Chronic renal failure
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| Chronic renal failure | |
| ICD-10 | N18 |
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| ICD-9 | 585 |
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Chronic renal failure Microchapters |
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Chronic renal failure On the Web |
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American Roentgen Ray Society Images of Chronic renal failure |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
Pathophysiology
Epidemiology & Demographics
Natural History, Complications & Prognosis
Diagnosis
- History and symptoms | Lab tests | Electrocardiogram | CT | Echocardiograpgy or Ultrasound | Other Imaging Findings | Other Diagnostic Studies
Causes
Common Causes
Causes by Organ System
Causes in Alphabetical Order
The most common causes of CRF are diabetic nephropathy, hypertension, and glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy.
Historically, kidney disease has been classified according to the part of the renal anatomy that is involved, as:
- Vascular, includes large vessel disease such as bilateral renal artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome and vasculitis
- Glomerular, comprising a diverse group and subclassified into
- Primary Glomerular disease such as focal segmental glomerulosclerosis and IgA nephropathy
- Secondary Glomerular disease such as diabetic nephropathy and lupus nephritis
- Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy
- Obstructive such as with bilateral kidney stones and diseases of the prostate
Treatment
The goal of therapy is to slow down or halt the otherwise relentless progression of CRF to ESRD. Control of blood pressure and treatment of the original disease, whenever feasible, are the broad principles of management. Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression to ESRD.[1][2]
Replacement of erythropoietin and vitamin D3, two hormones processed by the kidney, is usually necessary, as is calcium. Phosphate binders are used to control the serum phosphate levels, which are usually elevated in chronic renal failure.
After ESRD occurs, renal replacement therapy is required, in the form of either dialysis or a transplant.
- Treatment of Reversible Exacerbants
- Volume Depletion
- May be subtle
- Autoregulation impaired with DM, hypertension, CRI--decreases GFR with mild volume depletion
- Careful trial of volume repletion may--return of baseline renal function
- (Increase dietary Na, reduce diuretic dosing)
- Nephrotoxins
- NSAIDs
- Most toxic in setting of volume depletion, CHF, diuretic use
- Reduce prostaglandin (PG) synthesis--unopposed vasoconstriction with decreased GFR
- Can also cause ATN (acute tubular necrosis)
- Aminoglycosides
- Nonoliguric ARF typically occurs at 7-10 days
- Increased risk with older patients, prolonged therapy and greater total dose
- IV contrast
- ARF usually occurs within 24-48 hours of dye administration
- Peak Cr after 5-7 days with return to baseline at 10-14 days
- Risk ARF increased with DM and higher volume of dye
- Note: certain meds increase serum Cr (via inhibiting Cr secretion or interfering with assay) without changing GFR, e.g. cimetidine, trimethoprim (TMP), cefoxitin, flucytosine; BUN will not rise because GFR is preserved
- NSAIDs
- Urinary Tract Obstruction
- Most commonly due to prostatic hypertrophy in men
- Other causes:
- Results in reduced GFR and impaired tubular function
- Consider ultrasound, urologic evaluation
- Volume Depletion
- Reduce Progression
- Protective therapy most effective if initiated early, before Cr > 1.5-2.0 mg/dL
- Treat Hypertension
- Systemic hypertension--elevated intraglomerular pressure +/or glom hypertrophy
- Blood Pressue (BP) control shown in multiple trials to slow progression of renal disease
- Goal BP < 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 renoprotective 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 CRI (GFR 13-25 mL/min)
- Close follow-up by dietician given risk of malnutrition in CRI population
- Control blood sugar:
- Tight control (A1c < 7.0, FBS 70-120) reduces progression in DM I
- Unclear if as beneficial in DM II, but potentially helpful
- Treat complications
- Volume Overload
- Impaired excretion of Na/H2O due to decreased GFR +/- AII/aldo activation
- Restrict dietary Na to 1-2 g/d if hypertension or edema
- Diuretics
- Hyperkalemia
- K usually maintained until GFR < 15-20 mL/min
- Increased risk of hyperkalemia with oliguria, high K diet, (ACEI therapy)
- Increased risk with many meds: ACEI, NSAIDs, K-sparing diuretics, digoxin, TMP
- Increased risk in diabetics with type IV RTA
- Management
- Low K diet (< 60 mEq/d) once GFR < 15 mL/min
- Avoidance of salt substitutes (may contain K salts)
- +/- loop diuretic
- Low dose Kayexelate (5 g with meals) if needed
- Ca/PO4 Abnormalities
- Reduced renal synthesis 1,25-(OH)2D--low serum Ca-- 2° hyperparathyroidism
- (Occurs when GFR < 40 mL/min)
- Reduced GFR--phosphate retention
- Elevated parathyroid hormone (PTH)--mobilization of Ca from bone; increased excretion PO4
- Allows maintenance of normal Ca/PO4 while GFR > 30 mL/min
- Causes renal osteodystrophy
- Once GFR < 25-30 mL/min, hyperphosphatemia occurs
- Therapy goals = normalize Ca/PO4 and maintain parathyroid hormone (PTH)< 200 (2-3x uln)
- Ca/PO4 management should be initiated when Cr ~ 2
- CaxPO4 product should be < 60 to prevent met calcification
- Low PO4 diet: < 800 mg/d (challenging)
- Ca-based oral PO4 binders: Ca acetate or CaCO3 with meals
- Avoid Al-based PO4 binders except for acute therapy of hi CaxPO4 products
- (Al toxicity = osteomalacia, anemia, encephalopathy)
- Avoid Ca citrate (increases gastrointestinal absorption of aluminum)
- RenaGel = new non-Ca/Al-containing PO4 binder (cationic polymer)
- (For patients who cannot tolerate CaCO3 or need additional agent)
- Calcitriol 0.125-0.25 mg/d improves Ca & PTH levels, decreases bone disease
- (Monitor Ca--reduce dose if hyercalcemic)
- Reduced renal synthesis 1,25-(OH)2D--low serum Ca-- 2° hyperparathyroidism
- Metabolic Acidosis
- Occurs when GFR < 25 mL/min due to inability to excrete H+ ions
- Underlying cause = impaired renal NH3 prodxn and HCO3 reabsorption
- Risk = bone buffering of acidosis--worsened osteodystrophy via Ca/PO4 loss
- Increased skeletal muscle breakdown--loss of lean body mass
- Therapy goal = HCO3 > 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 Fe/folate deficiency, etc.
- Generally occurs when Cr > 2-3 mg/dL
- If untreated, hematocrit (Hct) usually stabilizes at ~ 25
- Therapy recommendations = erythropoietin if symptomatic anemia or Hgb < 10 g/dL (in pre-dialysis patients)
- Goal Hct 33-36
- Must replete Fe stores first (oral FeSO4)
- Initial dose ~ 150 U/kg sc weekly to increase Hct
- Maintenance dose ~ 75 U/kg weekly once Hct 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
- Volume Overload
- Plan for Renal Replacement Therapy (RRT)
- Indications for Dialysis
- Malnutrition
- CrCl 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 ESRD 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
Prognosis
See also
References
- ↑ Ruggenenti P, Perna A, Gherardi G, Gaspari F, Benini R, Remuzzi G. Renal function and requirement for dialysis in chronic nephropathy patients on long-term ramipril: REIN follow-up trial. Gruppo Italiano di Studi Epidemiologici in Nefrologia (GISEN). Ramipril Efficacy in Nephropathy. Lancet. 1998 Oct 17;352(9136):1252-6. PMID 9788454.
- ↑ Ruggenenti P, Perna A, Gherardi G, Garini G, Zoccali C, Salvadori M, Scolari F, Schena FP, Remuzzi G. Renoprotective properties of ACE-inhibition in non-diabetic nephropathies with non-nephrotic proteinuria. Lancet. 1999 Jul 31;354(9176):359-64. PMID 10437863.
External links
- National Kidney Foundation
- Renal Failure, Chronic and Dialysis Complications - emedicine.com
- Chronic Renal Failure - emedicine.com
de:Chronisches Nierenversagen id:Gagal ginjal kronis it:Insufficienza renale sv:Kronisk njursvikt