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BYDR ANUM YAQOOB

H.O MED-4

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Acute renal failure (ARF), or acute kidneyinjury (AKI), as it is now referred to in theliterature, is defined as an abrupt or rapiddecline in renal filtration function. This

condition is usually marked by a rise in serumcreatinine concentration or by azotemia (arise in blood urea nitrogen [BUN]concentration)

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However, immediately after a kidney injury,BUN or creatinine levels may be normal, andthe only sign of a kidney injury may bedecreased urine production

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AKI may be classified into 3 general categories, as

follows:

Prerenal - as an adaptive response to severe volumedepletion and hypotension, with structurally intactnephrons

Intrinsic - in response to cytotoxic, ischemic, orinflammatory insults to the kidney, with structuraland functional damage

Postrenal - from obstruction to the passage of urine While this classification is useful in establishing a

differential diagnosis, many pathophysiologicfeatures are shared among the different categories.

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In 2004, the Acute Dialysis Quality Initiative workgroup set forth a definition and classificationsystem for acute renal failure, described by theacronym RIFLE (Risk of renal dysfunction, Injury

to the kidney, Failure or Loss of kidney function,and End-stage kidney disease.

Investigators have since applied the RIFLE Systemto the clinical evaluation of AKI, although it was

not originally intended for that purpose. AKIresearch increasingly uses RIFLE.

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Stage GFR** Criteria Urine Output Criteria ProbabilityRisk SCreat increased 1.5

or

GFR decreased >25%

UO < 0.5 mL/kg/h 6h

High sensitivity (Risk>Injury >Failure)

Injury SCreat increased 2

or

GFR decreased >50%

UO < 0.5 mL/kg/h 12 h

Failure SCreat increased 3

or

GFR decreased 75%

or

SCreat 4 mg/dL; acuterise 0.5 mg/dL

UO < 0.3 mL/kg/h 24 h

(oliguria)

or

anuria 12 h

Loss Persistent acute renal failure: complete loss ofkidney function >4 wk

High specificity

ESKD* Complete loss of kidney function >3 mo

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Note: Patients can be classified by GFR criteriaand/or UO criteria. The criteria that support themost severe classification should be used. Thesuperimposition of acute on chronic failure is

indicated with the designation RIFLE-FC; failure ispresent in such cases even if the increase inSCreat is less than 3-fold, provided that the newSCreat is greater than 4.0 mg/dL (350 mol/L)

and results from an acute increase of at least 0.5mg/dL (44 mol/L).

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The driving force for glomerular filtration isthe pressure gradient from the glomerulus tothe Bowmans space. Glomerular pressure isprimarily dependent on renal blood flow (RBF)

and is controlled by combined resistances ofrenal afferent and efferent arterioles

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Prerenal failure - Defined by conditions withnormal tubular and glomerular function; GFRis depressed by compromised renal perfusion

Intrinsic renal failure - Includes diseases ofthe kidney itself, predominantly affecting theglomerulus or tubule, which are associatedwith release of renal afferentvasoconstrictors; ischemic renal injury can

ultimately leads to intrinsic renal failure b/cof the death of tubular cells and is the mostcommon cause.

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A physiologic hallmark of ATN is a failure tomaximally dilute or concentrate urine(isosthenuria). The injured kidney fails togenerate and maintain a high medullary solutegradient, because the accumulation of solute in

the medulla depends on normal distal nephronfunction. (Failure to excrete concentrated urineeven in the presence of oliguria is a helpfuldiagnostic clue in distinguishing prerenal fromintrinsic renal disease; in prerenal azotemia,

urine osmolality is typically more than 500mOsm/kg, whereas in intrinsic renal disease,urine osmolality is less than 300 mOsm/kg.)

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Postobstructive renal failure - Initially causesan increase in tubular pressure, decreasingthe filtration driving force; this pressuregradient soon equalizes, and maintenance of

a depressed GFR is then dependent on renalefferent vasoconstrictionwhich ultimatelyfails.

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PRE RENAL AKI:Volume depletion which can result from:

Renal losses (diuretics, polyuria)

GI losses (vomiting, diarrhea) Cutaneous losses (burns, Stevens-Johnson

syndrome)

Hemorrhage

Pancreatitis

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DECREASED CARDIAC OUTPUT: Heart failure

Pulmonary embolus

Acute myocardial infarction Severe valvular disease

Abdominal compartment syndrome (tenseascites

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SYSTEMIC VASODILATION: Sepsis Anaphylaxis

Anesthetics

Drug overdoseAFFERENT ARTEIOLAR VASOCONSTRICTION: Hypercalcemia

Drugs (NSAIDs, amphotericin B,norepinephrine, radiocontrast agents)

Hepatorenal syndrome

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INTRINSIC RENAL DISEASE:(VASCULAR CAUSES) Renal artery obstruction (thrombosis, emboli, dissection, vasculitis)

Renal vein obstruction (thrombosis)

Microangiopathy (TTP, HUS, disseminatedintravascular coagulation [DIC], preeclampsia)

Malignant hypertension

Scleroderma renal crisis

Transplant rejection Atheroembolic disease

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GLOMERULAR CAUSES: Anti-glomerular basement membrane (GBM)

disease (Goodpasture syndrome) Anti-neutrophil cytoplasmic antibody-

associated glomerulonephritis (ANCA-associated GN) (Wegener granulomatosis,Churg-Strauss syndrome, microscopicpolyangiitis)

Immune complex GN (lupus, postinfectious,cryoglobulinemia, primarymembranoproliferative glomerulonephritis)

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TUBULAR CAUSES: Heme pigment (rhabdomyolysis, intravascular

hemolysis)

Crystals (tumor lysis syndrome, seizures,ethylene glycol poisoning, megadose vitaminC, acyclovir, indinavir, methotrexate)

Drugs (aminoglycosides, lithium,

amphotericin B, pentamidine, cisplatin,ifosfamide, radiocontrast agents)

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INTERSTITIAL CAUSES: Drugs (penicillins, cephalosporins, NSAIDs,

proton-pump inhibitors, allopurinol,rifampin, indinavir, mesalamine,sulfonamides)

Infection (pyelonephritis, viral nephritides)

Systemic disease (Sjgren syndrome, sarcoid,

lupus, lymphoma, leukemia, tubulonephritis,uveitis)

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Ureteric obstruction (stone disease, tumor, fibrosis,ligation during pelvic surgery) Bladder neck obstruction (benign prostatic

hypertrophy [BPH], cancer of the prostate [CAprostate or prostatic CA], neurogenic bladder,tricyclic antidepressants, ganglion blockers, bladdertumor, stone disease, hemorrhage/clot)

Urethral obstruction (strictures, tumor, phimosis) Intra-abdominal hypertension (tense ascites) Renal vein thrombosis

Retroperitoneal tumor, retroperitoneal fibrosis(methysergide, propranolol, hydralazine), urolithiasis,or papillary necrosis.

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A detailed and accurate history is crucial tothe diagnosis of the type of acute kidneyinjury (AKI) that a patient has and to

determining the diseases subsequenttreatment.

Distinguishing AKI from chronic renal failureis important, yet making the distinction can

be difficult. A history of chronic symptomsfatigue, weight loss, anorexia, nocturia, andpruritussuggests chronic renal failure

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Nephrotoxic drug ingestion

History of trauma or unaccustomed exertion

Blood loss or transfusions

Evidence of connective tissue disorders orautoimmune diseases

Exposure to toxic substances, such as ethylalcohol or ethylene glycol

Exposure to mercury vapors, lead, cadmium, orother heavy metals, which can be encountered inwelders and miners

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Hypertension Congestive cardiac failure

Diabetes

Multiple myeloma Chronic infection

Myeloproliferative disorder

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Urine output history can be useful. Oliguriagenerally favors AKI. Abrupt anuria suggestsacute urinary obstruction, acute and severeglomerulonephritis, or embolic renal artery

occlusion. A gradually diminishing urineoutput may indicate a urethral stricture orbladder outlet obstruction due to prostateenlargement.

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Patients commonly present with symptoms related tohypovolemia, including thirst, decreased urineoutput, dizziness, and orthostatic hypotension.

Elders with vague mental status change arecommonly found to have prerenal or normotensiveischemic AKI.

Ask about volume loss from vomiting, diarrhea,sweating, polyuria, or hemorrhage.

Patients with advanced cardiac failure leading todepressed renal perfusion may present withorthopnea and paroxysmal nocturnal dyspnea.

Insensible fluid losses can result in severehypovolemia in patients with restricted fluid accessand should be suspected in elderly patients and incomatose or sedated patients.

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Intravascular volume

depletion

Altered Intrarenal

hemodynamics

Decreased effective

arterial blood volume

Abdominal

Compartment

Syndrome

Etiologies ofPre renal ARF

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GLOMERULAR TUBULAR

Nephritic syndrome ofhematuria, edema, andHTN indicates aglomerular etiology of

AKI. Query about priorthroat or skininfections.

ATN should be suspected in any patientpresenting after a period of hypotensionsecondary to cardiac arrest, hemorrhage,sepsis, drug overdose, or surgery.

A careful search for exposure tonephrotoxins should include a detailed listof all current medications and any recentradiologic examinations (ie, exposure toradiologic contrast agents).

Pigment-induced AKI should be suspectedin patients with possible rhabdomyolysis(muscular pain, recent coma, seizure,intoxication, excessive exercise, limbischemia) or hemolysis (recent bloodtransfusion).

Allergic interstitial nephritis should besuspected with fevers, rash, arthralgias,and exposure to certain medications,including NSAIDs and antibiotics.

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Postrenal failure usually occurs in older men withprostatic obstruction and symptoms of urgency,frequency, and hesitancy. Patients may present withasymptomatic, high-grade urinary obstructionbecause of the chronicity of their symptoms.

A history of prior gynecologic surgery orabdominopelvic malignancy often can be helpful inproviding clues to the level of obstruction.

Flank pain and hematuria should raise a concernabout renal calculi or papillary necrosis as the sourceof urinary obstruction.

Use of acyclovir, methotrexate, triamterene, indinavir,or sulfonamides implies the possibility of tubularobstruction by crystals of these medication

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Skin Skin examination may reveal the following:

Livido reticularis, digital ischemia, butterfly rash,palpable purpura - Systemic vasculitis

Maculopapular rash - Allergic interstitial nephritis

Track marks (ie, intravenous drug abuse) -Endocarditis

Petechiae, purpura, ecchymosis, and livedo reticularisprovide clues to inflammatory and vascular causes of

AK. Infectious diseases, TTP, DIC, and embolic

phenomena can produce typical cutaneous changes.

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Eyes Eye examination may reveal the following: Keratitis, iritis, uveitis, dry conjunctivae - Autoimmune

vasculitis Jaundice - Liver diseases Band keratopathy (ie, hypercalcemia) - Multiple myeloma Signs of diabetes mellitus Signs of hypertension Atheroemboli (retinopathy) Evidence of uveitis may indicate interstitial nephritis and

necrotizing vasculitis. Findings suggestive of severe hypertension, atheroembolic

disease, and endocarditis may be observed on carefulexamination of the eyes.

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Ears Ear examination may reveal the following:

Hearing loss - Alport disease and aminoglycosidetoxicity

Mucosal or cartilage ulcerations - WegenergranulomatosisCardiovascular system

Cardiovascular examination may reveal the following:

Irregular rhythms (ie, atrial fibrillation) -

Thromboemboli Murmurs - Endocarditis

Increased jugulovenous distention, rales, S3 - CHF

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Abdomen Abdominal examination may reveal the following: Pulsatile mass or bruit - Atheroemboli Costovertebral angle tenderness - Nephrolithiasis, papillary

necrosis Pelvic, rectal masses; prostatic hypertrophy; distended bladder

Urinary obstruction Limb ischemia, edema - Rhabdomyolysis Abdominal examination findings can be useful to help detect

obstruction at the bladder outlet as the cause of renal failure,which may be due to cancer or an enlarged prostate. (P/Rexamination)

The presence of tense ascites can indicate elevated intra-abdominal pressure that can retard renal venous return andresult in AKI.

The presence of an epigastric bruit suggests renal vascularhypertension, which may predispose to AKI.

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Pulmonary Pulmonary examination may reveal the

following:

Rales - Goodpasture syndrome, Wegenergranulomatosis

Hemoptysis - Wegener granulomatosis

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The physical examination must include pulse rate andblood pressure recordings measured in the supineposition and the standing position; close inspection of the

jugular venous pulse; careful examination of the heart,lungs, skin turgor, and mucous membranes; andassessment for the presence of peripheral edema.

In hospitalized patients, accurate daily records of fluidintake and urine output and daily measurements of patientweight are important. Hypovolemia leads to hypotension;however, hypotension may not necessarily indicatehypovolemia.

Severe CHF may also cause hypotension. .

Severe hypertension with renal failure suggestsrenovascular disease, glomerulonephritis, vasculitis, oratheroembolic disease.

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Anuria (< 100 mL/d) - Urinary tractobstruction, renal artery obstruction, rapidlyprogressive glomerulonephritis, bilateraldiffuse renal cortical necrosis

Oliguria (100-400 mL/d) - Prerenal failure,hepatorenal syndrome Nonoliguria (>400 mL/d) - Acute interstitial

nephritis, acute glomerulonephritis, partial

obstructive nephropathy, nephrotoxic andischemic ATN, radiocontrast-induced AKI,and rhabdomyolysis

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Alcoholic Ketoacidosis Anemia, Sickle Cell

Aneurysm, Abdominal

CHF and Pulmonary Edema Diabetic Ketoacidosis

Obstructive Uropathy

GI Bleeding

Protein Overloading Steroid Use

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Renal Calculi Renal Failure, Chronic and Dialysis

Complications

Toxicity, Alcohols

Urinary Obstruction

Urinary Tract Infection

Metabolic Acidosis

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Blood Urea Nitrogen and Serum Creatinine CBC

Peripheral Smear and Serology

Urinalysis

Urine Electrolytes Bladder Pressure

Emerging Biomarkers

Ultrasonography

Nuclear Scanning Aortorenal Angiography

Renal Biopsy.

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Although increased levels of BUN and creatinineare the hallmarks of renal failure, the rate of riseis dependent on the degree of renal insult as wellas on protein intake with respect to BUN.

The ratio of BUN to creatinine is an importantfinding, because the ratio can exceed 20:1 inconditions in which enhanced reabsorption ofurea is favored (eg, in volume contraction); thissuggests prerenal acute kidney injury (AKI).

BUN may be elevated in patients with GI ormucosal bleeding, steroid treatment, or proteinloading.

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Assuming no renal function, the rise in BUN over 24hours can be roughly predicted using the followingformula: 24-hour protein intake in milligrams X 0.16divided by total body water in mg/dL added to the BUNvalue.

Assuming no renal function, the rise in creatinine can

be predicted using the following formulas: For males: weight in kilograms X [28 - 0.2(age)] divided

by total body water in mg/dL added to the creatininevalue

For females: weight in kilograms X [23.8 - 0.17(age)]divided by total body water added to the creatininevalue

As a general rule, if serum creatinine increases to morethan 1.5 mg/dL/d, rhabdomyolysis must be ruled out.

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The peripheral smear may show schistocytes in conditionssuch as HUS or TTP. A finding of increased rouleaux formation suggests

multiple myeloma, and the workup should be directedtoward immunoelectrophoresis of serum and urine.

The presence of myoglobin or free hemoglobin, increased

serum uric acid level, and other related findings may helpto further define the etiology of acute kidney injury (AKI). Serologic tests for antinuclear antibody (ANA), ANCA, anti-

GBM antibody, hepatitis, and antistreptolysin (ASO) andcomplement levels may help to include and excludeglomerular disease.

Although serologic tests can be informative, the costs canbe prohibitive if these tests are not ordered judiciously.

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Findings of granular, muddy-brown casts are suggestiveof tubular necrosis . The presence of tubular cells ortubular cell casts also supports the diagnosis of ATN.Often, oxalate crystals are observed in cases of ATN.

Reddish brown or cola-colored urine suggests thepresence of myoglobin or hemoglobin, especially in the

setting of a positive dipstick for heme and no red bloodcells (RBCs) on the microscopic examination. The dipstick assay may reveal significant proteinuria as a

result of tubular injury. The presence of RBCs in the urine is always pathologic.

Eumorphic RBCs suggest bleeding along the collecting

system. Dysmorphic RBCs or RBC casts indicate glomerularinflammation, suggesting glomerulonephritis is present.

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The presence of WBCs or WBC casts suggestspyelonephritis or acute interstitial nephritis. Thepresence of urine eosinophils is helpful inestablishing a diagnosis but is not necessary forallergic interstitial nephritis to be present.

The presence of eosinophils, as visualized withWright stain or Hansel stain, suggests interstitialnephritis but can also be seen in urinary tractinfections, glomerulonephritis, and atheroembolicdisease.

The presence of uric acid crystals may represent ATN

associated with uric acid nephropathy. Calcium oxalate crystals are usually present in cases

of ethylene glycol poisoning.

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Urine electrolyte findings also can serve as valuableindicators of functioning renal tubules. The fractionalexcretion of sodium (FENa) is the commonly usedindicator. However, the interpretation of results frompatients in nonoliguric states, those withglomerulonephritis, and those receiving or ingesting

diuretics can lead to an erroneous diagnosis. FENa can be a valuable test for helping to detect

extreme renal avidity for sodium in conditions suchas hepatorenal syndrome. The formula for calculatingthe FENa is as follows:

FENa = (UNa/PNa) / (UCr/PCr) X 100 Calculating the FENa is useful in acute kidney injury

(AKI) only in the presence of oliguria.

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In patients with prerenal azotemia, the FENa isusually less than 1%. In ATN, the FENa is greaterthan 1%. Exceptions to this rule are ATN causedby radiocontrast nephropathy, severe burns,

acute glomerulonephritis, and rhabdomyolysis. In the presence of liver disease, FENa can be less

than 1% in the presence of ATN. On the otherhand, because administration of diuretics may

cause the FENa to be greater than 1%, thesefindings cannot be used as the sole indicators inAKI.

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In patients who are receiving diuretics, afractional excretion of urea (FEUrea) can beobtained, since urea transport is not affectedby diuretics. The formula for calculating the

FEUrea is as follows: FEUrea = (Uurea/Purea) / (UCr/PCr) X 100

FEUrea of less than 35% is suggestive of aprerenal state

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An intra-abdominal pressure of less than 10mm Hg is considered normal and suggeststhat abdominal compartment syndrome is notthe cause of AKI. Patients with an intra-

abdominal pressure below 15-25 mm Hg areat risk for abdominal compartmentsyndrome, and those with bladder pressuresabove 25 mm Hg should be suspected of

having AKI as a result of abdominalcompartment syndrome.

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A number of biomarkers are being investigatedto risk stratify and predict acute kidney injury(AKI) in patients at risk for the disease. Thereason for this is because creatinine is a late

marker for renal dysfunction and, once elevated,reflects a severe reduction in GFR.

The most promising biomarker to date is urinaryneutrophil gelatinase-associated lipocalin

(NGAL), which has been shown to predict AKI inchildren undergoing cardiopulmonary bypasssurgery.

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Renal ultrasonography is useful for evaluatingexisting renal disease and obstruction of theurinary collecting system. The degree ofhydronephrosis does not necessarily correlate

with the degree of obstruction. Mildhydronephrosis may be observed withcomplete obstruction if found early.

Ultrasonographic scans or other imaging

studies showing small kidneys suggestchronic renal failure

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Doppler scans are useful for detecting thepresence and nature of renal blood flow.

Because renal blood flow is reduced inprerenal or intrarenal AKI, test findings are of

little use in the diagnosis of AKI. However,Doppler scans can be quite useful in thediagnosis of thromboembolic or renovasculardisease.

Increased resistive indices can be observed inpatients with hepatorenal syndrome.

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Because of a marked delay intubular excretion of radionuclidein prerenal disease and intrarenal

disease, the value of these scansis limited

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This can be helpful in establishing thediagnosis of renal vascular diseases,including renal artery stenosis, renalatheroembolic disease, and atherosclerosis

with aortorenal occlusion, and in certaincases of necrotizing vasculitis (eg,polyarteritis nodosa).

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A renal biopsy may also be indicated whenrenal function does not return for aprolonged period and a prognosis is requiredto develop long-term management.

Acute cellular or humoral rejection in atransplanted kidney can be definitivelydiagnosed only by performing a renal biopsy.

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Measures to correct underlying causes ofacute kidney injury (AKI) should begin at theearliest indication of renal dysfunction. Alarge proportion of the renal mass is

damaged before any biochemical evidence ofrenal dysfunction is appreciated, because therelationship between the GFR and the serumcreatinine level is not linear, especially early

in disease; the rise of serum creatinine maynot be evident before 50% of the GFR is lost.

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The Acute Renal Failure Trial Network (ATN) Study,completed in 2008, was designed to compare clinicaloutcomes between patients allocated to an intensivedose versus a less-intensive dose of renalreplacement therapy.]No additional benefit

(morbidity/mortality) was conferred to patients whoreceived more intensive dialysis (either intermittentor continuous dialysis). The best evidence suggeststhat patients with dialysis-dependent AKI shouldreceive at least 3 hemodialysis treatments per week

with delivered Kt/V value of 1.2 or continuoushemodialysis (continuous venovenous hemodialysisor hemofiltration) of 20 mg/kg/h (prescribed).

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Maintenance of volume homeostasis andcorrection of biochemical abnormalities remainthe primary goals of treatment.

Daily fluid intake should equal urinary output

plus an additional 500ml to cover insensibleloses.

Fluid intake and urinary output should bemeasured and patient should be weighed daily.

Furosemide can be used to correct volumeoverload when the patients are still responsive;this often requires high intravenous (IV) doses.

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NSAIDS ACE inhibitors

Radiocontrasts agents

Aminoglycosides and other antibiotics

Heavy metal preparations

Chemotherapeutic Agents

Similarly, all medications cleared by renal

excretion should be avoided or their dosesshould be adjusted appropriately.

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A prophylactic strategy shown to decrease theincidence of contrast nephropathy is the IVadministration of fluids.

Normal saline solution of 1 ml/kg/h administered 12hours before the procedure and then 12 hours after

the procedure is recommended. In patients who are at high risk for volume overload,isotonic NaHCO3 solution should be administeredbefore and after the procedure.

Another prophylactic agent, used with varying

success, isN

-acetylcysteine at a dosage of 1200 mgPO q12h. This is administered to high-risk patientsthe day before a contrast study is performed and iscontinued the day of the procedure. Diuretics,NSAIDs, and possibly ACEIs should be withheld nearthe time of the procedure.

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Correcting severe acidosis with bicarbonateadministration can be important as a bridgeto dialysis.

Hyperkalemia, which can be life-threatening,

should be treated by decreasing the intake ofpotassium in diet or tube feeds, exchangingpotassium across the gut lumen usingpotassium-binding resins, promotingintracellular shifts in potassium with insulinand dextrose solutions, and institutingdialysis.

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Patients with ARF are at risk of intercurrentinfection so regular clinical examination andmicrobial investigationas clinically indicatedare required.

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Calculation of the nitrogen balance can bechallenging, especially in the presence ofvolume contraction, hypercatabolic states, GIbleeding, and diarrheal disease. Critically ill

patients should receive at least 1 g/kg/dprotein intake but should avoidhyperalimentation, which can lead to anelevated BUN level and water loss resulting in

hypernatremia.

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If there is an obstruction of the urinary tract,relieve the obdtruction.If that is not possibleurgent nephrostomy may be done.

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Great controversy exists regarding the timing of dialysis.Dialysis, especially hemodialysis, may delay the recoveryof patients with AKI.

There seems to be no difference in outcome between theuse of intermittent hemodialysis and continuous renalreplacement therapy (CRRT), but this is currently under

investigation. However, CCRT may have a role in patientswho are hemodynamically unstable and who have hadprolonged renal failure after a stroke or liver failure. Suchpatients may not tolerate the rapid shift of fluid andelectrolytes caused during conventional hemodialysis.Although not frequently used, peritoneal dialysis can alsotechnically be used in acute cases and probably istolerated better hemodynamically than conventionalhemodialysis.

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Indications for dialysis in patients with AKIare as follows:

Volume expansion that cannot be managedwith diuretics

Hyperkalemia refractory to medical therapy

Correction of severe acid-base disturbancesthat are refractory to medical therapy

Severe azotemia (BUN >80-100) Uremia

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Pulmonary complicationsPulmonary complications have been reported in

approximately 54% of patients with AKI andare the single most significant risk factor for

death in patients with AKI.Hypoxia commonly occurs during hemodialysisand can be particularly significant in thepatient with pulmonary disease. This dialysis-related hypoxia is thought to occur secondaryto white blood cell (WBC) lung sequestrationand alveolar hypoventilation.

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Cardiovascular complicationsCardiovascular complications (eg, congestive heartfailure [CHF], myocardial infarction, arrhythmias,cardiac arrest) have been observed in as many as 35%of patients with AKI. Fluid overload secondary tooliguric AKI is a particular risk for elderly patients

with little cardiac reserve. GI complicationsGI symptoms of nausea, vomiting, and anorexia are

frequent complications of AKI and represent one ofthe cardinal signs of uremia. GI bleeding occurs in

approximately one third of patients with AKI. Mostepisodes are mild, but GI bleeding accounts for 3-8%of deaths in patients with AKI.

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Infectious complicationsInfections commonly complicate the course of AKI andhave been reported to occur in as many as 33% ofpatients with AKI. Most common sites are pulmonaryand urinary tracts. Infections are the leading cause ofmorbidity and death in patients with AKI. Various

studies have reported mortality rates of 11-72% ininfections complicating AKI.

Neurologic complicationsNeurologic signs of uremia are a common complication

of AKI and have been reported in approximately 38%

of patients with AKI. Neurologic sequelae includelethargy, somnolence, reversal of the sleep-wakecycle, and cognitive or memory deficits.

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This is indicated by a gradual return ofurinary output and subsequent improvementin plasma biochemistry.

Some patients primarily those with ATN or

after relief of chronic obstruction develop adiuretic phase.This is due in part to the lossof medullary cocentration gradient whichnormally allows concentration of urine in thecollecting duct.Not all patients have diureticphase depending on the severity of renaldamage and rate of recovery.

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Renal recovery in most cases is not completeand that the kidneys remain vulnerable tonephrotoxic effects of all therapeutic agents.Therefore, agents with nephrotoxic potential arebest avoided.

Renal recovery is usually observed within the first2 weeks, and many nephrologists tend todiagnose patients with end-stage (ie, irreversible)renal failure 6-8 weeks after the onset of acute

kidney injury (AKI). It is always better to checkthese patients periodically, because somepatients may regain renal function much later.

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