Chronic renal failure secondary prevention: Difference between revisions
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{{Chronic renal failure}} | {{Chronic renal failure}} | ||
{{CMG}} {{AE}} {{AN}} | {{CMG}} {{AE}} {{AN}}{{SSW}} | ||
== Overview == | |||
Effective measures for the secondary prevention of chronic renal failure include reducing [[progression]], treating [[Complication (medicine)|complication]], and [[renal replacement therapy]](RRT). | |||
==Secondary Prevention== | ==Secondary Prevention== | ||
===Reduce Progression=== | ===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 antagonist|Angiotensin II receptor blockers]] (ARB) preferred 1st line agents due to reno-protective effects.<ref name="pmid3651580">{{cite journal |vauthors=Lerche D, Kozlov MM, Markin VS |title=Electrostatic free energy and spontaneous curvature of spherical charged layered membrane |journal=Biorheology |volume=24 |issue=1 |pages=23–34 |date=1987 |pmid=3651580 |doi= |url=}}</ref> | |||
*** 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 [[Uremia|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 [[Diabetes Mellitus Type 1|DM I]]. | |||
*** Unclear if as beneficial in [[Diabetes Mellitus Type 2|DM II]], but potentially helpful. | |||
* | ===Treat complications=== | ||
* | * Volume Overload | ||
* | ** Impaired excretion of sodium and water due to decreased [[GFR]] +/- [[Aldosterone|AII/aldo]] activation. | ||
*:* | ** Restrict dietary sodium to 1-2 g/d if [[hypertension]] or [[edema]]. | ||
* | ** [[Diuretic]]s | ||
* | *** [[Thiazide]]s 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 [[K|potassium]] diet, ([[ACEI|ACE inhibitors]] therapy). | ||
* | ** Increased risk with many meds: [[ACEI]], [[NSAID]]s, [[Potassium-sparing diuretic]]s, [[digoxin]], [[TMP]]. | ||
* | ** Increased risk in diabetics with [[Renal tubular acidosis|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 [[Hypercalcemia|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 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]] 10-15 mL/min | |||
**[[acidosis]] not responsive to medical therapy | |||
**Volume overload / [[CHF]] | |||
**[[Uremic pericarditis]] | |||
**[[Uremic encephalopathy]] | |||
**Intractable [[muscle cramps]] | |||
**[[Anorexia]] and [[nausea]] not attributable to reversible causes such as [[peptic ulcer disease]] | |||
**[[Protein energy malnutrition]] | |||
**[[Hyperkalemia]] | |||
**Extracellular fluid volume overload | |||
Recent studies have shown no benefits of initiating early dialysis with improved patient survival. <ref name="pmid20581422">{{cite journal |author=Cooper BA, Branley P, Bulfone L, ''et al.'' |title=A randomized, controlled trial of early versus late initiation of dialysis |journal=[[The New England Journal of Medicine]] |volume=363 |issue=7 |pages=609–19 |year=2010 |month=August |pmid=20581422 |doi=10.1056/NEJMoa1000552 |url=}}</ref>However, advanced preparation for [[dialysis]] can help avoid complications like poorly functioning fistula for [[hemodialysis]] or malfunctioning [[peritoneal dialysis]] catheter, [[sepsis]], [[bleeding]] and [[thrombosis]]. | |||
*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== | ==References== |
Latest revision as of 19:11, 6 August 2018
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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]Sargun Singh Walia M.B.B.S.[3]
Overview
Effective measures for the secondary prevention of chronic renal failure include reducing progression, treating complication, and renal replacement therapy(RRT).
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.[1]
- 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 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 10-15 mL/min
- acidosis not responsive to medical therapy
- Volume overload / CHF
- Uremic pericarditis
- Uremic encephalopathy
- Intractable muscle cramps
- Anorexia and nausea not attributable to reversible causes such as peptic ulcer disease
- Protein energy malnutrition
- Hyperkalemia
- Extracellular fluid volume overload
Recent studies have shown no benefits of initiating early dialysis with improved patient survival. [2]However, advanced preparation for dialysis can help avoid complications like poorly functioning fistula for hemodialysis or malfunctioning peritoneal dialysis catheter, sepsis, bleeding and thrombosis.
- 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 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
- ↑ Lerche D, Kozlov MM, Markin VS (1987). "Electrostatic free energy and spontaneous curvature of spherical charged layered membrane". Biorheology. 24 (1): 23–34. PMID 3651580.
- ↑ Cooper BA, Branley P, Bulfone L; et al. (2010). "A randomized, controlled trial of early versus late initiation of dialysis". The New England Journal of Medicine. 363 (7): 609–19. doi:10.1056/NEJMoa1000552. PMID 20581422. Unknown parameter
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