14 Ri Acute Nonoliguric Renal Failure


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  • The mortality rate was 46.5% and the most important causes of death were: sepsis (38%), respiratory failure (19%), and multiple organ failure (11%).
  • 14 Ri Acute Nonoliguric Renal Failure

    1. 1. Acute nonoliguric renal failure Ri 黃正憲 2003/10/27
    2. 2. Acute Renal Failure <ul><li>Definitions: </li></ul><ul><ul><li>An increase in the serum creatinine of  0.5 mg/dl over baseline value </li></ul></ul><ul><ul><li>An increase in the serum creatinine of more than 50% over base line value </li></ul></ul><ul><ul><li>A reduction in the calculated creatinine clearance of 50% </li></ul></ul><ul><ul><li>A decrease in the renal function that results in the need for dialysis </li></ul></ul>
    3. 3. Category <ul><li>1. urine output </li></ul><ul><ul><li>Anuric: <100 mL/d </li></ul></ul><ul><ul><li>Oliguric: 100-500 mL/d </li></ul></ul><ul><ul><li>Nonoliguric: >500 mL/d </li></ul></ul><ul><li>2. the more common </li></ul><ul><ul><li>Pre-renal </li></ul></ul><ul><ul><li>Intrinsic </li></ul></ul><ul><ul><li>Post-renal </li></ul></ul>
    4. 4. Acute Renal Failure <ul><li>Pre Renal Causes </li></ul><ul><li>- Intravascular volume depletion from vomiting diarrhea, </li></ul><ul><li>poor fluid intake, fever, use of diuretics </li></ul><ul><li>- Decreased glomerular perfusion in the setting of </li></ul><ul><li>renal artery atherosclerotic disease with decreased </li></ul><ul><li>systolic head of BP, use of ACE inhibitors or NSAIDS </li></ul><ul><li>- Decreased effective arterial blood volume in CHF, liver dysfunction, septic shock, anesthesia </li></ul>
    5. 5. Acute Renal Failure <ul><li>Pre Renal Causes </li></ul>Post Renal Causes - External compression to the outflow tract from tumors, increased intra abdominal pressure, retroperitoneal fibrosis - Intrinsic blockage from tumor, calculi, blood clots, papillary necrosis - Intratubular obstruction from crystals and myeloma chains - Blocked Foley catheter
    6. 6. Acute Renal Failure <ul><li>Pre Renal Causes </li></ul>Post Renal Causes Intrinsic causes Tubulo- Glomerular Vascular Interstitial
    7. 7. Acute Renal Failure <ul><li>Pre Renal Causes </li></ul>Post Renal Causes Intrinsic causes Tubular Interstitial Acute necrosis nephritis glomerulonephritis (10% of cases) (5% of cases) Ischemia Toxins (50% of cases) (35% of cases)
    8. 8. Ischemic Acute Renal Failure <ul><li>Intravascular volume depletion and hypotension </li></ul><ul><li>Gastrointestinal, renal, dermal losses, hemorrhage, shock </li></ul>Generalized or localized reduction in renal blood flow Ischemic Acute Renal Failure Decreased effective intravascular volume : CHF, cirrhosis, nephrosis, peritonitis Medications : ACE inhibitors, NSAIDS, radiocontrast agents, Ampho B, Cyclosporin Hepatorenal syndrome Large vessel renal vascular disease : Renal artery thrombosis or embolism, operative arterial cross clamping, renal artery stenosis Small vessel renal vascular disease : Atheroembolism, vasculitis, malignant hypertension, hypercalcemia, transplant rejection Sepsis
    9. 9. Toxin induced Acute Renal Failure <ul><li>Reduction in renal perfusion through alteration of intra renal hemodynamics </li></ul><ul><li>Direct tubular injury </li></ul><ul><li>Heme pigment induced ARF </li></ul><ul><li>Intratubular obstruction </li></ul><ul><li>Allergic Interstitial Nephritis </li></ul><ul><li>Hemolytic Uremic Syndrome </li></ul><ul><li>NSAIDs, ACE inhibitors, Cyclosporin, Tacrolimus, IV contrast, Ampho B </li></ul><ul><li>Aminoglycosides, IV contrast, Cyclosporin, Cisplatin, Ampho B, Heavy metals, IV immunoglobulins </li></ul><ul><li>Rhabdomyolysis, Hemolysis, Cocaine, Ethanol, Statins </li></ul><ul><li>Acyclovir, Sulfonamides, Ethylene glycol, myoglobin </li></ul><ul><li>Penicillins, Cephalosporins, Sulfonamides, Rifampin, Cipro, NSAIDs, Thiazides, Cimetidine, Allopurinol </li></ul><ul><li>Cyclosporin, Cocaine, Mitomycin, Quinine </li></ul>
    10. 10. <ul><li>Categories of anuria, oliguria, and nonoliguria may be useful in differential diagnosis of ARF. </li></ul><ul><li>Anuria - Urinary tract obstruction, renal artery obstruction, RPGN, bilateral diffuse renal cortical necrosis </li></ul><ul><li>Oliguria - Prerenal failure, hepatorenal syndrome </li></ul><ul><li>Nonoliguria – AIN, AGN, partial obstructive nephropathy, nephrotoxic and ischemic ATN, radiocontrast-induced ARF, and rhabdomyolysis </li></ul>
    11. 11. Nonoliguric ARF <ul><li>Oliguria is a frequent but not invariable clinical feature (~50%). </li></ul><ul><li>Harrison’s 15ed </li></ul>
    12. 12. Nonoliguric ARF <ul><li>ATN: aminoglycoside, streptomycin, polymyxin B, lithium, or cisplatin nephrotoxicity. </li></ul><ul><li>Case report: </li></ul><ul><ul><ul><li>Celecoxib-induced nonoliguric acute renal failure </li></ul></ul></ul><ul><ul><ul><li>Annals of Pharmacotherapy. 36(1):52-4, 2002 Jan. </li></ul></ul></ul><ul><ul><ul><li>Lupus nephritis </li></ul></ul></ul><ul><ul><ul><ul><li>American Journal of the Medical Sciences. 321(6):381-7, 2001 Jun. </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Isoniazid-induced crescentic glomerulonephritis </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Omeprazole-induced acute interstitial nephritis . </li></ul></ul></ul></ul><ul><ul><ul><li>…… . </li></ul></ul></ul>
    13. 13. Nonoliguric ARF <ul><ul><li>Glomerular alterations in experimental oliguric and nonoliguric acute renal failure. </li></ul></ul><ul><ul><li>tubular damage was more pronounced in oliguric kidneys…. There was no significant difference in these glomerular changes between oliguric and nonoliguric kidneys. </li></ul></ul><ul><ul><li>The findings suggest that less reduction in the whole-kidney GFR in nonoliguric ARF kidneys is ascribed largely to less pronounced tubular damage rather than to less severe glomerular morphologic alterations. </li></ul></ul><ul><ul><ul><ul><ul><li>Renal Failure. 15(2):215-24, 1993. </li></ul></ul></ul></ul></ul>
    14. 14. Nonoliguric ARF <ul><ul><li>Acute renal failure: clinical outcome and causes of death. </li></ul></ul><ul><ul><li>Higher mortality was observed in oliguric patients (62.9%) than nonoliguric (34.5%) (p < 0.05) and in ischemic renal failure (56.7%) when compared to nephrotoxic renal failure (14.7%) (p < 0.05). </li></ul></ul><ul><ul><li>Renal Failure. 19(2):253-7, 1997 Mar </li></ul></ul>
    15. 15. Nonoliguric ARF <ul><ul><li>Acute renal failure in a teaching hospital. </li></ul></ul><ul><ul><li>… Compared with nonoliguric patients, oliguric patients had higher mortality (56.3% vs 18.9%, p < 0.01), and needed dialysis more frequently (43.8% vs 12.9%, p < 0.01) </li></ul></ul><ul><ul><li>Singapore Medical Journal. 36(3):278-81, 1995 Jun. </li></ul></ul>
    16. 16. Conclusion <ul><li>Nonoliguric acute renal failure </li></ul><ul><li>Although the causes of nonoliguric renal failure varied, nephrotoxic failure occurred more frequently in nonoliguric than in oliguric subjects (P <0.01). </li></ul><ul><li>As compared to oliguric patients, those without oliguria had significantly lower urinary sodium concentrations (P<0.05) and FENa (P < 0.02), had shorter hospital stay (P < 0.01), had fewer septic episodes, neurologic abnormalities, gastrointestinal bleeding and acidemia, required dialysis less frequently (P < 0.001) and had lower mortality rate (P < 0.05). </li></ul><ul><li>NEJM. 296(20):1134-38,1977 May </li></ul>
    17. 17. Management of acute renal failure <ul><li>Management of volume homeostasis </li></ul><ul><li>Management of electrolyte homeostasis </li></ul><ul><li>Management of acid- base homeostasis </li></ul><ul><li>Management of uremia </li></ul><ul><li>Nutritional management in acute renal failure </li></ul><ul><li>Dialysis in acute renal failure </li></ul>
    18. 18. Management of volume homeostasis <ul><li>Record I/O </li></ul><ul><li>Physical examination </li></ul><ul><li>Fluid = urine output + 300-500 </li></ul><ul><li>Sodium intake<2 g/day </li></ul><ul><li>Diuretics </li></ul><ul><li>Low dose dopamin ( 0.3 ug/kg/min) </li></ul><ul><li>CVP or pulmonary capillary wedge pressure </li></ul>
    19. 19. Management of electrolyte homeostais <ul><li>Hypernatremia and hyponatremia </li></ul><ul><li>Hyperkalemia </li></ul><ul><li>Hypocalcemia </li></ul><ul><li>Hypomagnesemia </li></ul><ul><li>Hyperphosphatemia </li></ul>
    20. 20. Management of acid- base homeostasis <ul><li>Dietary protein restriction 0.8-1.0g/kg of body weight 30 kcal /kg/day ( except hypercatabolism ) </li></ul><ul><li>Look for cause of acidosis </li></ul><ul><li>Sodium bicarbonate </li></ul><ul><li>Dialysis </li></ul>
    21. 21. Management of uremia <ul><li>Fatigue, lethargy, mental dullness, norexia and nausea </li></ul><ul><li>More serious– myoclonus, confusion, delirium or coma, seizure and pericarditis </li></ul><ul><li>Diet protein control </li></ul><ul><li>Check GI bleeding </li></ul><ul><li>Hemodialysis </li></ul>
    22. 22. Nutritional management in acute renal failure <ul><li>Minimal recommand protein intake0.6-0.8g/kg/day </li></ul><ul><li>Carbohydrate and lipid should maximal with a target of providing 30-65kcal /kg/day </li></ul><ul><li>Limit fluid volume potassium , magnesium, and phosphorus should avoid. </li></ul>
    23. 23. Indications for dialysis <ul><li>Absolute indications </li></ul><ul><li>uremic symptoms </li></ul><ul><li>uremic pericarditis </li></ul><ul><li>Relative indications </li></ul><ul><li>volume overlosd </li></ul><ul><li>hyperkalemia </li></ul><ul><li>metabolic acidosis </li></ul><ul><li>Other electrolyte abnormalities </li></ul>
    24. 24. Drug management in acute renal failure <ul><li>Stop nephrotoxic drugs </li></ul><ul><li>Adjust medication dose </li></ul><ul><li>Check drug level </li></ul>
    25. 25. Thanks for your attention