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ACUTE RENAL FAILURE

ACUTE RENAL FAILURE

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ACUTE RENAL FAILURE

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    1. ACUTE RENAL FAILURE Shahzad Qureshi M.D. Division of Nephrology Loyola University Medical Center

    2. Objectives Define and review classification of ARF Epidemiology of ARF Measurement of kidney function Pathophysiology of ARF Management and treatment of ARF Review clinical cases

    3. What is ARF? A) Increase in serum Creatinine 0.5mg/dL. B) An increase in serum Creatinine of more then 50% from baseline. C) A reduction in the calculated Creatinine Clearance of 50%

    4. RIFLE Classification 2004 ADQI group classification Risk (R) -Increase Cr x1.5 or Decrease GFR x 25% or UO <0.5 ml/kg/hr x 6hrs Injury (I)- Increase Cr x2.0 or Decrease GFR x 50% or UO <0.5 ml/kg/hr x 12hrs Failure (F)- Increase Cr x3.0 or Decrease GFR x75% or anuria x 12 hours Loss (L)- Persistent ARF, complete loss of kidney function x 4 weeks (needing RRT) End Stage Kidney Disease (E)- Loss of kidney function x 3 months

    5. Measurement of Kidney Function

    6. Serum Creatinine Serum creatinine is a reflection of creatinine clearance Creatinine production is determined by muscle mass and must be interpreted with respect to pts age, weight and sex. Creatinine is filtered and secreted and tends to over estimate GFR. Certain diseases and medications interfere with correlation between serum Cr and GFR. (i.e.. Acute glomerulonephritis, trimethoprim, cimetidine)

    7. Serum Creatinine (cont.) Cockcroft-Gault equation Cr Cx= (140 - age y)(weight kg)(0.85 if female)/(72 X serum creatinine mol/L) MDRD (Modified Diet and Renal Disease) GFR, in mL/min per 1.73 mm2 = 186.3 X ((serum creatinine) exp[-1.154]) X (Age exp[-0.203]) X (0.742 if female) X (1.21 if African American)

    8. Serum Creatinine (cont.) None of the equations accurately determine GFR in ARF. (Assume Cr is stable) More accurate techniques involve nuclear medicine studies and GFR scans. New biochemical markers investigated (i.e.. Cystatin C)

    9. Epidemiology 5 % of hospitalized patients dev. ARF. 0.5% of these patients require dialysis. 20% of critical care admissions dev. ARF. Hospital acquired ARF usually develops in the setting of ICU secondary to multisystem organ failure.

    10. Causes of ARF in Hospitalized Patients 45% ATN Ischemia, Nephrotoxins 21% Prerenal CHF, volume depletion, sepsis 10% Urinary obstruction 4% Glomerulonephritis or vasculitis 2% AIN 1% Atheroemboli

    11. Mortality/Morbidity Mortality rates range from 7-80% depending on patients other co morbidities. This rate has remained unchanged since the advent of dialysis because of increasing age and co morbid conditions. Most common cause of death associated with ARF are sepsis, cardiac failure and respiratory failure. Mortality rates are lower for nonoliguric (>400ml/day) then oliguric ARF (<400 ml/day).

    12. Pathophysiology 1) As an adaptive response to severe volume depletion and hypotension with structurally and functionally intact nephrons. (Pre renal azotemia) 2) In response to cytoxic or ischemic insults to the kidney with structural and functional damage. (Intrinsic Renal failure) 3) With obstruction to passage of urine. (Post obstructive uropathy)

    13. History Nausea? Vomiting? Diarrhea? Hx of heart disease, liver disease, previous renal disease, kidney stones, BPH? Any recent illnesses? Any edema, change in urination? Any new medications? Any recent radiology studies? Rashes?

    14. Physical Exam Volume Status Mucus membranes, orthostatics Cardiovascular JVD, rubs Pulmonary Decreased breath sounds Rales Rash (Allergic interstitial nephritis, Livedo reticularis) Large prostate Extremities (Skin turgor, Edema)

    15. Workup for ARF BMP Urine Urine sediment (U/A): casts, cells, protein Urine electrolytes (UNa and UUN) and urine Cr to calculate FeNa/FeUrea Urine osmolarity Urine protein Urine eosinophils Kidney U/S - r/o hydronephrosis

    17. Pre Renal Azotemia Impaired renal blood flow as a result of true intravascular depletion, decreased effective circulating volume to the kidneys, or agents that impair renal blood flow. Urine and blood studies are helpful in diagnosing pre renal ARF. Hyaline casts can be seen (Not an abnormal finding). Treat with fluid boluses or continuous IVF, monitor urine output.

    18. Prerenal Causes Intravascular volume depletion Hemorrhage Vomiting, diarrhea Third spacing Diuretics Reduced Cardiac output Cardiogenic shock, CHF, tamponade, huge PE.... Systemic vasodilation Sepsis Anaphylaxis, Antihypertensive drugs Renal vasoconstriction - Hepatorenal syndrome Medications - ACE-I, NSAIDS

    19. Urine Indices in ARF

    20. Acute Renal Failure Urinary Indices As discussed, the main differential in the oliguric patient with acute renal failure is between pre-renal azotemia (PR) and acute tubular necrosis (ATN). Although a careful history and physical examination coupled with a careful urinalysis will often distinguish between these two conditions, the use of urinary electrolytes provides further information. The basis of the urinary electrolytes is the different tubular responses to salt and water conservation. Tubular function with pre-renal azotemia is normal allowing maximum tubular sodium and water reabsorption resulting in a concentrated urine that is low in sodium. In acute tubular necrosis, tubular dysfunction leads to sodium wasting and an inability to concentrate the urine. The ratio of urine to plasma creatinine concentrations (U/P)Cr has also been proposed as a discriminating marker. In pre-renal ARF, UCr is high due to water reabsorption without Cr reabsorption and PCr is usually only mildly increased resulting in a high (U/P)Cr ratio. In ATN, the UCr is lower due to an inability to concentrate the urine and the PCr is increased in proportion to the degree of renal failure so the U/P cr is generally lower than that seen in pre-renal azotemia. Unfortunately, as shown in the slide, there is considerable overlap (grey zone) in all these indices. The so-called renal failure index [RFI = UNa/(U/P)Cr] and the more commonly employed fractional excretion of Na [FENa= 100(UNa X PCr) / (PNa X UCr)], which combine different single indices, provide better discrimination. Recent data have demonstrated that the fractional excretion of sodium (FENa) , which expresses the fraction of filtered sodium that escapes reabsorption and eventually appears in the urine, is a more discriminating test to distinguish between pre-renal azotemia and oliguric ATN. FENa > 1 % strongly suggests ATN while FENa < 1 % suggests pre-renal azotemia. However, the FENa is not infallible, and there are a number of exceptions where pre-renal azotemia can be associated with FENa values greater than 1 % - e.g., recent diuretic use or pre-renal azotemia superimposed on chronic renal insufficiency. In a similar manner, many instances of ATN will have FENa < 1 % - e.g., early phase of contrast-induced ATN, rhabdomyolysis or septic ATN. Thus, the clinician should utilize the FENa in conjunction with the overall clinical picture and other lab tests and should not be wedded to a particular FENa result when other data suggest a different cause for ARF. As discussed, the main differential in the oliguric patient with acute renal failure is between pre-renal azotemia (PR) and acute tubular necrosis (ATN). Although a careful history and physical examination coupled with a careful urinalysis will often distinguish between these two conditions, the use of urinary electrolytes provides further information. The basis of the urinary electrolytes is the different tubular responses to salt and water conservation. Tubular function with pre-renal azotemia is normal allowing maximum tubular sodium and water reabsorption resulting in a concentrated urine that is low in sodium. In acute tubular necrosis, tubular dysfunction leads to sodium wasting and an inability to concentrate the urine. The ratio of urine to plasma creatinine concentrations (U/P)Cr has also been proposed as a discriminating marker. In pre-renal ARF, UCr is high due to water reabsorption without Cr reabsorption and PCr is usually only mildly increased resulting in a high (U/P)Cr ratio. In ATN, the UCr is lower due to an inability to concentrate the urine and the PCr is increased in proportion to the degree of renal failure so the U/P cr is generally lower than that seen in pre-renal azotemia. Unfortunately, as shown in the slide, there is considerable overlap (grey zone) in all these indices. The so-called renal failure index [RFI = UNa/(U/P)Cr] and the more commonly employed fractional excretion of Na [FENa= 100(UNa X PCr) / (PNa X UCr)], which combine different single indices, provide better discrimination. Recent data have demonstrated that the fractional excretion of sodium (FENa) , which expresses the fraction of filtered sodium that escapes reabsorption and eventually appears in the urine, is a more discriminating test to distinguish between pre-renal azotemia and oliguric ATN. FENa > 1 % strongly suggests ATN while FENa < 1 % suggests pre-renal azotemia. However, the FENa is not infallible, and there are a number of exceptions where pre-renal azotemia can be associated with FENa values greater than 1 % - e.g., recent diuretic use or pre-renal azotemia superimposed on chronic renal insufficiency. In a similar manner, many instances of ATN will have FENa < 1 % - e.g., early phase of contrast-induced ATN, rhabdomyolysis or septic ATN. Thus, the clinician should utilize the FENa in conjunction with the overall clinical picture and other lab tests and should not be wedded to a particular FENa result when other data suggest a different cause for ARF.

    21. What is FENa The fraction of filtered sodium excreted in the urine. FeNa = (urine Na x plasma Cr) (plasma Na x urine Cr)

    22. ARF syndromes with Low FENA Pre renal ARF Vasoconstriction Mediated Intrinsic Renal Failure -Tacrolimus, cyclosporine, cocaine - Hepatorenal syndrome - Radiocontrast Injury - Rhabdomyolysis - Sepsis (early), burn injury - Acute Glomerulonephritis

    23. Calculating FeNa after pt has gotten Lasix... Caution with calculating FeNa if pt has gotten Loop Diuretics in past 24-48 h Loop diuretics cause natriuresis (incr urinary Na excretion) that raises U Na-even if pt is prerenal So if FeNa>1%, you dont know if this is because pt is euvolemic or because Lasix increased the U Na So helpful if FeNa still <1%, but not if FeNa >1% 1. Fractional Excretion of Lithium (endogenous) 2. Fractional Excretion of Uric Acid 3. Fractional Excretion of Urea

    25. Post Obstructive Uropathy Occurs if both urinary outflow tracts are obstructed or outflow tract of solitary kidney is obstructed. Patients with SUDDEN ONSET of anuria are likely to have post obstructive uropathy. Primary causes include BPH, prostate and cervical cancer, stones, strictures and retroperitoneal fibrosis. Bladder catheterization and Renal U/S to assess hydronephrosis. Can have obstruction w/o hydronephrosis on U/S Monitor for post obstructive diuresis, hemorrhagic cystitis? Diagnose with CT urogram or MRIDiagnose with CT urogram or MRI

    27. Intrinsic Acute Renal Failure Tubular (ATN) Interstitial (AIN) Glomerular (Glomerulonephritis) Vascular

    28. ATN Most common cause of ARF in hospitalized patients Contrast and aminoglycosides most often associated with nonischemic ATN. 3 phases: 1) Initiation phase- Renal injury lasting hours to days. 2) Maintenance phase- Lasts days to weeks. GFR and U.O at lowest. 3) Recovery Phase- Postacute tubular necrosis diuresis. Can still exp. uremia and hypovolemia as tubular function not completely restored.

    29. Figure 3. Tubular-Cell Injury and Repair in Ischemic Acute Renal Failure. After ischemia and reperfusion, morphologic changes occur in the proximal tubules, including loss of the brush border, loss of polarity, and redistribution of integrins and Na+/K+-ATPase to the apical surface. Calcium, reactive oxygen species, purine depletion, and phospholipases probably have a role in these changes in morphology and polarity as well as in the subsequent cell death that occurs as a result of necrosis and apoptosis. There is a sloughing of viable and nonviable cells into the tubular lumen, resulting in the formation of casts and luminal obstruction and contributing to the reduction in the glomerular filtration rate. The severely damaged kidney can completely restore its structure and function. Spreading and dedifferentiation of viable cells occur during recovery from ischemic acute renal failure, which duplicates aspects of normal renal development. A variety of growth factors probably contribute to the restoration of a normal tubular epithelium.Figure 3. Tubular-Cell Injury and Repair in Ischemic Acute Renal Failure. After ischemia and reperfusion, morphologic changes occur in the proximal tubules, including loss of the brush border, loss of polarity, and redistribution of integrins and Na+/K+-ATPase to the apical surface. Calcium, reactive oxygen species, purine depletion, and phospholipases probably have a role in these changes in morphology and polarity as well as in the subsequent cell death that occurs as a result of necrosis and apoptosis. There is a sloughing of viable and nonviable cells into the tubular lumen, resulting in the formation of casts and luminal obstruction and contributing to the reduction in the glomerular filtration rate. The severely damaged kidney can completely restore its structure and function. Spreading and dedifferentiation of viable cells occur during recovery from ischemic acute renal failure, which duplicates aspects of normal renal development. A variety of growth factors probably contribute to the restoration of a normal tubular epithelium.

    30. Treatment Reverse underlying causes and correct fluid and electrolyte balances Treatment is supportive. Drugs such as mannitol, loop diuretics, dopamine and CCB successful in promoting diuresis in animals but not in humans. Dialysis as needed (IHD vs. CRRT)

    32. Acute Interstitial Nephritis 70% Drug hypersensitivity 30% Antibiotics: PCNs (Methicillin), Cephalosporins, Cipro Sulfa drugs NSAIDs Allopurinol... 15% Infection Strep, Legionella, CMV, other bact/viruses 8% Idiopathic 6% Autoimmune Dz (Sarcoid, Tubulointerstitial nephritis/Uveitis)

    33. AIN from Drugs Renal damage is NOT dose-dependent May take wks after initial exposure to drug Up to 18 mos to get AIN from NSAIDS! But only 3-5 d to develop AIN after second exposure to drug Fever (27%) Serum Eosinophilia (23%) Maculopapular rash (15%) Bland sediment or WBCs, sterile pyuria most commonly seen WBC Casts are common Urine eosinophils on Wrights or Hansels Stain - Also see urine eos in RPGN, renal atheroemboli... Treatment is to remove offending agents. Most patients recover complete kidney function w/I one year.

    35. Acute Glomerulonephritis Nephrotic Syndromes 1 Disorders - Minimal Change Disease - Membranous Nephropathy - FSGS 2 Disorders- DM - SLE - Hepatitis B - Amyloid - Heroin

    36. Nephrotic Syndromes Edema (Anasarca) Proteinuria (>3.5gm/24hrs) Lipidemia Can have normal serum creatinine (Not oliguric) Usually do NOT see RBC casts

    37. Nephritic Syndromes Type 1: Anti-GBM dz (Anti GBM Ab positive) Goodpastures Disease Anti-GBM Type 2: Immune complex (Low compliment, elevated ESR) IgA nephropathy (Normal Compliment levels) Postinfectious glomerulonephritis Lupus nephritis Mixed cryoglobulinemia MPGN IBE Type 3: Pauci-immune (ANCA positive, assoc with vasculitis) Wegners Disease Microscopic Polyangitis Churg-Strauss

    38. Nephritic Syndromes Fever Oliguria Hematuria Htn RBC casts Proteinuria (1-2grams usually) Treatment varies based on underlying disease

    40. Renal Atheroembolic Dz 1% of Cardiac caths: atheromatous debris scraped from the aortic wall will embolize Retinal Cerebral Skin (Livedo Reticularis, Purple toes) Renal (ARF) Gut (Mesenteric ischemia) Cr will NOT improve with IVF Diagnosis of exclusion: will NOT show up on MRI or Renal U/S; WILL show up on renal bx Tx: supportive

    41. You are called to evaluate a 45 y/o female in the ER admitted for heart palpatations. BUN 80, Cr 3.0, Potassium 6.5

    42. Treatment of Hyperkalemia EKG/Telemetry Calcium Gluconate Glucose and Insulin Sodium Bicarbonate Diuretics (Lasix) Cation-exchange resins (Kayexalate) Dialysis

    43. Case (cont.) You admit the pt to telemetry and give appropriate medications. You recheck labs 4h later and BUN=105, Cr=4.0, K=7.0. Suddenly the pt starts to seize. Now what?

    44. Acute Indications for Dialysis AEIOU Acidosis (metabolic) Electrolytes (hyperkalemia) Ingestion of drugs/Ischemia Overload (fluid) Uremia

    45. Uremia General Fatigue, weakness Pruritis Mental status change Uremic encephalopathy Seizures Asterixis GI disturbance Anorexia, early satiety, N/V, Uremic Pericarditis Plt dysfunction/bleeding