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Main Menu RENAL FAILURE RENAL FAILURE

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Page 1: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

Main Menu

RENAL FAILURERENAL FAILURE

Page 2: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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ClassificationsClassifications

Acute versus chronicAcute versus chronic Pre-renal, renal, post-renalPre-renal, renal, post-renal Anuric, oliguric, polyuricAnuric, oliguric, polyuric

Page 3: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Renal Physiology ReviewRenal Physiology ReviewThe Kidneys:The Kidneys:

a.a. Control the fluid/electrolyte balance for the Control the fluid/electrolyte balance for the bodybody

b.b. Remove metabolic wastes from the blood & Remove metabolic wastes from the blood & excrete them to the outsideexcrete them to the outside

c.c. Regulate red-blood cell productionRegulate red-blood cell production

d.d. Regulate blood-pressureRegulate blood-pressure

e.e. Important in calcium ion absorptionImportant in calcium ion absorption

f.f. Control volume, composition and pH of the Control volume, composition and pH of the bloodblood

Page 4: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Renal Hormone RegulationRenal Hormone Regulation

Synthesis and activation of hormones by Synthesis and activation of hormones by the kidney include:the kidney include:

• Active form of Vitamin DActive form of Vitamin D• ErythropoietinErythropoietin

Renal blood flow regulated by:Renal blood flow regulated by:

Renin-angiotensin aldosterone system (RAAS)

Page 5: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Fluid and Electrolyte ControlFluid and Electrolyte ControlMechanismsMechanisms

RAAS – Renin-Angiotensin Aldosterone RAAS – Renin-Angiotensin Aldosterone SystemSystem

AldosteroneAldosterone ADH – Anti-Diuretic HormoneADH – Anti-Diuretic Hormone

Page 6: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Aldosterone

Increases rate of sodium ion absorptionIncreases rate of sodium ion absorption Chloride moves along with sodium Chloride moves along with sodium

because of + charge of sodiumbecause of + charge of sodium Increases rate of potassium & hydrogen Increases rate of potassium & hydrogen

ion secretionion secretion

Result:Result:

Fluid and sodium retention increases blood-Fluid and sodium retention increases blood-pressurepressure

Page 7: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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ACUTE RENAL FAILUREACUTE RENAL FAILURE

Page 8: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Acute Renal FailureAcute Renal Failure

DefinitionDefinition The loss of renal function (measured as GFR) The loss of renal function (measured as GFR)

over hours to daysover hours to days Expressed clinically as the retention of Expressed clinically as the retention of

nitrogenous waste products in the bloodnitrogenous waste products in the blood

Page 9: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Acute Renal FailureAcute Renal Failure

DefinitionsDefinitions Azotemia - the accumulation of nitrogenous Azotemia - the accumulation of nitrogenous

wasteswastes Uremia - symptomatic renal failureUremia - symptomatic renal failure Oliguria - urine output < 400-500 mL/24 hoursOliguria - urine output < 400-500 mL/24 hours Anuria - urine output < 100 mL/24 hoursAnuria - urine output < 100 mL/24 hours

Page 10: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Causes of ARFCauses of ARF Pre-renal =Pre-renal =

vomiting, diarrhea, poor fluid intake, fever, use of diuretics, and heart vomiting, diarrhea, poor fluid intake, fever, use of diuretics, and heart failure failure

cardiac failure, liver dysfunction, or septic shock cardiac failure, liver dysfunction, or septic shock Intrinsic Intrinsic

Interstitial nephritis, acute glomerulonephritis, tubular necrosis, Interstitial nephritis, acute glomerulonephritis, tubular necrosis, ischemia, toxinsischemia, toxins

Post-renal =Post-renal = prostatic hypertrophy, cancer of the prostate or cervix, or prostatic hypertrophy, cancer of the prostate or cervix, or

retroperitoneal disorders retroperitoneal disorders neurogenic bladder neurogenic bladder bilateral renal calculi, papillary necrosis, coagulated blood, bladder bilateral renal calculi, papillary necrosis, coagulated blood, bladder

carcinoma, and fungus carcinoma, and fungus

Page 11: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Symptoms of ARFSymptoms of ARF

Decrease urine output (70%)Decrease urine output (70%) Edema, esp. lower extremityEdema, esp. lower extremity Mental changesMental changes Heart failureHeart failure Nausea, vomitingNausea, vomiting PruritusPruritus AnemiaAnemia TachypenicTachypenic Cool, pale, moist skinCool, pale, moist skin

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Hyperkalemia SymptomsHyperkalemia Symptoms WeaknessWeakness LethargyLethargy Muscle crampsMuscle cramps ParesthesiasParesthesias DysrhythmiasDysrhythmias

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Hyperkalemia TreatmentHyperkalemia Treatment

Calcium gluconate (carbonate)Calcium gluconate (carbonate) Sodium BicarbonateSodium Bicarbonate Insulin/glucoseInsulin/glucose Diuretics (Furosemid)Diuretics (Furosemid) AlbuterolAlbuterol HemodialysisHemodialysis

Page 14: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Prerenal Acute Renal FailurePrerenal Acute Renal Failure

Volume DepletionVolume Depletion Decreased effective blood volumeDecreased effective blood volume

congestive heart failurecongestive heart failure cirrhosiscirrhosis nephrotic syndromenephrotic syndrome sepsissepsis

Renal vasoconstrictionRenal vasoconstriction hepatorenal syndromehepatorenal syndrome hypercalcemiahypercalcemia nonsteroidal anti-inflammatory drugsnonsteroidal anti-inflammatory drugs

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Prerenal Acute Renal Failure:Prerenal Acute Renal Failure:Clinical PresentationClinical Presentation

HistoryHistory volume loss (e.g., diarrhea, acute blood loss)volume loss (e.g., diarrhea, acute blood loss) heart diseaseheart disease liver diseaseliver disease evidence of infectionevidence of infection diuretic usediuretic use thirstthirst orthostatic symptomsorthostatic symptoms

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Prerenal Acute Renal Failure:Prerenal Acute Renal Failure:Clinical PresentationClinical Presentation

Physical ExaminationPhysical Examination Blood pressure and pulseBlood pressure and pulse Orthostatic changes in blood pressureOrthostatic changes in blood pressure Skin turgorSkin turgor Dryness of mucous membranes and axillaeDryness of mucous membranes and axillae Neck veinsNeck veins Cardiopulmonary examCardiopulmonary exam Peripheral edemaPeripheral edema

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Prerenal Acute Renal Failure:Prerenal Acute Renal Failure: Clinical Presentation Clinical Presentation

BUN:Creatinine ratioBUN:Creatinine ratio > 20:1> 20:1

Urine indicesUrine indices OliguriaOliguria

• usually < 500 mL/24 hours; but may be non-oliguricusually < 500 mL/24 hours; but may be non-oliguric Elevated urine concentrationElevated urine concentration

• UUOsmOsm > 700 mmol/L > 700 mmol/L• specific gravity > 1.020specific gravity > 1.020

Evidence of high renal sodium avidityEvidence of high renal sodium avidity• UUNaNa < 20 mmol/L < 20 mmol/L

• FEFENaNa < 0.01 < 0.01 Inactive urine sedimentInactive urine sediment

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Fractional Excretion of SodiumFractional Excretion of SodiumFractional Excretion of SodiumFractional Excretion of Sodium

Etiologies of a fractional excretion of Etiologies of a fractional excretion of sodium <0.01sodium <0.01 normal renal functionnormal renal function prerenal azotemiaprerenal azotemia hepatorenal syndromehepatorenal syndrome early obstructive uropathyearly obstructive uropathy contrast nephropathycontrast nephropathy rhabdomyolysisrhabdomyolysis acute glomerulonephritisacute glomerulonephritis

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Treatment of Treatment of Prerenal Acute Renal FailurePrerenal Acute Renal Failure

Correction of volume deficitsCorrection of volume deficits Discontinuation of antagonizing Discontinuation of antagonizing

medicationsmedications NSAIDs/COX-2 inhibitorsNSAIDs/COX-2 inhibitors DiureticsDiuretics

Optimization of cardiac functionOptimization of cardiac function

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Postrenal Acute Renal FailurePostrenal Acute Renal Failure

Urinary tract obstructionUrinary tract obstruction level of obstructionlevel of obstruction

• upper tract (ureters)upper tract (ureters)• lower tract (bladder outlet or urethra)lower tract (bladder outlet or urethra)

degree of obstructiondegree of obstruction• partialpartial• completecomplete

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Pathophysiology of Renal Failure in Pathophysiology of Renal Failure in Obstructive UropathyObstructive Uropathy

EarlyEarly Increased intratubular pressureIncreased intratubular pressure Initial increase followed by decrease in renal Initial increase followed by decrease in renal

plasma flowplasma flow LateLate

Normal intratubular pressureNormal intratubular pressure Marked decrease in renal plasma flowMarked decrease in renal plasma flow

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Etiologies of Postrenal Etiologies of Postrenal Acute Renal FailureAcute Renal Failure

Upper tract obstructionUpper tract obstruction IntrinsicIntrinsic

• nephrolithiasisnephrolithiasis• papillary necrosispapillary necrosis• blood clotblood clot• transitional cell cancertransitional cell cancer

ExtrinsicExtrinsic• retroperitoneal or pelvic retroperitoneal or pelvic

malignancymalignancy• retroperitoneal fibrosisretroperitoneal fibrosis• endometriosisendometriosis• abdominal aortic abdominal aortic

aneurysmaneurysm

Lower tract Lower tract obstructionobstruction

• benign prostatic benign prostatic hypertrophyhypertrophy

• prostate cancerprostate cancer• transitional cell cancertransitional cell cancer• urethral strictureurethral stricture• bladder stonesbladder stones• blood clotblood clot• neurogenic bladderneurogenic bladder

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Postrenal Acute Renal Failure:Postrenal Acute Renal Failure:Clinical PresentationClinical Presentation

HistoryHistory Symptoms of bladder outlet obstructionSymptoms of bladder outlet obstruction

• urinary frequencyurinary frequency• urgencyurgency• intermittencyintermittency• hesitancyhesitancy• nocturianocturia• incomplete voidingincomplete voiding

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Postrenal Acute Renal Failure:Postrenal Acute Renal Failure:Clinical PresentationClinical Presentation

HistoryHistory Changes in urine volumeChanges in urine volume

• anuriaanuria• polyuriapolyuria• fluctuating urine volumefluctuating urine volume

Flank painFlank pain HematuriaHematuria History of pelvic malignancyHistory of pelvic malignancy

Page 25: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Postrenal Acute Renal Failure:Postrenal Acute Renal Failure:Clinical PresentationClinical Presentation

Physical ExaminationPhysical Examination Suprapubic massSuprapubic mass Prostatic enlargementProstatic enlargement Pelvic massesPelvic masses AdenopathyAdenopathy

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Postrenal Acute Renal Failure:Postrenal Acute Renal Failure:Clinical EvaluationClinical Evaluation

Diagnostic studiesDiagnostic studies BUN: Creatinine ratio > 20:1BUN: Creatinine ratio > 20:1 Unremarkable urine sedimentUnremarkable urine sediment Variable urine chemistriesVariable urine chemistries

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Postrenal Acute Renal Failure:Postrenal Acute Renal Failure:Clinical EvaluationClinical Evaluation

Diagnostic studiesDiagnostic studies Post-void residual bladder volumePost-void residual bladder volume

• > 100 mL consistent with voiding dysfunction> 100 mL consistent with voiding dysfunction Radiologic studiesRadiologic studies

• UltrasoundUltrasound• CT scanCT scan• Nuclear medicineNuclear medicine• Retrograde pyelographyRetrograde pyelography• Antegrade nephrostogramsAntegrade nephrostograms

Page 28: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Treatment of Treatment of Postrenal Acute Renal FailurePostrenal Acute Renal Failure

Relief of obstructionRelief of obstruction Lower tract obstructionLower tract obstruction

• bladder catheterbladder catheter Upper tract obstructionUpper tract obstruction

• ureteral stentsureteral stents• percutaneous nephrostomiespercutaneous nephrostomies

Recovery of renal function dependent Recovery of renal function dependent upon duration of obstructionupon duration of obstruction

Risk of post-obstructive diuresisRisk of post-obstructive diuresis

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Intrinsic Acute Renal FailureIntrinsic Acute Renal Failure

Acute tubular necrosis (ATN)Acute tubular necrosis (ATN) Acute interstitial nephritis (AIN)Acute interstitial nephritis (AIN) Acute glomerulonephritis (AGN)Acute glomerulonephritis (AGN) Acute vascular syndromes Acute vascular syndromes Intratubular obstructionIntratubular obstruction

Page 30: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Acute Tubular NecrosisAcute Tubular Necrosis

IschemicIschemic• prolonged prerenal prolonged prerenal

azotemiaazotemia

• hypotensionhypotension

• hypovolemic shockhypovolemic shock

• cardiopulmonary cardiopulmonary arrestarrest

• cardiopulmonary cardiopulmonary bypass bypass

SepsisSepsis

NephrotoxicNephrotoxic drug-induceddrug-induced

• radiocontrast agents radiocontrast agents

• aminoglycosidesaminoglycosides

• amphotericin Bamphotericin B

• cisplatinumcisplatinum

• acetaminophenacetaminophen pigment nephropathypigment nephropathy

• hemoglobinhemoglobin

• myoglobinmyoglobin

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Pathophysiology of Pathophysiology of Acute Tubular NecrosisAcute Tubular Necrosis

Mechanisms of decreased renal functionMechanisms of decreased renal function VasoconstrictionVasoconstriction Tubular obstruction by sloughed debrisTubular obstruction by sloughed debris Backleak of glomerular filtrate across Backleak of glomerular filtrate across

denuded tubular basement membranedenuded tubular basement membrane

Page 32: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Acute Tubular Necrosis:Acute Tubular Necrosis: Clinical Presentation Clinical Presentation

HistoryHistory Acute illnessAcute illness Exposure to nephrotoxinsExposure to nephrotoxins Episodes of hypotensionEpisodes of hypotension

Physical examinationPhysical examination Hemodynamic statusHemodynamic status Volume statusVolume status Features of associated illnessFeatures of associated illness

Laboratory dataLaboratory data BUN:Creatinine ratio < 10:1BUN:Creatinine ratio < 10:1 Evidence of toxin exposureEvidence of toxin exposure

Page 33: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Acute Tubular Necrosis:Acute Tubular Necrosis: Clinical Presentation Clinical Presentation

Urine indicesUrine indices Urine volumeUrine volume

• may be oliguric or non-oliguricmay be oliguric or non-oliguric Isosthenuric urine concentrationIsosthenuric urine concentration

• UUOsmOsm 300 mmol/L 300 mmol/L• specific gravity specific gravity 1.010 1.010

Evidence of renal sodium wastingEvidence of renal sodium wasting• UUNaNa > 40 mmol/L > 40 mmol/L

• FEFENaNa > 0.02 > 0.02 Urine sedimentUrine sediment

• tubular epithelial cellstubular epithelial cells• granular castsgranular casts

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Acute Tubular Necrosis:Acute Tubular Necrosis:TreatmentTreatment

Supportive therapySupportive therapy No specific pharmacologic treatmentsNo specific pharmacologic treatments Acute dialysis for:Acute dialysis for:

volume overload volume overload metabolic acidosis metabolic acidosis hyperkalemiahyperkalemia uremic syndromeuremic syndrome

• pericarditispericarditis• encephalopathyencephalopathy

azotemiaazotemia

Page 35: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Prognosis ofPrognosis ofAcute Tubular NecrosisAcute Tubular Necrosis

Mortality dependent upon comorbid conditionsMortality dependent upon comorbid conditions overall mortality ~ 50%overall mortality ~ 50%

Recovery of renal function seen in ~ 90% of Recovery of renal function seen in ~ 90% of patients who survive - although not necessarily patients who survive - although not necessarily back to prior baseline renal functionback to prior baseline renal function

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Acute Interstitial NephritisAcute Interstitial Nephritis

Acute renal failure due to lymphocytic Acute renal failure due to lymphocytic infiltration of the interstitiuminfiltration of the interstitium

Classic triad ofClassic triad of feverfever rashrash eosinophiliaeosinophilia

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Acute Interstitial NephritisAcute Interstitial Nephritis

Drug-inducedDrug-induced penicillinspenicillins cephalosporinscephalosporins sulfonamidessulfonamides rifampinrifampin phenytoinphenytoin furosemidefurosemide NSAIDsNSAIDs

MalignancyMalignancy IdiopathicIdiopathic

Infection-relatedInfection-related bacterialbacterial viralviral rickettsialrickettsial tuberculosistuberculosis

Systemic diseasesSystemic diseases SLESLE sarcoidosissarcoidosis Sjögren’s syndromeSjögren’s syndrome tubulointerstitial nephritis tubulointerstitial nephritis

and uveitisand uveitis

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Acute Interstitial Nephritis:Acute Interstitial Nephritis:Clinical PresentationClinical Presentation

HistoryHistory preceding illness or drug exposurepreceding illness or drug exposure

Physical examinationPhysical examination feverfever rashrash

Laboratory FindingsLaboratory Findings eosinophiliaeosinophilia

Page 39: Main Menu Main Menu RENAL FAILURE Main Menu Main MenuClassifications  Acute versus chronic  Pre-renal, renal, post-renal  Anuric, oliguric, polyuric

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Acute Interstitial Nephritis:Acute Interstitial Nephritis:Clinical PresentationClinical Presentation

Urine findingsUrine findings non-nephrotic protinurianon-nephrotic protinuria hematuriahematuria pyuriapyuria WBC castsWBC casts eosinophiluriaeosinophiluria

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Acute Interstitial Nephritis:Acute Interstitial Nephritis:TreatmentTreatment

Discontinue offending drugDiscontinue offending drug Treat underlying infectionTreat underlying infection Treat systemic illnessTreat systemic illness Glucocorticoid therapy may be used in patients Glucocorticoid therapy may be used in patients

who fail to respond to more conservative therapywho fail to respond to more conservative therapy

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Acute GlomerulonephritisAcute Glomerulonephritis

Nephritic presentationNephritic presentation proteinuriaproteinuria

• may be in nephrotic range (> 3 g/day)may be in nephrotic range (> 3 g/day) hematuriahematuria RBC castsRBC casts

Diagnosis usually requires renal biopsyDiagnosis usually requires renal biopsy

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Acute GlomerulonephritisAcute Glomerulonephritis

EtiologiesEtiologies poststreptococcal glomerulonephritispoststreptococcal glomerulonephritis postinfectious glomerulonephritispostinfectious glomerulonephritis endocarditis-associated glomerulonephritisendocarditis-associated glomerulonephritis systemic vasculitissystemic vasculitis thrombotic microangiopathy thrombotic microangiopathy

• hemolytic-uremic syndromehemolytic-uremic syndrome• thrombotic thrombocytopenic purpurathrombotic thrombocytopenic purpura

rapidly progressive glomerulonephritis rapidly progressive glomerulonephritis

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Acute Vascular SyndromesAcute Vascular Syndromes

Renal artery thromboembolismRenal artery thromboembolism Renal artery dissectionRenal artery dissection Renal vein thrombosisRenal vein thrombosis

Atheroembolic diseaseAtheroembolic disease

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Intratubular ObstructionIntratubular Obstruction

Intratubular crystal depositionIntratubular crystal deposition tumor lysis syndrometumor lysis syndrome

• acute urate nephropathyacute urate nephropathy ethylene glycol toxicity ethylene glycol toxicity

• calcium oxylate depositioncalcium oxylate deposition

Intratubular protein depositionIntratubular protein deposition multiple myelomamultiple myeloma

• -Bence-Jones protein deposition-Bence-Jones protein deposition

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Differential Diagnosis of Differential Diagnosis of Acute Renal FailureAcute Renal Failure

Prerenal ARFPrerenal ARF Postrenal ARFPostrenal ARF Intrinsic ARFIntrinsic ARF

acute tubular necrosisacute tubular necrosis acute interstitial nephritisacute interstitial nephritis acute glomerulonephritisacute glomerulonephritis acute vascular syndromesacute vascular syndromes intratubular obstructionintratubular obstruction

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Acute Renal Failure: Acute Renal Failure: Diagnostic EvaluationDiagnostic EvaluationAcute Renal Failure: Acute Renal Failure: Diagnostic EvaluationDiagnostic Evaluation

Evaluate for prerenal causesEvaluate for prerenal causes clinical examclinical exam

• blood pressureblood pressure• orthostasisorthostasis

central venous pressures and cardiac outputcentral venous pressures and cardiac output intake/output recordintake/output record urine sedimenturine sediment urine sodiumurine sodium

• UUNaNa < 20 mmol/L < 20 mmol/L

therapeutic trial of volume replacementtherapeutic trial of volume replacement

– skin turgorskin turgor– mucosal membrane hydrationmucosal membrane hydration

– FEFENaNa < 0.01 < 0.01

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Acute Renal Failure:Acute Renal Failure:Diagnostic EvaluationDiagnostic Evaluation

Evaluate for postrenal causesEvaluate for postrenal causes bladder catheterizationbladder catheterization renal ultrasoundrenal ultrasound

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Acute Renal Failure:Acute Renal Failure:Diagnostic EvaluationDiagnostic EvaluationAcute Renal Failure:Acute Renal Failure:

Diagnostic EvaluationDiagnostic Evaluation

Evaluation for intrinsic ARFEvaluation for intrinsic ARF clinical historyclinical history

• medicationsmedications• hypotensionhypotension

physical examphysical exam urinalysisurinalysis

• crystalscrystals• paraproteinsparaproteins

– radiocontrast agentsradiocontrast agents– sepsissepsis

– cellscells– castscasts

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Diagnostic Evaluation of ARFDiagnostic Evaluation of ARF

Form of ARF BUN:Cr UNa (mEq/L) FENa Urine Sediment

Prerenal >20:1 <20 < 1% Normal

Postrenal >20:1 >20 variable Normal or RBC’s

Intrinsic

ATN <10:1 >40 > 2% Muddy brown casts; tubular epithelial cells

AIN <20:1 >20 >1% WBC’s WBC casts, RBC’s, eosinophils

AGN variable <40 <1% RBC’s, RBC casts

Vascular variable >20 variable Normal or RBC’s

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Acute Renal Failure: Acute Renal Failure: ManagementManagement

Prerenal ARFPrerenal ARF volume repletionvolume repletion inotropic supportinotropic support discontinue diureticsdiscontinue diuretics

Postrenal ARFPostrenal ARF bladder catheterizationbladder catheterization percutaneous nephrostomy or ureteral stentspercutaneous nephrostomy or ureteral stents fluid management during post-obstructive fluid management during post-obstructive

diuresisdiuresis

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Acute Renal Failure: ManagementAcute Renal Failure: Management

Intrinsic ARFIntrinsic ARF General supportive careGeneral supportive care

• fluid managementfluid management• diureticsdiuretics• bicarbonate supplementationbicarbonate supplementation• potassiumpotassium• phosphatephosphate• drug dosingdrug dosing• nutritionnutrition

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Acute Renal Failure: ManagementAcute Renal Failure: ManagementAcute Renal Failure: ManagementAcute Renal Failure: Management

Indications for dialysisIndications for dialysis volume overload volume overload metabolic acidosis metabolic acidosis hyperkalemiahyperkalemia uremic syndromeuremic syndrome

• pericarditispericarditis• encephalopathyencephalopathy

azotemiaazotemia

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Dialysis IndicationsDialysis Indications

Refractory hyperkalemiaRefractory hyperkalemia

Metabolic acidosisMetabolic acidosis

Volume overloadVolume overload

Mental status changesMental status changes

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CHRONIC RENAL FAILURECHRONIC RENAL FAILURE

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Pathophysiology of CRFPathophysiology of CRF

What is Chronic Renal Failure?What is Chronic Renal Failure?

It is progressive tissue destruction with It is progressive tissue destruction with

permanent loss of nephrons and renal permanent loss of nephrons and renal function.function.

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Risk Factors

AgeAge > 60 years > 60 years Race or ethnic backgroundRace or ethnic background African-AmericanAfrican-American HispanicHispanic American IndianAmerican Indian AsianAsian History of exposure to chemicals/toxinsHistory of exposure to chemicals/toxins Cigarette smokeCigarette smoke Heavy metalsHeavy metals Family history of chronic kidney diseaseFamily history of chronic kidney disease

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Chronic vs. Acute Renal FailureChronic vs. Acute Renal Failure

Acute Renal Failure (ARF):Acute Renal Failure (ARF):

a.a. Abrupt onsetAbrupt onset

b.b. Potentially reversiblePotentially reversible Chronic Renal Failure (CRF):Chronic Renal Failure (CRF):

a.a. Progresses over at least 3 monthsProgresses over at least 3 months

b.b. Permanent- non-reversible damage to Permanent- non-reversible damage to nephronsnephrons

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Pathophysiology of CRFPathophysiology of CRF

Progressive destruction of nephrons leads to:Progressive destruction of nephrons leads to:

a.a. Decreased glomerular filtration, tubular Decreased glomerular filtration, tubular reabsorption & renal hormone regulation reabsorption & renal hormone regulation

b.b. Remaining functional nephrons compensate Remaining functional nephrons compensate

c.c. Functional and structural changes occurFunctional and structural changes occur

d.d. Inflammatory response triggeredInflammatory response triggered

e.e. Healthy glomeruli so overburdened they Healthy glomeruli so overburdened they become stiff, sclerotic and necroticbecome stiff, sclerotic and necrotic

Lippincott Williams & Wilkins (2005). Pathophysiology A 2-1 reference for nurses (1st ed.) Ambler, Pa.:Lippincott Williams & Wilkins

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Functional Changes of CRFFunctional Changes of CRF

The Kidneys are unable to:The Kidneys are unable to: Regulate fluids and electrolytesRegulate fluids and electrolytes Balance fluid volume and renin-angiotensin Balance fluid volume and renin-angiotensin

systemsystem Control blood pressureControl blood pressure Eliminate nitrogen and other wastesEliminate nitrogen and other wastes Synthesize erythropoietinSynthesize erythropoietin Regulate serum phosphate and calcium levelsRegulate serum phosphate and calcium levels

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4 Stages of CRF4 Stages of CRF

1.1. Reduced Renal Reserve (Silent):Reduced Renal Reserve (Silent): no no symptoms evident- GFR up to 50ml/minsymptoms evident- GFR up to 50ml/min

2.2. Renal Insufficiency:Renal Insufficiency: ½ function of both ½ function of both kidneys lost- GFR 25-50 ml/minkidneys lost- GFR 25-50 ml/min

3.3. Renal Failure:Renal Failure: GFR 5-25 ml/min GFR 5-25 ml/min

4.4. End Stage Renal Disease:End Stage Renal Disease: GFR less GFR less than 5 ml/minthan 5 ml/min

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Causes of CRFCauses of CRF

1)1) Diabetic Nephropathy Diabetic Nephropathy 2)2) HypertensionHypertension3)3) Vascular DiseaseVascular Disease4)4) Polycystic Kidney Disease/GeneticsPolycystic Kidney Disease/Genetics5)5) Chronic InflammationChronic Inflammation6)6) ObstructionObstruction7)7) Glomerular Disorders/ Glomerular Disorders/

GlomerulonephritisGlomerulonephritis

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SIGNS & SYMPTOMS Lab Value Cues

1. Anemia’s - d/t decreased erythropoietin secretion & uremic toxin damage to RBC’s

2. Azotemia – (elevated nitrogen) d/t retention of nitrogenous wastes

3. Creatinine – a component of muscle & it’s non-protein waste product. Normally filtered in the glomerulus & lost in the urine. Glomerular damage increases reabsorption into the blood. Serum creatinine 3 x normal shows a 75% loss of renal function.

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SIGNS & SYMPTOMS Lab Value Cues

4. Hypocalcemia – impaired regulation of Vitamin D leads to decreased absorption & low calcium levels. High phosphorus levels also cause low serum calcium levels.

5. Hyperkalemia – impaired excretion of potassium by the kidneys leads to elevated potassium levels.

6. Hyperlipidemia – decreased serum albumin leads to increased synthesis of LDL’s & cholesterol by the liver, contributing to elevated lipid levels

7. Proteinuria – increased protein filtration d/t glomeruli damage

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SIGNS & SYMPTOMSSIGNS & SYMPTOMSVisual / Verbal CuesVisual / Verbal Cues

1)1) Dry mouth, fatigue, Dry mouth, fatigue, nauseanausea – d/t – d/t hyponatremia & uremiahyponatremia & uremia

2)2) HypertensionHypertension – d/t – d/t sodium & water sodium & water retentionretention

3)3) Hypervolemia Hypervolemia – d/t – d/t sodium & water sodium & water retentionretention

4)4) Gray/yellow skinGray/yellow skin – d/t – d/t accumulated urine accumulated urine pigmentspigments

5)5) Cardiac irritabilityCardiac irritability – d/t – d/t hyperkalemiahyperkalemia

6)6) Muscle crampsMuscle cramps – d/t – d/t hypocalcemiahypocalcemia

7)7) Bone & muscle painBone & muscle pain – d/t – d/t hypocalcemia / hypocalcemia / hyperphosphatemia hyperphosphatemia

8)8) Restless leg syndromeRestless leg syndrome – – d/t toxins’ effects on the d/t toxins’ effects on the nervous systemnervous system

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Genetics of Kidney DiseaseGenetics of Kidney DiseaseGenetic diseases that Genetic diseases that

cause CRF:cause CRF:

Polycystic Kidney Polycystic Kidney Disease (PKD)Disease (PKD)

Nephropathic CystinosisNephropathic Cystinosis (Fanconi’s Syndrome)(Fanconi’s Syndrome)

Alport SyndromeAlport Syndrome

Sanford, R. (2004). Sanford, R. (2004). Autosomal dominant polycystic kidney disease.Autosomal dominant polycystic kidney disease. Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/cam-Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/cam-genetics/sanford.htmgenetics/sanford.htm

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Metabolic ImpactMetabolic Impact

Hyperlipidemia common in CRF- Hyperlipidemia common in CRF- especially in Nephrotic Syndromeespecially in Nephrotic Syndrome

Excessive lipids accelerate progression of Excessive lipids accelerate progression of renal diseaserenal disease

Cholesterol increases glomerular injuryCholesterol increases glomerular injury

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Contributing MechanismsContributing Mechanisms

Two known paths of hyperlipidemia Two known paths of hyperlipidemia progression in CRF:progression in CRF:

Hyperlipidemia activates LDL receptors in Hyperlipidemia activates LDL receptors in mesangial cellsmesangial cells

Increased synthesis of lipoproteins in the Increased synthesis of lipoproteins in the liver related to increased albumin liver related to increased albumin productionproduction

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Albumin ContributionAlbumin ContributionNormal glomeruli structure limits proteins from filtering Normal glomeruli structure limits proteins from filtering

through the urinethrough the urine

Progression of glomeruli injury leads to increased Progression of glomeruli injury leads to increased capillary filtration of albumincapillary filtration of albumin

The liver compensates and increases albumin The liver compensates and increases albumin production - to replace albumin lost in urineproduction - to replace albumin lost in urine

This leads to increased synthesis of lipoproteins by the This leads to increased synthesis of lipoproteins by the liver secondary to the compensatory increase in albumin liver secondary to the compensatory increase in albumin production.production.

Results in increased LDL levels – predisposing to Results in increased LDL levels – predisposing to atherosclerosisatherosclerosis

Atherosclerosis further increases glomeruli injury Atherosclerosis further increases glomeruli injury

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InflammationInflammation

Inflammatory response can be triggered Inflammatory response can be triggered by: tissue injury, infections, toxins, immune by: tissue injury, infections, toxins, immune responses and/or Angiotensin IIresponses and/or Angiotensin II

Can be acute or chronicCan be acute or chronic Can affect the renal pelvis and interstitial Can affect the renal pelvis and interstitial

tissue as in pyelonephritistissue as in pyelonephritis Can affect the glomeruli as in Can affect the glomeruli as in

glomerulonephritisglomerulonephritis

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Inflammation- (Cont.)

Renal Failure- prolongs inflammatory reactionsRenal Failure- prolongs inflammatory reactions Adverse effects of chronic inflammation=Adverse effects of chronic inflammation=

Decreased appetiteDecreased appetite

Muscle and fat wastingMuscle and fat wasting

Endothelial damageEndothelial damage

AtherosclerosisAtherosclerosis

HypoalbuminemiaHypoalbuminemia

Increased cardiovascular disease riskIncreased cardiovascular disease risk

Legg, V.(2005). Complications of chronic kidney disease. Legg, V.(2005). Complications of chronic kidney disease. AJN,AJN,105(6),40-105(6),40-5050

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Causes of Inflammation in CRF

InfectionInfection AnemiaAnemia Uremia Uremia – increases oxidation of proteins, – increases oxidation of proteins,

lipids & carbohydrates, leading to vascular lipids & carbohydrates, leading to vascular inflammationinflammation

Malnutrition – Malnutrition – decreases antioxidantsdecreases antioxidants Low serum albumin Low serum albumin – decreases – decreases

antioxidantsantioxidantsLegg, V.(2005). Complications of chronic kidney disease. Legg, V.(2005). Complications of chronic kidney disease. AJN,AJN,105(6),40-50105(6),40-50

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Angiotensin II in theInflammatory Process

Inflammatory mediator causing:Inflammatory mediator causing:

• Increased vascular permeabilityIncreased vascular permeability• Increased leukocyte infiltration Increased leukocyte infiltration

(monocytes, macrophages)(monocytes, macrophages)• Cell proliferation & hypertrophyCell proliferation & hypertrophy

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Glomerular Inflammatory Disorders

Reminder:Reminder:The glomeruli filter blood & form urine filtrate. The

selectively permeable, capillary membrane allows H2O and small particles (i.e. glucose) to leave the capillary membrane. Large particles (i.e. proteins & blood cells) stay in the blood.

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Nephrotic vs. Nephritic Nephrotic vs. Nephritic SyndromesSyndromes

Nephrotic SyndromesNephrotic Syndromes - glomerular - glomerular disorders that affect the glomerular disorders that affect the glomerular capillary membrane & capillary membrane & increasesincreases permeability to plasma proteinspermeability to plasma proteins

Nephritic SyndromesNephritic Syndromes – glomerular – glomerular disorders that initiate the inflammatory disorders that initiate the inflammatory response within the glomeruli & initially response within the glomeruli & initially decreasesdecreases permeability of the membrane permeability of the membrane

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Nephritic Syndromes

GlomerulonephritisGlomerulonephritis• An inflammatory response in the endothelial, An inflammatory response in the endothelial,

epithelial & mesangial cells of the glomeruliepithelial & mesangial cells of the glomeruli• Inflammatory process damages the capillary Inflammatory process damages the capillary

wall-allowing RBCs into the urinewall-allowing RBCs into the urine

Symptoms:Symptoms:• 1st oliguria, followed by hematuria, azotemia, 1st oliguria, followed by hematuria, azotemia,

low GFR (d/t hemodynamic changes), low GFR (d/t hemodynamic changes), hypertensionhypertension

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Nephrotic Syndromes

Primary causes:Primary causes: Lipoid NephrosisLipoid Nephrosis Focal Segmental Focal Segmental

glomerulosclerosisglomerulosclerosis Membranous Membranous

glomerulonephritisglomerulonephritis

Secondary causes:Secondary causes: Diabetes MellitusDiabetes Mellitus SLESLE AmyloidosisAmyloidosis

Characterized by:Characterized by: Proteinuria > 3.5g/dayProteinuria > 3.5g/day LipiduriaLipiduria HypoalbuminemiaHypoalbuminemia HyperlipidemiaHyperlipidemia

Increased permeability of Increased permeability of glomerular membrane glomerular membrane allows proteins to escape allows proteins to escape into the filtrateinto the filtrate

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Chronic GlomerulonephritisChronic Glomerulonephritis A slow, progressive disease that can be caused A slow, progressive disease that can be caused

by primary ( Nephrotic & Nephritic Syndromes) by primary ( Nephrotic & Nephritic Syndromes) or secondary disorders ( SLE, Good pasture's)or secondary disorders ( SLE, Good pasture's)

Typically develops asymptomatically over many Typically develops asymptomatically over many yearsyears

Hypertension, proteinuria and hematuria Hypertension, proteinuria and hematuria exhibited with progression of diseaseexhibited with progression of disease

Late stages display uremic symptoms of Late stages display uremic symptoms of azotemia, nausea, vomiting, dyspnea and azotemia, nausea, vomiting, dyspnea and pruritispruritis

Leads to CRFLeads to CRF Treatment includes: control of hypertension, Treatment includes: control of hypertension,

control of fluid/electrolyte imbalances, reduce control of fluid/electrolyte imbalances, reduce edema, prevent heart failureedema, prevent heart failure

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Pharmacology in CRF

Pharmacokinetics –

drug absorption, distribution, metabolism & excretion

Pharmacodynamics –

A drug’s mechanism of action and effect at the target site

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Alterations in Drug Responses in CRF

Gastrointestinal impairments affect absorption of Gastrointestinal impairments affect absorption of medicationsmedications

Volume of distribution (VVolume of distribution (Vdd) – the availability of a ) – the availability of a drug distributed in body tissues is increased or drug distributed in body tissues is increased or decreased by alterations in body composition or decreased by alterations in body composition or protein bindingprotein binding

Metabolism of medications altered -the kidneys Metabolism of medications altered -the kidneys produce many enzymes involved in drug produce many enzymes involved in drug metabolism including cytochrome P-450metabolism including cytochrome P-450

Decreased glomerular filtration rate affects drug Decreased glomerular filtration rate affects drug excretionexcretion

Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72.

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Medication Considerations in CRF

DilantinDilantin – increased V – increased Vd d related to protein binding related to protein binding changes and low albumin, increasing risk of changes and low albumin, increasing risk of drug toxicitydrug toxicity

DigoxinDigoxin – increased V – increased Vd d leading to toxicity due to leading to toxicity due to decreased renal excretiondecreased renal excretion

InsulinInsulin – metabolism of insulin decreases, – metabolism of insulin decreases, requiring dose reductionrequiring dose reduction

Tylenol and procainamideTylenol and procainamide – liver metabolized – liver metabolized drugs with metabolites that are excreted renally, drugs with metabolites that are excreted renally, can accumulate leading to drug toxicitycan accumulate leading to drug toxicity

Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72.

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Medication Considerations (Cont.)

Impaired renal excretion leads to toxic drug accumulations Impaired renal excretion leads to toxic drug accumulations with:with:

Aminoglycoside antibiotics -Aminoglycoside antibiotics -(tobramycin & gentamycin)(tobramycin & gentamycin)

AtenololAtenololAIECAIEC

LithiumLithiumVancomycinVancomycinMetforminMetformin

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Over-the-Counter Medicationsand CRF

NSAIDS – inhibit prostaglandins decreasing GFR and reduced sodium excretion

Antacids and laxatives (containing magnesium & aluminum) – causes mineral accumulation and metabolic complications

Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72.

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Acute Problems in CRFAcute Problems in CRF

Relating to underlying diseaseRelating to underlying disease Relating to ESRDRelating to ESRD Dialysis related problemsDialysis related problems

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Problems Related to ESRDProblems Related to ESRD

Metabolic – K/CaMetabolic – K/Ca Volume overloadVolume overload Anemia, platelet disorder, GI bleedAnemia, platelet disorder, GI bleed HTN, pericarditisHTN, pericarditis Peripheral neuropathy, dialysis dementiaPeripheral neuropathy, dialysis dementia Abnormal immune functionAbnormal immune function

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DialysisDialysis

½ of patients with CRF eventually require ½ of patients with CRF eventually require dialysisdialysis

Diffuse harmful waste out of bodyDiffuse harmful waste out of body Control BPControl BP Keep safe level of chemicals in bodyKeep safe level of chemicals in body 2 types 2 types

HemodialysisHemodialysis Peritoneal dialysis Peritoneal dialysis

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HemodialysisHemodialysis

3-4 times a week3-4 times a week Takes 2-4 hours Takes 2-4 hours Machine filters Machine filters

blood andblood and

returns it toreturns it to

bodybody

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Types of AccessTypes of Access

Temporary siteTemporary site AV fistulaAV fistula

Surgeon constructs by combining an artery and a veinSurgeon constructs by combining an artery and a vein 3 to 6 months to mature3 to 6 months to mature

AV graftAV graft Man-made tube inserted by a surgeon to connect Man-made tube inserted by a surgeon to connect

artery and veinartery and vein 2 to 6 weeks to mature2 to 6 weeks to mature

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What This MeansWhat This Means

No BP on same arm as fistulaNo BP on same arm as fistula Protect arm from injuryProtect arm from injury Control obvious hemorrhageControl obvious hemorrhage

Bleeding will be arterialBleeding will be arterial Maintain direct pressureMaintain direct pressure

No IV on same arm as fistulaNo IV on same arm as fistula

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Access ProblemsAccess Problems

AV graft thrombosis AV graft thrombosis AV fistula or graft bleedingAV fistula or graft bleeding AV graft infectionAV graft infection Steal PhenomenonSteal Phenomenon

Early post-opEarly post-op Ischemic distallyIschemic distally

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Peritoneal DialysisPeritoneal Dialysis

Abdominal lining filters bloodAbdominal lining filters blood 3 types3 types

Continuous ambulatoryContinuous ambulatory Continuous cyclicalContinuous cyclical Intermittent Intermittent

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Dialysis Related ProblemsDialysis Related Problems

Lightheaded –give fluidsLightheaded –give fluids HypotensionHypotension DysrhythmiasDysrhythmias Disequilibration SyndromeDisequilibration Syndrome

At end of early sessionsAt end of early sessions Confusion, tremor, Confusion, tremor, Due to decrease concentration of blood Due to decrease concentration of blood

versus brain leading to cerebral edemaversus brain leading to cerebral edema