Acute Renal Failure

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Acute Renal Failure

• A. Symptoms
• Polyuria, Oliguria or Anuria hematuria
• Dysuria
• Uremia
• Definition symptomatic azotemia
• Acidosis ( tachypnea)
• Mental Status changes
• Hypervolemia / Hypertension
• Hyperkalemia
• Pericarditis

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• Duration
• Oliguria
• Absolute increase Scr by 0.5 or 1.0 mg/dl or
  relative increase 25
• Cockcroft Gault Equation
• (140-age) x wt(kg)
• ------------------------
• Serum Cr x 72

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• B. Etiologies
• Location of Lesion
• Prerenal - 70 of cases
• Intrinsic - 25 of cases
• Post-renal (obstructive) -
• FeNa urine Na x serum Cr
• ------------------------------- X 100
• serum Na x urine Cr
• Prerenal Renal (ATN)
• Urine Na 10
• FeNa 1
• response IVF good poor
• BUN/Scr 20 nl

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• Pre-renal azotemia
• Decreased effective arterial volume
• CHF,,Cirrhosis,,Nephrotic syndrome,,Sepsis
• Renal Artery Stenosis (atherosclerosis,
  fibromuscular dysplasia)
• Cardiopulmonary bypass (3 hours)
• Intravascular volume depletion
• GI lossVomiting..diarrheaetc
• Renal loss diuretc..osmotic diuresis..etc
• Cutaneous loss hyperthermia..burns
• Hemorrhage
• Third space pancreatitis..severe
  hypoalbuminemia..cappillary leak

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• II.Parenchymal Damage
• Nephritis (inflammation) glomerular vs.
  interstitial
• Tubular Injury most common cause of ARF
  Nephrotic Syndrome (total protein losses)
• III. Obstruction of Outflow (5) Urinary Tract
  Infection (UTI) with Pyelonephritis
• Urinary Calculus disease (renal stones)
• Crystal Deposition
• Bladder tumors with extensive invasion
• Prostatic Enlargement BPH vs. Carcinoma
• Unilateral obstruction with only one functioning
  kidney

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• Vascular hypertension
• Atherosclerotic (atheroembolism) - cholesterol
  emboli, 5-10 of hospitalized ARF Trauma
• Vasculitides
• Post-operative - aortic aneurysm repair, aortic
  cross-clamping
• Vasoconstricting Agents - NSAIDs, vasopressors

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• Drug Induced
• ACE Inhibitors
• Radiocontrast Dye Interstitial Nephritis -
  sulfonamides, NSAIDS, other antibiotics
• Amphotericin
• Cis-Platinum
• Aminoglycosides
• Non-steroidal anti-inflammatory drugs (NSAIDs)

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• Pathophysiology
• Ischemia is the underlying problem in ARF
• leads to depletion of cellular ATP and release of
  calcium
• Reactive oxygen species produced leading to
  further cell death
• Calcium release leads to phospholipase activation
  
• Neutrophils may mediate reperfusion injury
  (ICAM-1 is involved)
• Many nephrotoxins are renal vasocontrictors (eg.
  cyclosporine, radiocontrast)

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• C. Initial Evaluation
• Consider possible etiologies and direct
  evaluation
• Medications should always be suspected
• Standard Blood Testing
• Electrolyte/renal panel, Ca2, Phosphate, Mg2,
  Albumin
• Complete Blood Count
• Foley catheter to rule out bladder obstruction

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• Urine for electrolytes, dipstick and microscopic
  analysis
• Osmolality, creatinine, Na, K, Cl-
• Urine spot protein to creatinine ratio (normal is
  
• Pigment Hemoglobin (myoglobin)
• Cells, Casts, Crystals, Organisms
• Consider Urine culture

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• Renal/Pelvic Sono - stones, hydronephrosis, mass
• Consider Abdominal radiograph if ultrasound is
  not done to rule out stones
• ESR, ASO titer, ANA, C3/C4 Anti-GBM Abs
• Renal Biopsy in rapidly progressing disease
• ANCA and Anti-GBM diseases - consider
  cyclophosphamide glucocorticoids
• Idiopathic rapidly progressive glomerulonephritis
  often ANCA positive (other inflammatory diseases
  such as bacterial endocarditis can given ANCA)

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• Pathology Summary
• Glomerular Involvement
• Diffuse all glomeruli in a section are diseased
• Focal some glomeruli in a section are diseased
• Segmental parts of individual glomerulus
  affected
• 2.Focal Glomerulonephritis
• Some glomeruli are dead( necrosis, collapse,
  sclerosis
• b.Acute or chronic inflamation is often seen
• 3.Crescent Glomerulonephritis (very poor
  prognosis)
• Crescent (moon shaped) formation in glomerulus
• Affected glomeruli are non-functional

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• Focal and Segmental Glomerulosclerosis portions
  of many glomeruli are destroyed
• 5. Minimal Change Glomerulonephritis
• a. Glomeruli appear okay, but function is poor
• b. Electron microscopic evidence of basement
  membrane disease
• c. Response to glucocorticoids is usually very
  good
• 6. IgA Deposition
• a.IgA nephropathy
• b.Deposition of IgA immune complexes
• c.Differential includes Systemic Lupus (SLE) and
  Henoch-Schonlein Purpura (HSP)

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• 7. Proliferative Glomerulonephritis
• a. Increase in mesangeal cell number
• b. Usually follows insults (eg.
  Post-Streptococcal)
• May be seen in collagen vascular disease, SLE
• 8. Collapsing Glomerulonephritis
• Major form seen in HIV nephropathy
• Usually late stage
• Rapid progression to renal failure (weeks-months)
  
• No effective therapy to date

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• 9. Tubular Necrosis
• a. Tubular cells die and slough off basement
  membrane
• b. The dead tubular cells form casts which can
  occlude lumen
• c. Glomular basement membrane may also be damaged
  

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• E. Management
• Renal Diet
• Low phosphate, potassium, sodium, and protein
• High calcium and vitamin D
• Various multivitamin formulas available for renal
  patients, eg. Nephrovit
• Low protein diet may slow progression slightly in
  chronic renal disease
• Phosphate and Calcium
• Dangerous if product of Calcium and Phosphage
  70 (mg/dl) (will lead to precipitation)

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• If product is close to 70, then phosphate should
  be lowered with aluminum compounds
• These compounds should be given with meals to
  bind the phosphate directly
• If product is 500-1000mg po tid with meals
• If calcium is low but phosphate normal, then
  calcium should be given before meals
• Consider using 1,25 dihyroxyvitamin D supplements
  

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• 1. Acidosis
• Renal tublar acidosis (RTA) is common in early
  renal failure
• Oral bicitra (citrate replaces bicarbonate) may
  be used
• Bicitra is contraindicated in edematous states
  due to high sodium content
• 2. Hyperuricemia
• Check uric acid levels
• Uric acid deposition in renal tubules may worsen
  progression of renal failure
• Allopurinol may be given (100-200mg po qd) to
  attempt normalization of uric acid

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• 3. Hypertension
• a. ACE inhibitors generally contraindicated in
  moderate to severe renal failure
• Calcium blockers such as nifedipine
• Labetolol is also very effective but patient
  should have LV EF50 and no bronchospasm
• d. Consider Hydralazine for afterload reduction
• e. Pure alpha-adrenergic blocking agents may be
  effective, but tachyphylaxis may occur
• Diuretic improve hypertension/ volume overload

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• 4. Volume overload
• a. Attempt to maximize cardiac output and improve
  intravascular volume
• b. Diuretics often worsen renal failure but may
  be necessary to prevent pulmonary edema
• c. In general, potassium sparing diuretics should
  be avoided (high risk hyperkalemia)
• e. Dopamine or mannitol can be tried, but are
  usually not effective
• f. Albumin infusions are probably not helpful,
  but may help diuresis in low albumin states
• g. Dialysis may be required particularly in
  severe volume overload situations

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• 5. Protein Load
• Reducing protein load is thought to reduce
  azotemia
• Appears to slow progression of CRF
• Patients with moderate renal disease - some
  decrease in progression on low protein diet
• Patients with severe renal disease show no
  benefit on low protein diet
• 6. Hospital inpatients with ARF 50 mortality
  rate

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• 7. Newer Agents
• Atrial natriuretic factor (ANF) dilators
  diuretic
• ANF (Auriculin) ? efficacy in oliguric ARF
• ANF may increase renal dysfunction in diabetics
  receiving radiocontrast
• Brain derived natriuretic factor (BDNF) may be
  effective some patients
• Other vasodilators (eg. calcium channel blockers)
  are not effective
• Investigation renal growth/regeneration factors

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• 8. Dialysis Indications
• Serum abnormalities unresponsive to medical
  therapy
• Severe Acidosis
• Severe Hyperkalemia
• II Uremia
• Mental status changes (usually delirium)
• Nausea and vomiting
• Pericarditis (pericardial friction rub)

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• III Volume Overload
• Hemofiltration or hemodialysis can be used to
  allow recovery of kidney after ARF
• Average duration of need for these therapies was
  9 days in ARF
• After this time, kidneys regain function and
  increase urine output
• Native kidneys may continue with minimal function
  for 6-12 months of hemodialysis
• After that, native kidneys usually shut down
  permanently

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• Kidney Transplantation
• Excellent (and improving) results with cadaveric
  grafts.
• Living Related Donor kidneys superior to CRT
• New kidney usually placed in extraperitoneally in
  the pelvis
• Cyclosporin ,Prednisone, OKT3, mycophenolic acid,
  FK506 immunosuppression
• Combined Kidney Pancreas transplant in Diabetic
  ESRD patients