful

Treat complications

• Volume Overload
  • Impaired excretion of sodium and water due to decreased GFR +/- AII/aldo activation
  • Restrict dietary sodium to 1-2 g/d if hypertension or edema
  • Diuretics
    • Thiazides ineffective if GFR < 25 mL/min (~Creatinine > 2-3)
    • Switch to Loop diuretic as Creatinine rises; may need bid dosing
    • Addition of thiazide to Loop diuretic can--additional Diuresis
    • Watch for excessive volume depletion
• Hyperkalemia
  • Potassium usually maintained until GFR < 15-20 mL/min
  • Increased risk of hyperkalemia with Oliguria, high potassium diet, (ACE inhibitors therapy)
  • Increased risk with many meds: ACEI, NSAIDs, Potassium-sparing diuretics, digoxin, TMP
  • Increased risk in diabetics with type IV RTA
• Management
  • Low potassium diet (< 60 mEq/d) once GFR < 15 mL/min
  • Avoidance of salt substitutes (may contain potassium salts)
  • +/- loop diuretic
  • Low dose Kayexelate (5 g with meals) if needed
• Calcium/phosphate Abnormalities
  • Reduced renal synthesis Calcitriol/Vitamin D--low serum Calcium-- Secondary hyperparathyroidism
  • (Occurs when GFR < 40 mL/min)
  • Reduced GFR--phosphate retention
  • Elevated parathyroid hormone (PTH)--mobilization of Calcium from bone; increased excretion phosphate
  • Allows maintenance of normal Calcium/phosphate while GFR > 30 mL/min
  • Causes renal osteodystrophy
  • Once GFR < 25-30 mL/min, hyperphosphatemia occurs
  • Therapy goals = normalize Calcium/Phosphate and maintain parathyroid hormone (PTH)< 200 (2-3x uln)
    • Calcium/Phosphate management should be initiated when Creatinine ~ 2
    • Calcium x phosphate product should be < 60 to prevent met calcification
    • Low phosphate diet: < 800 mg/d (challenging)
    • Calcium-based oral phosphate binders: Calcium acetate or Calcium carbonate with meals
    • Avoid Aluminium-based phosphate binders except for acute therapy of high Calcium x Phosphate products
      • (Aluminium toxicity = osteomalacia, anemia, encephalopathy)
    • Avoid Calcium citrate (increases gastrointestinal absorption of aluminum)
      • RenaGel = new non-Calcium/Aluminium-containing phosphate binder (cationic polymer)
        • (For patients who cannot tolerate Calcium carbonate or need additional agent)
      • Calcitriol 0.125-0.25 mg/d improves Calcium & Parathyroid hormone levels, decreases bone disease
        • (Monitor Calcium--reduce dose if hypercalcemic)
• Metabolic Acidosis
  • Occurs when GFR < 25 mL/min due to inability to excrete H+ ions
  • Underlying cause = impaired renal ammonia production and bicarbonate reabsorption
  • Risk = bone buffering of acidosis--worsened Osteodystrophy via Calcium/phosphate loss
  • Increased skeletal muscle breakdown--loss of lean body mass
  • Therapy goal = bicarbonate > 22 mEq/L via alkali therapy (NaHCO3 0.5-1 mEq/kg/d)
• Anemia
  • Normocytic normochromic hypoproliferative anemia due to reduced Erythropoietin production
  • May be exacerbated by reduced RBC survival, coexistent iron/folate deficiency, etc.
  • Generally occurs when Creatinine > 2-3 mg/dL
  • If untreated, hematocrit (Hct) usually stabilizes at ~ 25
  • Therapy recommendations = Erythropoietin if symptomatic anemia or Hemoglobin < 10 g/dL (in pre-dialysis patients)
  • Goal Hematocrit 33-36
  • Must replete iron stores first (oral ferrous sulfate)
  • Initial dose ~ 150 U/kg sc weekly to increase Hematocrit
  • Maintenance dose ~ 75 U/kg weekly once Hematocrit goal reached
  • Improves symtoms and may reduce left ventricle (LV) mass (via improvemt of hyperdynamic state)
  • Side effects = increased blood pressure (BP); may need to augment Antihypertensive regimen
• Plan for Renal Replacement Therapy (RRT)
  • Indications for Dialysis
    • Malnutrition
    • Creatinine clearance M 10-15 mL/min
    • Symptoms of uremia related complications (pericarditis, encephalopathy)
    • Hyperkalemia, acidosis not responsive to medical therapy
    • Volume overload / CHF
  • RRT modalities
    • Hemodialysis
    • Peritoneal dialysis
    • Renal transplant
  • Access for hemodialysis should be established when GFR < 25 mL/min (estimated Chronic renal failure within 1 year)
  • Diabetics tend to require dialysis sooner than non-diabetics because more symptomatic at given GFR
• Indications for referral to nephrologist
  • Unclear etiology of new or chronic renal insufficiency
  • For diagnostic evaluation, e.g. biopsy
  • GFR < 50 mL/min: i.e. before vascular access/RRT required

References

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