CHRONIC RENAL FAILURE

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CHRONIC RENAL FAILURE

• JAKUB ZÁVADA
• KLINIKA NEFROLOGIE 1.LF UK

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DEFINITION

• PROGRESSIVE AND IRREVERSIBLE LOSS OF RENAL
  FUNCTION
• K/DOQI CLASSIFICATION
• 1. NORMAL/INCREASED GFR BUT SOME EVIDENCE OF
  RENAL DISEASE
• (microalbuminuria/proteinuria, hematuria,
  histological changes)
• 2. MILD DECREASE OF GFR
• (60-89 ml/min/1,73m2 1-1,49 ml/s/1,73m2)
• 3. MODERATE DECREASE OF GFR
• (30-59 ml/min/1,73m2 0,5-0,99 ml/s/1,73m2)
• 4. SEVERE DECREASE OF GFR
• (15-30 ml/min/1,73m2 0,25-0,49 ml/s/1,73m2)
• 5. KIDNEY FAILURE, RRT TO BE CONSIDERED
• (GFR lt 15 ml/min/1,73m2 0,25ml/s/1,73m2)

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EPIDEMIOLOGY

• INCIDENCE OF ESRD 110 (UK)- 315 (USA)
  PTS/1000000/YEAR (IN 1999)
• PREVALENCE OF ESRD 659 (EU) 1217 (USA)
  PTS/1000000/YEAR (IN 1999)
• INCIDENCE OF ESRD IS RISING AT A RATE OF 6-7 PER
  YEAR
• MOST COMMON ETIOLOGY DM, HYPERTENSION, CHRONIC
  GLOMERULONEPHRITIS
• ESRDEND STAGE RENAL DISEASE
• RRTRENAL REPLACEMENT THERAPY
• CRFCHRONIC RENAL FAILURE
• GFRGLOMERULAR FILTRATION RATE

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FACTORS AFFECTING PROGRESSION OF CRF

• NONMODIFIABLE RISK FACTORS
• UNDERLYING NEPHROPATHY
• AGE, GENDER, RACE, GENES
• MODIFIABLE RISK FACTORS
• PROTEINURIA
• HYPERTENSION
• GLYCEMIA
• LIPIDS
• OBESITY
• HYPERURICEMIA
• SMOKING

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MECHANISMS OF PROGRESSION OF CRF

• GLOMERULOSCLEROSIS
• ENDOTHELIAL INJURY ? MESANGIAL PROLIFERATION ?
  GLOMERULAR SCLEROSIS
• TUBULOINTERSTICIAL SCARRING
• TUBULAR CELL INJURY ? RELEASE OF INFLAMMATORY
  MEDIATORS ? STIMULATION OF RENAL FIBROBLASTS ?
  FIBROSIS
• VASCULAR SCLEROSIS
• ARTERIOLAR HYALINOSIS, LOSS OF PERITUBULAR
  CAPILLARIES ? INTERSTITICIAL ISCHEMIA ?
  INTERSTICIAL FIBROSIS

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CLINICAL PRESENTATION OF CRF

• CHRONIC KIDNEY DISEASE (K/DOQI STAGES 2-4)
• ACUTE-ON-CHRONIC RENAL FAILURE
• LATE REFERRAL OF CRF, UREMIC EMERGENCY

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COMPLICATIONS AND CONSEQUENCES OF CRF

• CARDIOVASCULAR DISEASE
• ANEMIA
• RENAL BONE DISEASE
• METABOLIC ACIDOSIS
• MALNUTRITION
• HYPERVOLEMIA
• HYPERKALEMIA
• BLEEDING DIATHESIS
• DERMATOLOGIC MANIFESTATIONS
• NEUROLOGIC MANIFESTATIONS
• IMMUNOSUPRESSION

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MANAGEMENT OF CRF

• DEFINE THE CAUSE
• LOOK FOR REVERSIBILITY
• PRE-RENAL, DRUG TOXICITY, IMMUNE-MEDIATED,
  INFECTION, OBSTRUCTION, HYPERCALCEMIA,
  HYPERTENSION
• MINIMIZE PROGRESSION OF CRF
• PREVENT AND TREAT COMPLICATIONS OF CRF
• PREPARE FOR RENAL REPLACEMENT THERAPY
• DRUGS
• ADJUST DOSE ANTIMICROBIAL DRUGS, DIGOXIN,
  LITHIUM, CARBAMAZEPINE
• AVOID METFORMIN, NSAID, CYCLOSPORINE, MAGNESIUM

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DIETARY INTERVENTIONS IN CRF

• LOW PROTEIN DIET (?) MDRD STUDY FAILED TO SHOW
  BENEFIT
• LOW-PHOSPHATE DIET (HELPS TO CONTROL
  HYPERPHOSPHATEMIA AND RENAL OSTEODYSTROPHY)
• SUPPLEMENTAION OF FISH OILS (?) PERHAPS HELPFUL
  IN IGA NEPHROPATHY (CONTROVERSIAL)
• SALT RESTRICTION (HELPS TO CONTROL HYPERTENSION
  AND VOLUME OVERLOAD)

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PHARMACOLOGICAL INTERVENTIONS IN CRF

• BLOOD PRESSURE CONTROL
• BP GOAL
• GENERAL POPULATION 140/90
• CKD STAGE 1-4 PROTEINURIAlt1G/DAY 135/85
• CKD STAGE 1-4 PROTEINURIAgt1G/DAY 125/75
• ANTIHYPERTENSIVE AGENTS
• 1) ACEI (ACE INHIBITORS)
• 2) DIURETIC LOW SALT DIET
• 3) ATRA (ANGIOTENSIN RECEPTOR ANTAGONISTS)
• 4) NDCCB (NONDIHYDROPYRIDINE CALCIUM CHANNEL
  BLOCKERS)
• CAVE ACEI and ATRA are renoprotective via
  reduction of intraglomerular pressure, which
  could lead to mild decrease in GFR and mild
  increase in s-creatinin (not a reason to avoid
  them!).
• In older patients and patients with renovascular
  disease these drugs could lead to severe
  deterioration of renal function (close monitoring
  needed, if this happens, avoid them)
• ACEi and ATRA could cause hyperkalemia (close
  monitoring needed)

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SUPPORTIVE CARE AND PREPARATION OF RENAL
REPLACEMENT THERAPY

• SALT, POTASSIUM AND WATER BALANCE
• LOW SODIUM, LOW POTTASIUM DIET, DIURETICS
• SECONDARY HYPERPARATHYROIDISM AND BONE DISEASE
• LOW PHOSPHATE DIET, ORAL PHOSPHATE BINDERS
• VITAMIN D SUPPLEMENTATION
• ANEMIA
• ERYTHROPOETIN
• HBV VACCINATION
• CHOICE OF RRT
• HEMODIALYSIS, PERITONEAL DAILYSIS, PRE-EMPTIVE
  TRANSPLANTATION
• DIALYSIS ACCESS
• TIMING OF STARTING DIALYSIS TREATMENT

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