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123 123 Presentation Transcript

  • Acute Renal Failure   Presented by Peter Fumo, MD, FACP
  • Pre-renal Azotemia   Intra-renal Azotemia   Post-renal Azotemia
  •  
  • Counterregulatory Responses to Decrease in Effective Circulating Blood Volume   Increased Sympathetic Tone   Increase in renin-angiotensin system characterized by a increase in angiotensin II and aldosterone   Increase in ADH
  • Net Effects:   Increased efferent arteriolar tone due to AII to maintain SNGFR   Decreased afferent arteriolar tone due to increased nitric oxide and prostaglandin synthesis stimulated by AII to maintain SNGFR   Increased tubular sodium reabsorption proximally due to AII and distally due to aldosterone   Increase in water reabsorption and urinary concentration due to ADH   Increase in urea reabsorption due to increased sodium and water reabsorption
  • Urinary indices will therefore display low urinary sodium (<20 Meq/l)   Low fractional excretion of sodium (< 1%)   Low fractional excretion of urea (< 35%)   High urine osmolarity (> 600 mOsm)   Urinalysis will show high urine SG and low urine pH   BUN/Cr ratio will be > 20:1
  •     Renal autoregulation will help maintain GFR and creatinine clearance Pre-renal azotemia simply means diminished renal blood flow and is reversible   Low cardiac output due to low preload due to volume depletion, third-spacing or pulmonary hypertension (e.g. acute PE)   Low cardiac output due to pump failure, valvular heart disease or tamponade   Systemic vasodilation with shunting of blood away from renal vasculature such as in septic shock or liver failure   Defects in autoregulation or medications that interfere with autoregulation
  • Treatments include:   Restoring intravascular volume   Stopping certain medications such as NSAIDs, ARBs or ACE Is   Allowing BP to drift up with defective autoregulation     Inotropic support with pump failure   Norepinephrine, volume and perhaps vasopressin with vasodilatory shock
  • Post-renal Azotemia   Due to obstruction to urinary outflow   Diagnosed usually by ultrasound   Urinalysis is bland   Hyperkalemic metabolic acidosis common   Treatment is to relieve the obstruction
  • Intrarenal Etiologies include:   Vascular   Acute Tubular Necrosis   Acute Glomerulonephritis   Acute Interstitial Nephritis   Tubular Obstruction
  • Acute Tubular Necrosis   Most common inpatient etiology   Can be ischemic or due to nephrotoxins   Urinalysis shows isosthenuric urine with granular casts, usually seen with ischemic oliguric ATN   Urinary sodium >40 mEq/l, fractional excretion of sodium > 3% and fractional excretion of urea >35% with oliguria   Urine osmolarity < 400 mOsm   BUN/Cr ratio < 10:1
  • Nephrotoxic ATN can be due to endogenous toxins such as hemoglobin and myoglobin, or exogenous toxins such as aminoglycosides or dye   Hemoglobin or myoglobin gives a positive dipstick for blood in the absence of RBCs   Rhabdomyalysis can give rise in serum creatinine > 2 mg/dl/day   Treatment of ischemic ATN is to restore renal perfusion   Treatment of nephrotoxic ATN is usually fluids and to stop offending nephrotoxins
  • Vascular etiologies:   Acute injury to renal vessels   Characterized by elevations in BP, nonspecific urinalysis but often proteinuria and hematuria   Urinary indices can look like pre-renal azotemia   Examples include malignant hypertension, TTP and HUS which are all characterized by schistocytes   Atheroemboli for which eosinophilia and eosinophiluria common   Renal infarction-elevated LDH, ALT
  • Acute Glomerulonephritis   Usually develops in outpatient setting   Urinalysis is key to diagnosis and show proteinuria, hematuria and RBC casts   Can see low urine sodium and isosthenuric urine   Relatively rare cause compared to others   Biopsy required for definitive diagnosis   Treatment usually entails immunosuppression
  • Acute Interstitial Nephritis   Usually allergic in origin from medications such as antibiotics   Can see rash, fever, eosinophilia   Urinalysis shows hematuria, pyuria, WBC casts and eosinophils   NSAIDs do not give eosinophilia, eosinophiluria or rash but does give proteinuria due to MCD   Treatment is to remove offending drug and perhaps steroids
  • Tubular obstruction   Can be due to endogenous proteins such as Bence-Jones proteins (SSA positive)   Can be due to endogenous crystals such as uric acid (acid urine, pleomorphic crystals and urine uric acid to creatinine ratio > 1)   Exogenous crystals due to medications such as acyclovir, sulfa drugs and indinivir   Treatment is intravenous fluids, forced diuresis and urinary alkalinization with uric acid
  •   Trial of intravenous fluids often helpful General Diagnostic Approach Careful assessment of volume status Careful look at medications Careful look at recent radiologic studies Urinalysis Urinary Indices especially if oliguric Differential for eosinophilia and smear for schistocytes CPK, LDH and uric acid levels Renal ultrasound
  • If renal ultrasound does not show obstruction, azotemic medication avoidance and trial of intravenous fluids does not improve BUN and creatinine, then most likely etiology is intrarenal   Renal biopsy usually indicated for suspicion of acute GN, unclear diagnosis, if immunosuppression being considered or if certain medication that cannot be withdrawn potentially implicated
  • Overview of Treatment   Avoid nephrotoxins and renal dose medications that are renally excreted   Low protein, low sodium and low potassium diet   Phosphate binders   Daily assessment of volume status and symptoms   Daily weight, I/Os and screen 8
  • Indications for Dialysis   Uremic symptoms   Uremic Signs   Congestive heart failure unresponsive to diuretics   Severe hyperkalemia especially if associated with EKG changes   Intractable acidosis