Farmakoterapi II Ginjal ARF

7/27/2019 Farmakoterapi II Ginjal ARF

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ACUTE RENAL FAILURE/

GAGAL GINJAL AKUT

Tunggul Adi P., M.Sc., Apt.

Lab Farmasi Klinik, Farmasi, FKIK, UNSOED


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Tujuan pembelajaran

Mahasiswa mampu menjelaskan definisi,

epidemiologi, prognosis, etiologi, patofisiologi

ARF atau GGA

Mahasiswa mampu menjelaskan gejala/tandadan pemeriksaan ARF

Mahasiswa mampu menjelaskan manajemen

terapi ARF


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Primary references

Di Piro

Koda-Kimble

Chapter of Acute Renal Failure


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KEY CONCEPTS

Acute renal failure (ARF) is a commoncomplication in the hospitalized patient and isassociated with a high mortality rate.

ARF is predominantly categorized based on the

anatomic area of injury or malfunction: (a)prerenaldecreased renal blood flow, (b)intrinsica structure within the kidney isdamaged, and (c) postrenalan obstruction ispresent within the urine collection system.

Risk factors for ARF include advanced age,acute infection, pre-existing chronicrespiratory or cardiovascular disease,dehydration, and chronic kidney disease


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KEY CONCEPTS

ARF lacks a specific and sensitive sign toherald its onset. Hence, a thorough patienthistory, including medications, recent

procedures and illnesses, physicalexamination, and laboratory assessment ofserum and urine are necessary componentsof an ARF evaluation after an elevated serumcreatinine (Scr ) is noted.

Prevention is key; there are very fewtherapeutic options for the therapeuticmanagement of established ARF.


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KEY CONCEPTS

Supportive management remains the primaryapproach to prevent or reduce thecomplications associated with ARF. Supportive

therapies include: renal replacement therapies(RRTs), nutritional support, avoidance ofnephrotoxins, and blood pressure and fluidmanagement.

For those patients with prolonged or severeARF, RRTs are the cornerstone of support andfacilitate an aggressive approach to fluid,electrolyte and waste management.


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DEFINISI

ARF is broadly defined as a decrease in glomerularfiltration rate (GFR), generally occurring over hours todays, sometimes over weeks, that is associated with anaccumulation of waste products, including urea andcreatinine.

This relatively abrupt decline in renal function is incontrast to CKD, which is defined by the presence ofproteinuria/albuminuria for at least 3 months, in combinationwith a GFR of 500 mL/day).


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Epidemiologi dan prognosis


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ETIOLOGI

The etiology of ARF can be divided into broadcategories based on the anatomic location of theinjury associated with the precipitating factor(s). Themanagement of patients presenting with this disorderis largely predicated on identification of the specificetiology responsible for the patients current acutekidney injury.

Traditionally, the causes of ARF have beencategorized as (a) prerenal, which results fromdecreased renal perfusion in the setting ofundamaged parenchymal tissue, (b) intrinsic, theresult of structural damage to the kidney, mostcommonly the tubule from a ischemic or toxic insult,and (c) postrenal, caused by obstruction of urine flowdownstream from the kidney


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ETIOLOGI

The most common cause of hospital-acquiredARF is prerenal ischemia as the result ofreduced renal perfusion secondary to sepsis,reduced cardiac output, and/or surgery.

Drug-induced ARF may account for18% to 33%of in-hospital occurrences.

Otherrisk factors for developing ARF whilehospitalized include advanced age (>60 years ofage), male gender, acute infection, andpreexisting chronic diseases of the respiratoryor cardiovascular systems.


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ETIOLOGI


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PATOFISIOLOGI


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Fungsional ARF

In functional ARF, a decline in GFR secondary to areduced glomerular hydrostatic pressure, which isthe driving force for the formation of ultrafiltrate, canoccur without damage to the kidney itself. The declinein glomerular hydrostatic pressure may be a directconsequence of changes in glomerular afferent(vasoconstriction) and efferent (vasodilation)arteriolarcircumference.

These clinical conditions are most commonly seen inindividuals who have reduced effective bloodvolume (e.g., heart failure, cirrhosis, severepulmonary disease, or hypoalbuminemia) orrenovascular disease (e.g., renal artery stenosis)and who cannot compensate for changes in afferentor efferent arteriolar tone.


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Fungsional ARF

Functional ARF is very common in individualswith heart failure who receive an ACEI or anARB in an attempt to improve their leftventricular function. Because the decline inefferent arteriolar resistance resulting from theinhibition of angiotensin II occurs within days,ifthe dose is increased too rapidly, adecline in GFR with a concomitant rise inthe serum creatinine will be noticeable. Ifthe increase in the serum creatinine is mildto moderate (an increase of less than 30%from baseline) the medication can becontinued


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PRERENAL ARF

Prerenal ARF results from hypoperfusion of the renalparenchyma, with or without systemic arterialhypotension.

Renal hypoperfusion with systemic arterial hypotensionmay be caused by a decline in intravascular or effective

blood volume that can occur in those with acute blood loss(hemorrhage), dehydration, hypoalbuminemia, or diuretictherapy.

Renal hypoperfusion without systemic hypotension ismost commonly associated with bilateral renal arteryocclusion, or unilateral occlusion in a patient with a

single functioning kidney. Otherthe most common causeis atherosclerosis, with severe abrupt occlusion sometimesoccurring as the result of an embolism


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INTRINSIC

Acute intrinsic renal failure results from

damage to the kidney itself. Conceptually,

acute intrinsic renal failure can be categorized

on the basis of the structures within thekidney that are injured: the renal vasculature,

glomeruli, tubules, and the interstitium.

Penyebab terbesar (sekitar 85 %) adalah

tubular damage.

Lihat tabel etiologi


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POST RENAL

Postrenal ARF may develop as the result ofobstruction atany level within the urinary collection system from therenal tubule to urethra

It is often caused by a prostatic process (hypertrophy,cancer or infection)

It may also be the result of an improperly placed urinarycatheter. Anticholinergic medications may also preventbladder emptying and cause ARF.

Lihat tabel etiologi

Wherever the location of the obstruction, urine will

accumulate in the renal structures above the obstructionand cause increased pressure upstream. The ureters,renal pelvis, and calyces all expand, and the net result is adecline in GFR.


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CLINICAL PRESENTATION OF

ARF


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General

The initiating sign or symptom prompting the

eventual diagnosis of ARF is highly variable,

depending on the etiology. It may be an

elevated Scr , decreased urine output, blood inthe urine, pain during voiding, or severe

abdominal or flank pain.

Determine if the renal complication is acute,

chronic, or the result of an acute change in

a patient with known CKD.


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URINE OUTPUT

Acute anuria (< 50 mL/day of urine output) istypically caused by either complete urinaryobstruction or a catastrophic event (e.g., shockor acute cortical necrosis).

Oliguria (< 500 mL/day of urine output), whichoften develops over several days, suggestsprerenal azotemia.

Nonoliguric (> 500 mL/day of urine output)renal failure usually results from acute intrinsicrenal failure or incomplete urinary obstruction.


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Physical examination finding in

ARF


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Diagnostic Parameters for

Differentiating Causes of ARF


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Urine Analysis Findings as a Guide

to the Etiology of ARFailure


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ISSUE of SCr

There is currently no consensus on the

degree and time frame of changes in Scr

values that clearly defines the presence of

ARF. The difficulty of using Scr as adiagnostic laboratory test for patients with ARF

is its lack of sensitivity to rapid changes in

GFR. An abrupt cessation in glomerular

filtration will not yield an immediatemeasurable change in Scr.


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ISSUE of SCr

Glomerular filtration rate(GFR; mL/min) and serumcreatinine (Scr ; g/dL) versustime following acute renalinjury. Prior to time 0, a GFRof 120 mL/min and a Scr of1.0 g/dL exist. At time 0, anabrupt renal artery thrombusforms, depriving one kidneyof renal blood flow.Composite GFR immediatelydeclines by 50% toapproximately 60 mL/min.However, Scr does notincrease immediately, as it isdependent on creatinineproduction and attainment ofsteady-state serumconcentrations.


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Perhatian dalam membaca hasil

lab

Instead of using fixed numbers to determine renal function,changes in the value, even if it remains within the normalrange, may indicate marked impairment of renal function.

Patients with reduced creatinine production, such as thosewith low muscle mass either because of being bedridden for

long periods of time, may have very low baseline Scr values(

Farmakoterapi II Ginjal ARF

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