Acute Renal Failure <ul><li>A. Symptoms  </li></ul><ul><ul><li>Polyuria, Oliguria or Anuria hematuria  </li></ul></ul><ul>...
<ul><ul><li>Duration <3 months   </li></ul></ul><ul><ul><li>Oliguria <400 ml urine/24 hours </li></ul></ul><ul><ul><li>Abs...
<ul><li>B. Etiologies  </li></ul><ul><li>Location of Lesion  </li></ul><ul><li>Prerenal - ~70% of cases  </li></ul><ul><li...
<ul><li>Pre-renal azotemia  </li></ul><ul><li>Decreased effective arterial volume </li></ul><ul><ul><li>CHF,,Cirrhosis,,Ne...
<ul><li>II.Parenchymal Damage  </li></ul><ul><li>Nephritis (inflammation): glomerular vs. interstitial  </li></ul><ul><li>...
<ul><li>Vascular hypertension  </li></ul><ul><li>Atherosclerotic (atheroembolism) - cholesterol emboli, 5-10% of hospitali...
<ul><li>Drug Induced  </li></ul><ul><li>ACE Inhibitors  </li></ul><ul><li>Radiocontrast Dye Interstitial Nephritis - sulfo...
<ul><li>Pathophysiology  </li></ul><ul><li>Ischemia is the underlying problem in ARF  </li></ul><ul><li>leads to depletion...
<ul><li>C. Initial Evaluation  </li></ul><ul><li>Consider possible etiologies and direct evaluation  </li></ul><ul><li>Med...
<ul><li>Urine for electrolytes, dipstick and microscopic analysis  </li></ul><ul><li>Osmolality, creatinine, Na+, K+, Cl- ...
<ul><li>Renal/Pelvic Sono - stones, hydronephrosis, mass  </li></ul><ul><li>Consider Abdominal radiograph if ultrasound is...
<ul><li>Pathology Summary </li></ul><ul><li>Glomerular Involvement  </li></ul><ul><li>Diffuse: all glomeruli in a section ...
<ul><li>Focal and Segmental Glomerulosclerosis: portions of many glomeruli are destroyed  </li></ul><ul><li>5. Minimal Cha...
<ul><li>7. Proliferative Glomerulonephritis  </li></ul><ul><li>a. Increase in mesangeal cell number  </li></ul><ul><li>b. ...
<ul><li>9. Tubular Necrosis  </li></ul><ul><li>a. Tubular cells die and slough off basement membrane  </li></ul><ul><li>b....
<ul><li>E. Management  </li></ul><ul><li>Renal Diet  </li></ul><ul><li>Low phosphate, potassium, sodium, and protein  </li...
<ul><li>If product is close to 70, then phosphate should be lowered with aluminum compounds  </li></ul><ul><li>These compo...
<ul><li>1. Acidosis  </li></ul><ul><li>Renal tublar acidosis (RTA) is common in early renal failure  </li></ul><ul><li>Ora...
<ul><li>3. Hypertension  </li></ul><ul><li>a. ACE inhibitors generally contraindicated in moderate to severe renal failure...
<ul><li>4. Volume overload  </li></ul><ul><li>a. Attempt to maximize cardiac output and improve intravascular volume  </li...
<ul><li>5. Protein Load  </li></ul><ul><li>Reducing protein load is thought to reduce azotemia  </li></ul><ul><li>Appears ...
<ul><li>7. Newer Agents  </li></ul><ul><li>Atrial natriuretic factor (ANF)= dilators + diuretic  </li></ul><ul><li>ANF (Au...
<ul><li>8. Dialysis Indications </li></ul><ul><li>Serum abnormalities unresponsive to medical therapy  </li></ul><ul><li>S...
<ul><li>III Volume Overload  </li></ul><ul><li>Hemofiltration or hemodialysis can be used to allow recovery of kidney afte...
<ul><li>Kidney Transplantation  </li></ul><ul><li>Excellent (and improving) results with cadaveric grafts. </li></ul><ul><...
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26 acute renal failure

  1. 1. Acute Renal Failure <ul><li>A. Symptoms </li></ul><ul><ul><li>Polyuria, Oliguria or Anuria hematuria </li></ul></ul><ul><ul><li>Dysuria </li></ul></ul><ul><ul><li>Uremia </li></ul></ul><ul><ul><ul><li>Definition: symptomatic azotemia </li></ul></ul></ul><ul><ul><ul><li>Acidosis (± tachypnea) </li></ul></ul></ul><ul><ul><ul><li>Mental Status changes </li></ul></ul></ul><ul><ul><ul><li>Hypervolemia / Hypertension </li></ul></ul></ul><ul><ul><ul><li>Hyperkalemia </li></ul></ul></ul><ul><ul><ul><li>Pericarditis </li></ul></ul></ul>
  2. 2. <ul><ul><li>Duration <3 months </li></ul></ul><ul><ul><li>Oliguria <400 ml urine/24 hours </li></ul></ul><ul><ul><li>Absolute increase Scr by 0.5 or 1.0 mg/dl or relative increase 25% </li></ul></ul><ul><ul><li>Cockcroft – Gault Equation </li></ul></ul><ul><li>(140-age) x wt(kg) </li></ul><ul><li>------------------------ </li></ul><ul><li>Serum Cr x 72 </li></ul>
  3. 3. <ul><li>B. Etiologies </li></ul><ul><li>Location of Lesion </li></ul><ul><li>Prerenal - ~70% of cases </li></ul><ul><li>Intrinsic - ~25% of cases </li></ul><ul><li>Post-renal (obstructive) - <5% of cases </li></ul><ul><li>FeNa= urine Na x serum Cr </li></ul><ul><li>------------------------------- X 100 </li></ul><ul><li> serum Na x urine Cr </li></ul><ul><li>Prerenal Renal (ATN) </li></ul><ul><li>Urine Na <10 >10 </li></ul><ul><li>FeNa <1% >1% </li></ul><ul><li>response IVF good poor </li></ul><ul><li>BUN/Scr >20 nl </li></ul>
  4. 4. <ul><li>Pre-renal azotemia </li></ul><ul><li>Decreased effective arterial volume </li></ul><ul><ul><li>CHF,,Cirrhosis,,Nephrotic syndrome,,Sepsis </li></ul></ul><ul><ul><li>Renal Artery Stenosis (atherosclerosis, fibromuscular dysplasia) </li></ul></ul><ul><ul><li>Cardiopulmonary bypass (>3 hours) </li></ul></ul><ul><li>Intravascular volume depletion </li></ul><ul><ul><li>GI loss…Vomiting..diarrhea…etc </li></ul></ul><ul><ul><li>Renal loss diuretc..osmotic diuresis..etc </li></ul></ul><ul><ul><li>Cutaneous loss hyperthermia..burns </li></ul></ul><ul><ul><li>Hemorrhage </li></ul></ul><ul><ul><li>Third space pancreatitis..severe hypoalbuminemia..cappillary leak </li></ul></ul>
  5. 5. <ul><li>II.Parenchymal Damage </li></ul><ul><li>Nephritis (inflammation): glomerular vs. interstitial </li></ul><ul><li>Tubular Injury: most common cause of ARF Nephrotic Syndrome (total protein losses) </li></ul><ul><li>III. Obstruction of Outflow (~5%) Urinary Tract Infection (UTI) with Pyelonephritis </li></ul><ul><li>Urinary Calculus disease (renal stones) </li></ul><ul><li>Crystal Deposition </li></ul><ul><li>Bladder tumors with extensive invasion </li></ul><ul><li>Prostatic Enlargement: BPH vs. Carcinoma </li></ul><ul><li>Unilateral obstruction with only one functioning kidney </li></ul>
  6. 6. <ul><li>Vascular hypertension </li></ul><ul><li>Atherosclerotic (atheroembolism) - cholesterol emboli, 5-10% of hospitalized ARF Trauma </li></ul><ul><li>Vasculitides </li></ul><ul><li>Post-operative - aortic aneurysm repair, aortic cross-clamping </li></ul><ul><li>Vasoconstricting Agents - NSAIDs, vasopressors </li></ul>
  7. 7. <ul><li>Drug Induced </li></ul><ul><li>ACE Inhibitors </li></ul><ul><li>Radiocontrast Dye Interstitial Nephritis - sulfonamides, NSAIDS, other antibiotics </li></ul><ul><li>Amphotericin </li></ul><ul><li>Cis-Platinum </li></ul><ul><li>Aminoglycosides </li></ul><ul><li>Non-steroidal anti-inflammatory drugs (NSAIDs) </li></ul>
  8. 8. <ul><li>Pathophysiology </li></ul><ul><li>Ischemia is the underlying problem in ARF </li></ul><ul><li>leads to depletion of cellular ATP and release of calcium </li></ul><ul><li>Reactive oxygen species produced leading to further cell death </li></ul><ul><li>Calcium release leads to phospholipase activation </li></ul><ul><li>Neutrophils may mediate reperfusion injury (ICAM-1 is involved) </li></ul><ul><li>Many nephrotoxins are renal vasocontrictors (eg. cyclosporine, radiocontrast) </li></ul>
  9. 9. <ul><li>C. Initial Evaluation </li></ul><ul><li>Consider possible etiologies and direct evaluation </li></ul><ul><li>Medications should always be suspected </li></ul><ul><li>Standard Blood Testing </li></ul><ul><li>Electrolyte/renal panel, Ca2+, Phosphate, Mg2+, Albumin </li></ul><ul><li>Complete Blood Count </li></ul><ul><li>Foley catheter to rule out bladder obstruction </li></ul>
  10. 10. <ul><li>Urine for electrolytes, dipstick and microscopic analysis </li></ul><ul><li>Osmolality, creatinine, Na+, K+, Cl- </li></ul><ul><li>Urine spot protein to creatinine ratio (normal is <0.2) </li></ul><ul><li>Pigment: Hemoglobin (myoglobin) </li></ul><ul><li>Cells, Casts, Crystals, Organisms </li></ul><ul><li>Consider Urine culture </li></ul>
  11. 11. <ul><li>Renal/Pelvic Sono - stones, hydronephrosis, mass </li></ul><ul><li>Consider Abdominal radiograph if ultrasound is not done to rule out stones </li></ul><ul><li>ESR, ASO titer, ANA, C3/C4 Anti-GBM Abs </li></ul><ul><li>Renal Biopsy in rapidly progressing disease </li></ul><ul><li>ANCA and Anti-GBM diseases - consider cyclophosphamide + glucocorticoids </li></ul><ul><li>Idiopathic rapidly progressive glomerulonephritis often ANCA positive (other inflammatory diseases such as bacterial endocarditis can given ANCA+) </li></ul>
  12. 12. <ul><li>Pathology Summary </li></ul><ul><li>Glomerular Involvement </li></ul><ul><li>Diffuse: all glomeruli in a section are diseased </li></ul><ul><li>Focal: some glomeruli in a section are diseased </li></ul><ul><li>Segmental: parts of individual glomerulus affected </li></ul><ul><li>2.Focal Glomerulonephritis: </li></ul><ul><li>Some glomeruli are dead( necrosis, collapse, sclerosis </li></ul><ul><li>b.Acute or chronic inflamation is often seen </li></ul><ul><li>3.Crescent Glomerulonephritis (very poor prognosis) </li></ul><ul><li>Crescent (moon shaped) formation in glomerulus </li></ul><ul><li>Affected glomeruli are non-functional </li></ul>
  13. 13. <ul><li>Focal and Segmental Glomerulosclerosis: portions of many glomeruli are destroyed </li></ul><ul><li>5. Minimal Change Glomerulonephritis </li></ul><ul><li>a. Glomeruli appear okay, but function is poor </li></ul><ul><li>b. Electron microscopic evidence of basement membrane disease </li></ul><ul><li>c. Response to glucocorticoids is usually very good </li></ul><ul><li>6. IgA Deposition </li></ul><ul><li>a.IgA nephropathy </li></ul><ul><li>b.Deposition of IgA immune complexes </li></ul><ul><li>c.Differential includes Systemic Lupus (SLE) and Henoch-Schonlein Purpura (HSP) </li></ul>
  14. 14. <ul><li>7. Proliferative Glomerulonephritis </li></ul><ul><li>a. Increase in mesangeal cell number </li></ul><ul><li>b. Usually follows insults (eg. Post-Streptococcal) </li></ul><ul><li>May be seen in collagen vascular disease, SLE </li></ul><ul><li>8. Collapsing Glomerulonephritis </li></ul><ul><li>Major form seen in HIV nephropathy </li></ul><ul><li>Usually late stage </li></ul><ul><li>Rapid progression to renal failure (weeks-months) </li></ul><ul><li>No effective therapy to date </li></ul>
  15. 15. <ul><li>9. Tubular Necrosis </li></ul><ul><li>a. Tubular cells die and slough off basement membrane </li></ul><ul><li>b. The dead tubular cells form casts which can occlude lumen </li></ul><ul><li>c. Glomular basement membrane may also be damaged </li></ul>
  16. 16. <ul><li>E. Management </li></ul><ul><li>Renal Diet </li></ul><ul><li>Low phosphate, potassium, sodium, and protein </li></ul><ul><li>High calcium and vitamin D </li></ul><ul><li>Various multivitamin formulas available for renal patients, eg. Nephrovit® </li></ul><ul><li>Low protein diet may slow progression slightly in chronic renal disease </li></ul><ul><li>Phosphate and Calcium </li></ul><ul><li>Dangerous if product of Calcium and Phosphage > ~70 (mg/dl) (will lead to precipitation) </li></ul>
  17. 17. <ul><li>If product is close to 70, then phosphate should be lowered with aluminum compounds </li></ul><ul><li>These compounds should be given with meals to bind the phosphate directly </li></ul><ul><li>If product is <60, then calcium should be given 500-1000mg po tid with meals </li></ul><ul><li>If calcium is low but phosphate normal, then calcium should be given before meals </li></ul><ul><li>Consider using 1,25 dihyroxyvitamin D supplements </li></ul>
  18. 18. <ul><li>1. Acidosis </li></ul><ul><li>Renal tublar acidosis (RTA) is common in early renal failure </li></ul><ul><li>Oral bicitra (citrate replaces bicarbonate) may be used </li></ul><ul><li>Bicitra is contraindicated in edematous states due to high sodium content </li></ul><ul><li>2. Hyperuricemia </li></ul><ul><li>Check uric acid levels </li></ul><ul><li>Uric acid deposition in renal tubules may worsen progression of renal failure </li></ul><ul><li>Allopurinol may be given (100-200mg po qd) to attempt normalization of uric acid </li></ul>
  19. 19. <ul><li>3. Hypertension </li></ul><ul><li>a. ACE inhibitors generally contraindicated in moderate to severe renal failure </li></ul><ul><li>Calcium blockers such as nifedipine </li></ul><ul><li>Labetolol is also very effective but patient should have LV EF>50% and no bronchospasm </li></ul><ul><li>d. Consider Hydralazine for afterload reduction </li></ul><ul><li>e. Pure alpha-adrenergic blocking agents may be effective, but tachyphylaxis may occur </li></ul><ul><li>Diuretic improve hypertension/ volume overload </li></ul>
  20. 20. <ul><li>4. Volume overload </li></ul><ul><li>a. Attempt to maximize cardiac output and improve intravascular volume </li></ul><ul><li>b. Diuretics often worsen renal failure but may be necessary to prevent pulmonary edema </li></ul><ul><li>c. In general, potassium sparing diuretics should be avoided (high risk hyperkalemia) </li></ul><ul><li>e. Dopamine or mannitol can be tried, but are usually not effective </li></ul><ul><li>f. Albumin infusions are probably not helpful, but may help diuresis in low albumin states </li></ul><ul><li>g. Dialysis may be required particularly in severe volume overload situations </li></ul>
  21. 21. <ul><li>5. Protein Load </li></ul><ul><li>Reducing protein load is thought to reduce azotemia </li></ul><ul><li>Appears to slow progression of CRF </li></ul><ul><li>Patients with moderate renal disease - some decrease in progression on low protein diet </li></ul><ul><li>Patients with severe renal disease show no benefit on low protein diet </li></ul><ul><li>6. Hospital inpatients with ARF ~50% mortality rate </li></ul>
  22. 22. <ul><li>7. Newer Agents </li></ul><ul><li>Atrial natriuretic factor (ANF)= dilators + diuretic </li></ul><ul><li>ANF (Auriculin®) ? efficacy in oliguric ARF </li></ul><ul><li>ANF may increase renal dysfunction in diabetics receiving radiocontrast </li></ul><ul><li>Brain derived natriuretic factor (BDNF) may be effective some patients </li></ul><ul><li>Other vasodilators (eg. calcium channel blockers) are not effective </li></ul><ul><li>Investigation renal growth/regeneration factors </li></ul>
  23. 23. <ul><li>8. Dialysis Indications </li></ul><ul><li>Serum abnormalities unresponsive to medical therapy </li></ul><ul><li>Severe Acidosis </li></ul><ul><li>Severe Hyperkalemia </li></ul><ul><li>II Uremia </li></ul><ul><li>Mental status changes (usually delirium) </li></ul><ul><li>Nausea and vomiting </li></ul><ul><li>Pericarditis (pericardial friction rub) </li></ul>
  24. 24. <ul><li>III Volume Overload </li></ul><ul><li>Hemofiltration or hemodialysis can be used to allow recovery of kidney after ARF </li></ul><ul><li>Average duration of need for these therapies was 9 days in ARF </li></ul><ul><li>After this time, kidneys regain function and increase urine output </li></ul><ul><li>Native kidneys may continue with minimal function for 6-12 months of hemodialysis </li></ul><ul><li>After that, native kidneys usually shut down permanently </li></ul>
  25. 25. <ul><li>Kidney Transplantation </li></ul><ul><li>Excellent (and improving) results with cadaveric grafts. </li></ul><ul><li>Living Related Donor kidneys superior to CRT </li></ul><ul><li>New kidney usually placed in extraperitoneally in the pelvis </li></ul><ul><li>Cyclosporin ,Prednisone, OKT3, mycophenolic acid, FK506 immunosuppression </li></ul><ul><li>Combined Kidney Pancreas transplant in Diabetic ESRD patients </li></ul>

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