04 Differential Diagnosis Of Acute Renal Failure
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Transcript of 04 Differential Diagnosis Of Acute Renal Failure
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臺灣大學附設醫院外科臺灣大學附設醫院外科4B4B 加護病房實習報告加護病房實習報告
報告者 : 李浩遠 (Intern, 學號 : B8601076)
臺北醫學大學醫學系七年級
Differential Diagnosis of Acute Renal Failure
Differential Diagnosis of Acute Renal Failure
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Definition Definition
Acute renal failure (ARF) is defined as a precipitous and significant (>50%) decrease in glomerular filtration rate (GFR) over a period of hours to days, with an accompanying accumulation of nitrogenous wastes in the body.
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Prerenal DiseasePrerenal Disease True volume depletion Advanced liver disease Congestive heart failure Renal arterial disease Perinatal or Neonatal hemorrhage Perinatal asphyxia and hyaline membrane dise
ase Gastroenteritis Congenital and acquired heart diseases
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Prerenal DiseasePrerenal Disease A reduction in renal blood flow - the most co
mmon cause of acute renal failure. Occur from true volume depletion or from se
lective renal ischemia (as in bilateral renal artery stenosis).
Causes of prerenal azotemia: true volume depletion, advanced liver disease, and congestive heart failure.
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Prerenal Azotemia Caused bPrerenal Azotemia Caused by True Volume Depletiony True Volume Depletion
In severe cases the patient may be in hypovolemic shock.
Oliguria is present in most individuals Normal or increased urine output indica
tes that an osmotic agent or other diuretic agent is acting, or that there is tubular dysfunction such as ATN.
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Prerenal Azotemia Caused bPrerenal Azotemia Caused by Advanced Liver Disease y Advanced Liver Disease
Liver disease: sodium retention, initially manifested as
ascites a progressive decline in GFR. Both humoral and hemodynamic factors pl
ay a primary role in the development of these problems.
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Prerenal Azotemia Caused bPrerenal Azotemia Caused by Congestive Heart Failure y Congestive Heart Failure
CHF is associated with two major alterations in renal function:
Sodium retention early in the course of the disease and a decline in GFR as cardiac function worsens.
Neurohumeroral factors and certain therapies may contribute to these problems.
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Prerenal Azotemia Caused bPrerenal Azotemia Caused by y Renal arterial diseaseRenal arterial disease
Renal arterial disease - Renal arterial stenosis (atherosclerotic, fibromuscular dysplasia), embolic disease (septic, cholesterol)
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Prerenal ARF of Newborns and InfantsPrerenal ARF of Newborns and Infants The most common cause of ARF is prerenal etio
logies.Prerenal ARF: Perinatal hemorrhage - Twin-twin transfusion,
complications of amniocentesis, abruptio placenta, birth trauma
Neonatal hemorrhage - Severe intraventricular hemorrhage, adrenal hemorrhage
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Prerenal ARF of Newborns and InfantsPrerenal ARF of Newborns and Infants Perinatal asphyxia and hyaline membran
e disease (newborn respiratory distress syndrome) both may result in preferential blood shunting away from kidneys (ie, prerenal) to central circulation.
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Prerenal ARF of Prerenal ARF of ChildrenChildren The most common cause of ARF is preren
al etiologies.Prerenal ARF: The most common cause of hypovolemi
a in children is gastroenteritis. Congenital and acquired heart diseases
are also important causes of decreased renal perfusion in this age group.
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Symptoms and Signs of Symptoms and Signs of Prerenal Failure Prerenal Failure Patients commonly present with sympto
ms related to hypovolemia, including thirst, decreased urine output, dizziness, and orthostatic hypotension.
Look for a history of excessive fluid loss via hemorrhage, GI losses, sweating, or renal sources.
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Symptoms and Signs of Symptoms and Signs of PrerenPrerenal Failureal Failure
Patients with advanced cardiac failure leading to depressed renal perfusion may present with orthopnea and paroxysmal nocturnal dyspnea.
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Intrinsic Renal FailureIntrinsic Renal Failure Tubular diseasesInterstitial diseasesGlomerular diseasesVascula diseases NephrotoxinsAllergic interstitial nephritis
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Intrinsic Renal FailureIntrinsic Renal Failure Glomerular diseases: Nephritic
syndrome of hematuria, edema, and HTN is synonymous with a glomerular etiology of ARF.
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Intrinsic Renal FailureIntrinsic Renal Failure Tubular diseases: ATN should
be suspected in any patient presenting after a period of hypotension secondary to cardiac arrest, hemorrhage, sepsis, drug overdose, or surgery.
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Intrinsic Renal FailureIntrinsic Renal Failure Interstitial diseases - Acute interstitial
nephritis, drug reactions, autoimmune diseases (eg, systemic lupus erythematosus [SLE]), infiltrative disease (sarcoidosis, lymphoma), infectious agents (Legionnaire disease, hantavirus)
Vascular diseases - Hypertensive crisis, polyarteritis nodosa, vasculitis
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Intrinsic Renal FailureIntrinsic Renal Failure A careful search for exposure to
nephrotoxins should include a detailed list of all current medications and any recent radiologic examinations (ie, exposure to radiologic contrast agents).
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Intrinsic Renal FailureIntrinsic Renal Failure Allergic interstitial nephritis sh
ould be suspected with recent drug ingestion, fevers, rash, and arthralgias.
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Acute Tubular Necrosis Acute Tubular Necrosis
Renal insults, including renal ischemia exposure to exogenous or endogenous nephr
otoxins.
The net effect is a rapid decline in renal function that may require a period of dialysis before spontaneous resolution occurs.
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Acute Tubular Necrosis Acute Tubular Necrosis
There are two major histiologic changes that take place in ATN:
(1) tubular necrosis with sloughing of the epithelial cells
(2) occlusion of the tubular lumina by casts and by cellular debris
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Acute Tubular Necrosis Acute Tubular Necrosis In addition of the tubular obstruction, two
other factors appear to contribute to the development of renal failure in ATN:
across the damaged tubular epithelia backleak of filtrate and
a primary reduction in glomerular filtration.
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Acute Tubular Necrosis Acute Tubular Necrosis The decrease in glomerular filtration results
both from arteriolar vasoconstriction and from mesangial contraction.
The decline in renal function begins abruptly following a hypotensive episode, rhabdomyolysis, or the administration of a radiocontrast media.
When aminoglycosides are the cause, the onset is more insidious, with the first rise in creatinine being at seven or more days.
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Major Causes of Acute Major Causes of Acute Tubular Necrosis Tubular Necrosis
Renal Ischemia:
* Severe prerenal disease from any cause. Exposure to Nephrotoxins:
* Amphotericin B
* Aminoglycosides * Heme Pigments * NSAID's (hemoglobinuria/myoglobinura)
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Intrinsic ARF of Children Intrinsic ARF of Children
Hemolytic uremic syndrome (HUS) often is cited as the most common cause of ARF in children. The most common form of the disease is associated with a diarrheal prodrome caused by Escherichia coli 0157:H7.
These children usually present with microangiopathic anemia, thrombocytopenia, colitis, mental status changes, and renal failure.
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Post-renal ARFPost-renal ARF
Diseases causing urinary obstruction from the level of the renal tubules to the urethra
– Tubular obstruction from crystals (eg, uric acid, calcium oxalate, acyclovir, sulfonamide, methotrexate, myeloma light chains)
– Ureteral obstruction - Retroperitoneal tumor, retroperitoneal fibrosis (methysergide, propranolol, hydralazine), urolithiasis, papillary necrosis
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Post-renal ARFPost-renal ARF
Urethral obstruction - Benign prostatic hypertrophy; prostate, cervical, bladder, colorectal carcinoma; bladder hematoma; bladder stone; obstructed Foley catheter; neurogenic bladder; stricture
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FeNaFeNa
Calculation of fractional excretion of sodium (FeNa)
FeNa = (urine Na/plasma Na)/(urine creatinine/plasma creatinine)
FeNa <1 % = prerenal ARF FeNa >1% = ATN
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FeNaFeNaExceptions (intrinsic renal failure with FeNa <1
%) Urinary tract obstruction Acute glomerulonephritis Hepatorenal syndrome Radiologic contrast induced ATN Myoglobinuric and hemoglobinuric ARF Renal allograft rejection Drug-related alterations in renal hemodynami
cs (eg, captopril, NSAIDs)
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Urine output Urine output Anuria (<100 mL/d)
Urinary tract obstruction, renal artery obstruction, rapidly progressive glomerulonephritis, bilateral diffuse renal cortical necrosis
Oliguria
(100-400 mL/d)
Prerenal failure, hepatorenal syndromeNon-oliguria
(>400 mL/d) Acute interstitial nephritis, acute glomerulonephritis, partial obstructive nephropathy, nephrotoxic and ischemic ATN, radiocontrast-induced ARF, and rhabdomyolysis
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UrinalysisUrinalysis Granular casts
ATN, glomerulonephritis, interstitial nephritis
RBC casts
Glomerulonephritis, malignant HTN
WBC casts
Acute interstitial nephritis, pyelonephritis
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UrinalysisUrinalysis
Eosino-philuria
Acute allergic interstitial nephritis, atheroembolism
Crystall-uria
Acyclovir, sulfonamides, methotrexate, ethylene glycol toxicity, radiocontrast agents
Normal prerenal and postrenal failure, HUS/thrombotic thrombocytopenic purpura (TTP), preglomerular vasculitis, or atheroembolism
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Complete blood countComplete blood count
Leukocytosis common in ARF
Leukopenia and thrombocytopenia
SLE or TTP
Anemia and rouleaux formation
multiple myeloma
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Complete blood countComplete blood count
Microangiopathic anemia
TTP or atheroemboli
Eosinophilia allergic interstitial nephritis, polyarteritis nodosa, or atheroemboli
Coagulation disturbances
liver disease or hepatorenal syndrome.
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Blood chemistry Blood chemistry
Creatine phosphokinase (CPK) elevations
rhabdomyolysis and myocardial infarction
Elevations in liver transaminases
rapidly progressive liver failure and hepatorenal syndrome
Hypocalcemia (moderate)
Hyperkalemia
common complication of ARF
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Urine indices Urine indices
prerenal ARF
ATN
Urine specific gravity >1.018 <1.012
Urine osmolality (mOsm/kg H2O) >500 <500
Urine sodium (mEq/L) <15-20 >40
Plasma BUN/creatinine ratio >20 <10-15
Urine/plasma creatinine ratio >40 <20
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Laboratory Findings in the Differential Laboratory Findings in the Differential
Diagnosis of Acute Renal Failure:Diagnosis of Acute Renal Failure:
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Laboratory Findings in the Differential Laboratory Findings in the Differential
Diagnosis of Acute Renal Failure:Diagnosis of Acute Renal Failure:
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References References 1 Liano F, Pascual J: Epidemiology of acute renal
failure: a prospective, multicenter, community-based study. Madrid Acute Renal Failure Study Group. Kidney Int 1996 Sep; 50(3): 811-8
2 Klahr S, Miller SB: Acute oliguria. N Engl J Med 1998 Mar 5; 338(10): 671-5
3 Akposso K, Hertig A, Couprie R, et al: Acute renal failure in patients over 80 years old: 25-years' experience [In Process Citation]. Intensive Care Med 2000 Apr; 26(4): 400-6
4 Druml W: Prognosis of Acute Renal Failure. Nephron 1996; 53: 8-15
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References References
5 Moghal NE, Brocklebank JT, Meadow SR: A review of acute renal failure in children: incidence, etiology and outcome. Clin Nephrol 1998 Feb; 49(2): 91-5
6 Ragaller MJ, Theilen H, Koch T: Volume replacement in critically ill patients with acute renal failure. J Am Soc Nephrol 2001 Feb; 12 Suppl 17: S33-9
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References References
7 San A, Selcuk Y, Tonbul Z, Soypacaci Z: Etiology and prognosis in 438 patients with acute renal failure. Ren Fail 1996 Jul; 18(4): 593-9
8 Renal Failure, AcuteSeptember 17, 2002
eMedicine.com, Inc.