Acute Renal Failure

Why do you think we should learn about

a specific disease in medical school?
 IMPORTANCE OF AKI
• AKI is common.

• AKI imposes a heavy burden of illness (morbidity and mortality).

• The cost of managing AKI is high.

• AKI is amenable to early detection and potential prevention.

• There is considerable variability in practice

 IMPORTANCE OF AKI
• AKI is common.

• AKI imposes a heavy burden of illness (morbidity and mortality).

• The cost of managing AKI is high.

• AKI is amenable to early detection and potential prevention.

• There is considerable variability in practice

How do we recognize – i.e. define
 DEFINITION OF ARF

• the abrupt loss of kidney function that

results in the retention of urea and other
nitrogenous waste products and in the
dysregulation of extracellular volume and
electrolytes.
RIFLE and AKIN Criteria
 DEFINITION AND STAGING OF AKI

• Increase in SCr by >0.3 mg/dl within 48 hours; or

• Increase in SCr by >1.5-fold above baseline, which is known or

presumed to have occurred within 7 days; or

• Urine volume <0.5 ml/kg/h for 6 hours.

 Overview of AKI, CKD, and AKD
Functional criteria Structural criteria
AKI Increase in SCr by 50% within 7 days, OR No criteria
Increase in SCr by 0.3 mg/dl (26.5 mmol/l)
within 2 days, OR
Oliguria
CKD GFR < 60 ml/min per 1.73m2 for Kidney damage
> 3 months
for > 3 months
AKD AKI, OR Kidney damage
GFR ≤ 60 ml/min per 1.73m2 for
< 3 months, OR
for < 3 months
Decrease in GFR by ≥ 35% or increase
in SCr by > 50% for < 3 months
 Overview of AKI, CKD, and AKD

Overlapping ovals show the relationships among AKI, AKD,

and CKD. AKI is a subset of AKD. Both AKI and AKD without
AKI can be superimposed upon CKD.
Afirmarea diagnosticului de insuficienta renala ACUTA
• World incidence of AKI: a meta-analysis. Susantitaphong P, et al.
• AKI Advisory Group of the American Society of Nephrology 
• Clin J Am Soc Nephrol. 2013;8(9):1482. Epub 2013 Jun 6.  
• A systematic review (2004-2012) of large cohort studies was conducted to
estimate the world incidence of AKI and its stages of severity and associated
mortality, and to describe geographic variations according to countries,
regions, and their economies.
• 154 studies (n=3,585,911) - the pooled incidence rates of AKI were 21.6% in
adults
• The pooled AKI-associated mortality rates were 23.9% in adults

• CONCLUSIONS Using the KDIGO definition, 1 in 5 adults

worldwide experience AKI during a hospital episode of care.
 INSUFICINETA RENALA ACUTA-
INCIDENTA

World Incidence of AKI: A Meta-Analysis, june 2013

Paweena Susantitaphong, Dinna N. Cruz
The growth of acute kidney injury

• US: the incidence of AKI rose

from 61 to 288 per 100,000
population (1988 to 2002) [8].

• The incidence of dialysis-

requiring AKI: +700%
• AKI-related hospitalizations:
+140% in diabetic and +230% in
nondiabetic individuals [10]

Eastern Europe Joanna Matuszkiewicz-Rowinska, June 2015

Insuficienta renala acuta
• Incidenta (cont.)
1990s, studiu prospectiv in comunitate (Feest)
• Durata de 2 ani, inclusi 440,000 pacienti
• creatinina > 500 umol/l
• 140 pmp / an
• 72% erau varstnici > 70 ani
• Incidenta de 17 / pmp daca pacientii erau < 50ani
• Incidenta de 949 pmp daca pacientii erau > 80 ani
• supravietuire 54% la 12 luni, 34% la 2 ani
Proportia de varstnici (> 80 ani) cu IRA internati in ATI
 INSUFICIENTA RENALA ACUTA-
ETIOLOGIE

O larga varietate de patologii care pot aparea intr-o larga

varietate de situatii clinice.

• ETIOLOGIE
• pre-renala
• renala
• post-renala
 IRA

Dobandite in comunitate Dobandita in spital Dobandita in ATI

Incidenta Mica Moderata (5%) Mare (10-20%)

Cauza Unica Multipla MSOF

pre>post>renal pre>NTA>post MSOF + NTA

Supravietuire Buna Medie Redusa

70-90% 30-50% 10-30%
INSUFICIENTA RENALA ACUTA PRERENALA - CAUZE
Anatomical and physiologic features of the renal cortex and medulla

Blood flow
PO2,
4.2 ml/min/g Macula densa
~ 50
Cortical labyrinths mm Hg

Medullary rays

PO2,
Outer
~ 10-20
medulla
Blood flow mm Hg
1.9 ml/min/g

Inner
medulla

Medullary tick
Cortex ascending limbs

Renal vein Renal artery

Brezis & Seymour, The New Engl. J. of Med., 332,647-655, 1995.

 INSUFICIENTA RENALA ACUTA PRERENALA - FIZIOPATOLOGIE

Fiziologie renala NORMALA

Autoreglarea
• Ca urmare a reducerii perfuziei renale scade tonusul
arteriolei aferente I creste tonusul arteriolei eferente
• Procesul este ANGIOTENSIN II dependent
• Permite mentinerea presiunii capilare glomerulare si
procesul de ultrafiltrare
INSUFICIENTA RENALA ACUTA PRERENALA - FIZIOPATOLOGIE

Fiziologie renala
Feedback-ul tubuloglomerular
• Macula densa sesizeaza modificarile dependente de
flux si ale conc de Cl- in fluidul tubular
• Fluxul plasmatic la nivelul nefronului se ajusteaza
prin alterarea rezistentei arteriolei aferente
• Modificarile sunt dependente de SRAA, adenozina,
prostaglandine
Autoreglarea fluxului plasmatic renal
INSUFICIENTA RENALA ACUTA PRERENALA - FIZIOPATOLOGIE

-> Mecanisme “Protectoare”

• Autoreglarea renala

-Eicosanoizi vasodilatatori -“NSAID”

-Angiotensina II -“ACE / AT1RA”
Importanta diferentierii AKI pre- / renala
INSUFICIENTA RENALA ACUTA PRERENALA - TRATAMENT

OBIECTIV CENTRAL
Refacerea perfuziei renale prin:

Corectarea depletiei volemice absolute

sau
Corectarea perfuziei renale efective
diminuate

REPREZINTA O URGENTA !
Clase de dezechilibre hidrice in ATI
DRY-DRY WET-DRY
deshidratare -IC cu deshirdratare prin
tratatament diuretic si
hipoperfuzie renala
-IC cu hipoperfuzie renala
in ciuda hiperhidratarii
generale

DRY-WET WET-WET
Spatiul trei: hiperhidratare, Hiperhidratare
darlichidul nu e in circulatie
evidenta
Mesajul este clar: examinati pacientul !!
 MONITORING - KEY
TO SUCCESS
PA Catheter

Oesophageal doppler
 Corectarea depletiei volemice

DEPLETIA VOLEMICA ABSOLUTA / REALA

• Transfuzii sanguine atunci cand etiologia este hemoragica sau
oricand Hb < 10 g/L
• Etiologie non-hemoragica sau in absenta sangelui:
• Abord vascular central +/- flexula de calibru mare (14G)
• Determinarea PVC
• PVC < 2 cm H2O – volemia insuficienta, necesitand refacere volemica
• Solutii cristaloide vs coloide?
 Corectarea depletiei volemice
Solutii cristaloide vs coloide?
• Review al trialurilor randomizate publicate - solutiile coloidale:
• Se asociaza cu un risc de deces crescut
• Eficacitate similara cu NaCl izotona
• Sunt mai scumpe

• CONCLUZIE: NaCl izotona va fi preferata pana in momentul stabilizarii

hemodinamice.
• Exceptie posibila – colapsul circulator deoarece solutiile coloidale, macromoleculare
sau saline hipertone corecteaza TA si volumul circulator mai rapid.
Curba de supravietuire Kaplan-Meier la pacientii critici tratati
cu albumina sau ser fiziologic.

albumin

SAFE study N Engl J Med 2004;350:2247-2256. SAFE study N Engl J Med 2004;350:2247-2256.
Mortalitatea globala in studiul « SAFE » la pacienti critici
(albumina vs ser fiziologic)

SAFE study N Engl J Med 2004;350:2247-2256 .

 Corectarea depletiei volemice

• Daca PVC > 8 cm H2O, se opreste aportul sodat si se reconsidera situatia –

tonicitatea si continutul electrolitic al lichidelor de substitutie se modifica
in functie de tipul pierderilor si de dinamica constantele plasmatice

• In formele cu hTA si PVC > 10 cm H2O se presupune existenta unui soc cu

rasunet cardiac si se recurge la droguri cardiotonice sau/si vasoactive.
 Corectarea depletiei volemice

• La pacientii la care IRA este prerenala, diureza si functia renala

excretorie se vor ameliora semnificativ dupa corectarea
volumului intravascular si a TA.

• Daca debitul urinar orar ramine scazut (< 30 ml/hr.), vor fi

utilizate si alte masuri pentru ameliorarea functiei renale
Testul de stres la Furosemid:
- bolus 1mg/kgC la pacientii naivi sau 1,5mg/kgC
- monitorizarea orara a diurezei si repletie volemica=diureza cu monitorizarea
statusului volemic (TA, edeme, asculatie pulmonara), timp de 6 ore
- diureza in primele 2 ore <200ml -> prezinta risc crescut de progresie catre AKIN 3

Dopamina piv:
- 2,5mcg/kgC in perfuzie continua
- vasodilatatie renala
- monitorizarea TA, FC (risc de aritmii)
FIZIOPATOLOGIA
HRS
Hepatorenal Syndrome-Current
Concepts in Pathophysiology
Piyush Mathur1* and Dinesh Agarwal
 TIPUL 1 = AKI-HRS TIPUL 2

• Declin rapid al functiei renale (<2 s) • cr <1,5mg/dl,

- dublarea cr initiale • Declin lent al functiei renale
- reducerea eGFR cu >50%

• Factor precipitant (infectie, diuretice, • Ascita refractara

nefrotoxice)
 IMPORTANTA HRS

• Incidenta anuala HRS de 8%

• probabilitatea de a dezvolta HRS la 1 an de 18% si de 39% la 5 ani

• mortalitate la doua saptamani de pana la 80% daca AKI-HRS

netratata

• in tipul 2 cronic de HRS, declinul functiei renale este gradual, dar

de asemenea prognostic rezervat, supravietuire medie de 3-6 luni
DIAGNOSTIC

EXCLUDEREA ALTOR
CAUZE DE IRA!!!
Treatments for HRS (mostly for AKI-HRS) are based on correcting the
different aspects of pathophysiology of HRS.

• Improving the effective arterial blood volume: Volume expanders

• Reducing arterial vasodilatation: Vasoconstrictors

• Eliminating portal hypertension: TIPS shunt

• Correcting liver dysfunction and portal hypertension: Liver

transplantation
 *MIDODRINA (precursor al
desglymidodrinei ->α1-receptor
Vasoconstrictoare agonist) - in combinatie cu octreotidul,
inferioara terliprsinei

*OCTREOTIDUL (analog de
somatostatina, vasoconstictie
periferica) - ineficient in monoterapie

*VASOPRESINA (=ADH, creste

rezistenta vasculara perferica)
ischemie!!

*TERLIPRESINA (analog
de vasopresina)

*NORADRENALINA
(catecolamina, creste FC
si TA) - reversia HRS
- All patients had severe hepatic dysfunction: hepatic
encephalopathy
- Four patients survived and completely recovered
the hepatic function
TRANSPLANTUL
HEPATIC
+
Transplant renal
 TAKE HOME MESSAGES!!!
1. Cirrhosis leads to a reduction in effective arterial blood volume, which stimulates renal
vasoconstriction via the various vasoconstrictor systems, predisposing patients to AKI

2. Any condition that causes a further reduction of the effective arterial blood volume can
precipitate AKI-HRS. These include sepsis, over-diuresis, large-volume paracentesis (5 liters)
without intravascular volume replacement, and gastrointestinal bleeding.

3. In hospitalized patients with cirrhosis, prerenal azotemia is the most common cause of
acute kidney injury. HRS can be considered a form of prerenal azotemia, which is not volume
responsive and which is seen exclusively in patients with severe liver dysfunction.

4. Type 1 HRS has been renamed AKI-HRS.

5. Pharmacologic treatment (terlipressin, norepinephrine) increases survival, but the only

definitive treatment is liver transplantation.
TIP Exemple

1 Acut cardiorenal Insuficienta cardiaca -> AKI SCA

2 Cronic cardiorenal Insuficienta cardiaca cronica -> ICC

CKD SINDROMUL
CARDIORENAL
3 Acut nefrocardiac AKI -> insuficienta cardiaca Cardiomiopatie
uremica

4 Cronic nefrocardiac CKD -> insuficienta cardiaca HVS/HFpEF

5 Secundar Boala sistemica -> IR, IC sepsis, vasculite, DZ

CRS-1:
-”warm”: vasoconstrictie
secundara activarii RAAS sau
reducerea volumului
circulant efectiv

-”cold”: cresterea PVC,

cresterea presiunii
interstitiale
Diagnosticul IC:
• clinic
• paraclinic:
-Rx
-echografie cardiaca
-”comete”
-bioimpedanta
-biomarkeri
Congestie pulmonara! -> comete?

Use of Lung Ultrasound for the Assessment of Volume Status in CK

Covic A1, Siriopol D2, Voroneanu L2.
BIOMARKERI?
 SINDROMUL CARDIORENAL-TRATAMENT

• Diuretice:
-de ansa:
Furosemid bolus i.v. sau piv?

no difference for all-cause mortality, length of hospital stay

continuous infusion superior urine output
 Rezistența la diuretice – combinatii + dozare frecventa
Se asociază cu risc crescut de HHF și deces

Tiazidice!

Loop diuretics are

not created equal CKD – reduces drug delivery
Bumetanide, HF – impaired sodium delivery
Torasemide >
Furosemide More frequent
Food, hypoalbuminemia, NSAID! dosing rather than
escalation
Probleme: 1. Evaluarea eficienței tratamentului diuretic
Output urinar/40 mg furosemid
sau
Sodiu urinar/furosemid urinar
sau
Sodiu urinar

The ESCAPE trial = 390 pacienți cu ICC

decompensată

Cei la care eficiența diureticului a fost sub medie –

risc de 3x mai mare de deces (HR, 2.86 [95% CI, 1.53–
5.36]).

Jeffrey M. Testani et al. Circ Heart Failure 2014

Eur Heart Journal 2020
Abordare practică

Eur Heart Journal 2020

 Administrarea de ser hiperton –
scade mortalitatea și spitalizările pentru IC
N - 1032 patients treated with HSS and 1032 controls; mean age < 65 yrs in only one study – Issa 2011

Menținerea unui volum

IV adecvat permite
menținerea unei perfuzii
renale adecvate

Int J Cardiol. 2014
Dopamina – crește outputul urinar dar nu previne
agravarea insuficienței renale sau decesul
Meta-analiză, 3553 pacienți

Jan O. Friedrich et al. Annals of Internal Medicine 2005

Care inotrop?
Differential Effects of Levosimendan and
Dobutamine on Glomerular Filtration
Rate in Patients With Heart Failure and
Renal Impairment: A Randomized
Double-Blind Controlled Trial
Lukas Lannemyr, MD; Sven-Erik Ricksten, MD, PhD

Levosimendan (0.1 lg/kg per

minute) vs dobutamine (7.5 lg/kg
per minute).
Ultrafiltrare?
The Cardiorenal Rescue Study in Acute Decompensated Heart Failure
(CARRESS-HF) - no benefits compared to diuresis

American Heart Association/American College of Cardiology and the

European Society of Cardiology treatment guidelines establish that IUF
is an option (class IIa, level of evidence B and C) if all diuretic strategies
have failed.
 SEPSISUL (SA-AKI)

- principala cauza de AKI in ATI

- asociata cu mortalitate crescuta
- mecanism complex

INCIDENCE OF AKI AKI REQUIRING DIALYSIS

Sepsis 4.2% 24%
Severe sepsis 22.7% 39%
Septic shock 52.8% 89%
SA-AKI - FIZIOPATOLOGIE

Update on sepsis-associated acute kidney injury:

emerging targeted therapies, Doyle JF, Forni LG
Clinical factors associated with worse outcomes?

a. Older age
b. More severe disease
c. Greater burden of illness
d. Longer stays in ICU and hospital
e. AKI severity as defined by criteria
f. Delay in the initiation of appropriate antimicrobial therapy
g. Fluid balance
“early goal-directed therapy” (EGDT) - 2012

a. In primele 3 ore::
i. Masurarea nivelului lactatului seric
ii. Recoltarea de HC inaintea initierii antibioterapiei
iii. Recoltare presepsina/procalcitonină
iv. Antibioterapie empirica cu spectru larg
v. Administrarea de solutii cristaloide 30 mL/kg in caz de hTA sau lactat seric > 4 mmol/L

b. In primele 6 ore:
i. Initierea vasopresoarelor (cu fluide) pentru a mentine MAP $ 65 mmHg
ii. In cazul hTA persistente sau a lactatului seric initial > 4 mmol/L:
1. Masurarea PVC (optim >8mmHg)
2. Masurarea ScvO2 (optim >70)
iii. Remasurarea lactatului seric
 14 trialuri randomizate incluse

balanced crystalloids or albumin is associated with

reduced mortality!!
 Timing of Renal-Replacement Therapy in Patients
with Acute Kidney Injury and Sepsis

• within 12 hours after documentation of

failure-stage acute kidney injury (early
strategy)

• or after a delay of 48 hours if renal

recovery had not occurred (delayed
strategy)

Stéphane Gaudry, M.D., David Hajage, M.D., Fréderique

Schortgen, June 2016
INSUFICIENTA RENALA ACUTA INTRINSECA-CAUZE
INSUFICIENTA RENALA ACUTA INTRINSECA-CAUZE
INSUFICIENTA RENALA ACUTA INTRINSECA-CAUZE
INSUFICIENTA RENALA ACUTA INTRINSECA-CAUZE
NECROZA TUBULARA ACUTA-FIZIOPATOLOGIE
ischemic ATN:

hypovolemic shock due to severe

trauma, acute pancreatitis,
septicemia; hemolytic crises,
myoglobinuria in crush syndrome,
which clogs the tubule causing
ischemia

nephrotoxic ATN:

heavy metals (e.g., mercury); organic

solvents (e.g., carbon tetrachloride);
drugs such as gentamicin and other
antibiotics, and radiographic
contrast
NECROZA TUBULARA ACUTA-FIZIOPATOLOGIE
 ISCHEMIE REPERFUZIE

Depletie ATP Acumulare de Xantine

hipoxantine

Generare de
superoxid
SOD
Crestere Ca2+
citosolic Peroxid hidrogen
Xantin oxidaza
Fe2+
Fenton reaction

Fe3+
Activarea proteazei Ca Radical hidroxyl
calmodulin dependente
Xantin
dehidrogenaza

1) Stresul oxidativ
 3) Rolul calciului
in leziunile de ischemie-reperfuzie renale.

Paller & Greene, Ann; Acad. Science, 723, 1994

Cell injury to hypoxic rat proximal is reduced by chelation
of extracellular Ca2+.

Wetzels et al, J. Pharmacol. Exp. Ther., 267, 176, 1993

 ISCHEMIE REPERFUZIE

Depletie ATP Acumulare de Xantine

hipoxantine

Generare de
superoxid
SOD
Crestere Ca2+ citosolic
Xantin oxidaza Peroxid hidrogen
Fe2+
Fenton reaction

Fe3+
Activarea proteazei Ca Radical hidroxyl
calmodulin dependente
Xantin
dehidrogenaza

1) Stresul oxidativ
Cortical Medullary Junction:
ischemia/reperfusion
2) Raspunsul
inflamator
4) Rolul oxidului nitric
Pathways of oxygen-derived Pathways of formation of reactive
A reactive species B nitrogen species

– disparitia posibiltatii de vasodilatatie

Induction of tubular epithelial cell injury

Microvillar Actin
NO

NO
Integrins

Lumen Basolateral
Cytoskeletal Targets of NO Membrane
 Anatomia patologica in NTA-faza de recuperare

Recovering ATN showing a tubular epithelial cell mitotic figure (arrow).

Fazele evoluției IAR ischemice
 NECROZA TUBULARA ACUTA-DIAGNOSTIC

-contextul clinic, anamneza atentă (medicamente, toxice industriale,

animale sau vegetale) pot permite identificarea factorilor declanșanți
 NECROZA TUBULARA ACUTA-DIAGNOSTIC

-ESU: epiteliile tubulare în număr mare, cilindri epiteliali și cei granuloși

 NECROZA TUBULARA ACUTA-DIAGNOSTIC

-excluderea succesivă a celorlalte forme patogenice ale IAR

DIAGNOSTIC DE SEVERITATE/PROGRESIE SPRE AKIN 3?
 NECROZA TUBULARA ACUTA-TRATAMENT

1. Tratamentul cauzei

2. Tratamentul complicatiilor
-frecvente în IAR
-agravează prognosticul
Complicatiile IAR:

1. Hiperhidratarea:
- edeme, HTA, dispnee, edem pulmonar, IC, revărsate pleurale;
- restrictie hidro-sodata, diuretice de ansă, dializă
Review, 15 September 2018

-little evidence is available especially from rigorous randomized controlled trials to support or
oppose this common clinical practice
-7 randomised controlled trials

Loop diuretics should be used for the

management of volume overload in AKI, but
there is no clear evidence that loop diuretics
enhance renal recovery or prevent the
development of AKI!
Complicatiile IAR:

2. Hiperpotasemia

- parestezii, paralizii, EKG (unde T

inalte, extrasistole, tulburari de
conducere AV pana la bloc total)
- glucoză + insulină, β-mimetice,
bicarbonat
- calciu i.v.
Complicatiile IAR:

3. Acidoza metabolica
-Bicarbonat i.v.
Complicatiile IAR:

4. Serozite -> tamponada cardiaca

Complicatiile IAR:

5. Disfunctie trombocitara - anticoagulare?

6. Malnutritia protein-calorica
CATABOLISMUL ESTE REGULA
Dat de rezistenta la insulina, efectul TSR, acidoza
– Necesarul de calorii creste si mai mult daca pacientul este septic
– Mortalitatea este direct proportionala cu balanta azotului
– Nu sunt date controlate care sa sustina efectul benefic al suportului nutritional
asupra supravietuirii.
Complicatiile IAR:

7. Gastro-intestinale

8. Anemia

9. Encefalopatia uremica!!!
A. Jörres 09-2005
 DIALIZA IN INSUFICIENTA RENALA ACUTA

• Atunci când complicațiile „uremiei acute” nu mai pot fi controlate, dializa

devine necesară, dar ca măsură de suport și nu de înlocuire a funcției
renale („supportive not replacement therapy”):
-EPA refractar
-oligurie persistenta
-hiperpotasemie severa
-acidoza matabolica severa
-pericardita uremica
-encefalopatie uremica

• Între 30-50% dintre pacienții cu IAR necesită dializă

 Terapia de supleere renala continua
pt pacientii cu IRA
Avantaje Dezavantaje
• Ameliorarea stabilitatii hemodinamice • Probleme abord vascular
• Reducere aritmii cardiace • Risc crescut de sangerare
• Ameliorare nutritie • Imobilizare prelungita
• Ameliorare schimburi gazoase • Frecvent, ruperea capilarelor filtrului
pulmonare • Cost ridicat
• Ameliorare control fluide • Acidoza lactica la utilizarea de solutii
• Ameliorare parametrii biochimici lactat
• Sedere mai scurta in ATI
 DIALIZA IN INSUFICIENTA RENALA ACUTA

-
1. When to iniate RRT?

EARLIER VS LATER?
DAR...
 In plus, initierea rapida “distruge” diureza

Stéphane Gaudry, M.D., David Hajage, M.D.,

Fréderique Schortgen, June 2016
 DIALIZA IN INSUFICIENTA RENALA ACUTA

Quantification of Dialysis in AKI: Intermittent Therapies

The Dose Response Multicentre International (DO-RE-MI)

- intensive vs. less intensive dose in an observational trial
- 88 received intermittent therapy only, while 46 received intermittent therapy plus
CRRT or another modality
- The median intermittent treatment duration was 5.5 h, and the median prescribed
Kt/V was 1.2 per treatment
- No significant association between RRT dose and patient outcome was reported.

The KDIGO AKI Clinical Practice Guideline recommends delivery of a weekly Kt/V of
3.9 when intermittent treatments are applied
 DIALIZA IN INSUFICIENTA RENALA ACUTA
-
3. HD vs CRRT vs SLED vs PD?
Retrospective cohort study, 58,635 with renal replacement therapy for acute kidney injury
 DIALIZA IN INSUFICIENTA RENALA ACUTA
-
4. When to stop?
The KDIGO guideline criteria for discontinuation of RRT

“it is no longer required” after sufficient renal recovery

RRT is “no longer consistent with the goals of care”.

.
 Recomandari actuale de tratament in IRA

• HD intermitenta
– Tratament de electie in IRA izolata, dar poate fi utilizata si in MSOF
– Asigurarea unei doze suficiente de dializa; este de preferat HD zilnica
– Se poate utiliza orice membrana (exceptie rabdomioliza sau substante contrast iodate
 High-Flux)
• CRRT
– Preferata in instabilitatea cardiocirculatorie, hiperhidratare, edem cerebral
– Asigurarea unei doze suficiente de dializa (35 ml/kg×h recomandata in CVVH )
TAKE HOME MESSAGES!!!
 prerenal azotemia is a functional form of AKI, which results from kidney perfusion,
so rapid normalization of kidney function when perfusion is restored

 a variety of renal parenchymal diseases can cause intrinsec AKI (ATN, AIN, AGN and
RPGN, acute vascular diseases, intratubular deposition of crystals/paraproteins)

 ATN is the most common cause of intrinsec AKI

 the most important risk factor for the development of AKI - preexisting CKD

 no specific interventions that have been reliably demonstrated to prevent AKI but
good medical care, avoidance of volume contraction, prevention of hypotension,
avoidance of nephrotoxic agents