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:
- Treat Hypertension
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)
- RenaGel = new non-Calcium/Aluminium-containing phosphate binder (cationic polymer)
- 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
- 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 Dialysis
- 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