SlideShare a Scribd company logo
RRT in AKI Time & Modality
Dr Ayman Seddik, MD, ECNeph, FASN
Prof. OF Nephrology Ain Shams University
Nephrology consultant Diaverum KSA
OUTLINE :
Definition of AKI
( what is new )
1
Q2
PATHOPHYSIOLOGY
of severe AKI
requiring RRT?
2
Q3
When ….. TIME TO
START RRT IN
AKI?
3
Q4
Which ……..
form of RRT?
4
Q1
OUTLINE :
Definition of AKI
( what is new )
1 2
Q3
3 4
Q1
KDIGO/AKIN Classification
OUTLINE :
1
Q2
PATHOPHYSIOLOGY
of severe AKI
requiring RRT?
2
Q3
3 4
Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021).
Main principles of the pathophysiology of AKI.
A) Mild acute kidney injury (AKI), defined by a transient decline in urinary output or excretory function, involves no or minimal kidney cell necrosis or loss. Precedent and subsequent nephron
numbers remain identical and no persistent adaptive cellular responses are necessary. In the long term, the risk of cardiovascular disease (CVD) is somewhat increased, which may also depend on the
underlying cause of AKI.
Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021).
Main principles of the pathophysiology of AKI.
B) Whenever AKI is associated with kidney cell or tubule necrosis, the affected cells are irreversibly lost during the phase of acute necroinflammation, as indicated by activated immune cells in the
interstitial compartment. Renal progenitor cells are more resistant to death and their clonal expansion may facilitate the structural and functional recovery of some injured nephrons. Nephrons in
which injured segments do not recover undergo atrophy, are irreversibly lost, and are replaced by fibrous tissue that stabilizes the structural integrity of remnant nephrons. Resulting hyperfiltration
requires an increase of the functional capacity of remnant nephrons achieved through an increase in their dimensions, with tubular epithelial cells (TECs) undergoing polyploidization, indicated by an
increased size of cytoplasm and cell nuclei. Depending on the number of remnant nephrons, their capacity for adaption (kidney reserve), and filtration load (dependent on body weight, fluid intake,
diet, and others), glomerular filtration rate (GFR) can return to baseline. This status already qualifies as CKD, even if GFR returns to baseline.
The adaptive changes of CKD imply a higher risk of CVD and possibly kidney cancer, and the irreversible loss of nephrons reduces kidney lifespan.
Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021).
Main principles of the pathophysiology of AKI.
C) When severe AKI involves extensive tubule necrosis, the consequences on nephron number are substantial. Tubule recovery occurs only in those nephrons with surviving progenitor cells. Adaptation
to filtration and metabolic demands results in large increases in the dimensions of the few surviving nephrons (megalonephrons). Such adaptations frequently exceed the adaptive capacity of podocytes,
leading to secondary focal segmental glomerulosclerosis and subsequent loss of the remnant nephrons (that is, progressive CKD). Cellular adaptation-related polyploidization and senescence, as well as
nephron loss-related scarring, drive interstitial fibrosis and progressive kidney atrophy. These adaptive changes strongly increase the risk of CVD and possibly kidney cancer. Kidney lifespan is
drastically reduced and some patients remain on kidney replacement therapy.
Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021).
Systemic consequences of AKI.
The kidneys maintain homeostasis; hence, acute kidney injury (AKI) affects almost all
systems of the body, albeit in different ways.
1- Fluid retention affects especially the lungs and the heart, frequently
with clinical signs of respiratory or circulatory failure. Fluid retention also compromises the
gastrointestinal system, for example, the liver or the intestine, promoting intestinal barrier
dysfunction and translocation of bacteria and bacterial toxins.
2- Impaired uremic toxin excretion affects the function
of the brain, the heart, the bone marrow, and the immune system, leading to neurocognitive
defects, anemia, and acquired immunodeficiency accompanied by persistent systemic
inflammation.
3-Kidney cell necrosis releases debris into the venous circulation,
which accumulates in the lungs and causes direct microvascular injury, thrombosis, and,
sometimes, acute respiratory distress syndrome.
OUTLINE :
1 2
Q3
When ….. TIME TO
START RRT IN
AKI?
3 4
Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021).
Management of AKI.
Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021).
Fluid management in acute kidney injury.
Joannidis, M., Meersch-Dini, M. & Forni, L.G. Acute kidney injury. Intensive Care Med 49, 665–668 (2023). https://doi.org/10.1007/s00134-023-07061-4
Both hypovolaemia (kidney hypoperfusion) and hypervolaemia (kidney congestion) compromise kidney
function. Impaired cardiac function adds to both problems as renal and cardiac dysfunction aggravate each
other, referred to as cardiorenal syndromes.
An injured kidney or heart increases the likelihood of developing clinical symptoms of hypovolaemia or
hypervolaemia compared with healthy organs. An increasing severity of symptoms requires escalating
therapeutic interventions. Hypotension frequently indicates kidney hypoperfusion despite clinically apparent
hypervolaemia whenever fluid redistributes to the venous system, into tissue interstitium or third
compartments, for example, in hepatorenal syndrome, congestive heart failure or capillary leakage during
sepsis.
Kidney and/or heart failure drastically decrease both organs’ capacity to maintain function during
hypovolaemia or hypervolaemia. In a euvolemic patient with AKI, a single bolus of buffered crystalloid fluid
can indicate the presence of subclinical hypovolaemia and hypoperfusion of the kidney (prerenal AKI).
Prolonged administration of balanced crystalloids should be handled with caution in order not to promote
oedema or congestion and not to decrease tissue oxygenation. Patients with hypervolaemia should not
receive fluids for AKI but loop natriuretics. In patients who are critically ill with suppressed vasomotor
response, vasopressors are frequently needed to improve cardiac output.
WHEN RRT
AKI
LATE
EARLY
hospital mortality and 90-day RRT dependence rates were higher in
the early RRT group than in the delayed RRT group. HOWEVER
WITHOUT STATISTICAL SIGNIFICANCE
Hemodynamic instability is a common complication during RRT, which can increase hospital mortality
and limit kidney recovery.
Many factors contribute to hemodynamic instability, including excessive ultrafiltration, rapid
osmotic/oncotic shifts, decreased cardiac output, and decreased peripheral resistance.
The incidence of hypotension was 15.7% and 11.0% in the early-strategy group and in the delayed-
strategy group, respectively.
studies that reported hypotension events all involved intermittent hemodialysis (IHD), which was more
likely to result in hemodynamic instability than CRRT.
A remarkable higher incidence of RRT-associated infection events was also
found in the early RRT group. Patients treated with RRT are more susceptible
to infection, as they are exposure to catheters and invasive treatments
Moreover, RRT may enhance the elimination of antibiotics, leading to
suboptimal antibiotic concentrations
Conclusions
• This meta-analysis suggested that early initiation of RRT was not associated with survival
benefit in critically ill patients with AKI.
• In addition, early initiation of RRT could lead to unnecessary RRT exposure in some
patients, resulting in a waste of health resources and a higher incidence of RRT-associated
adverse events.
• Maybe, only critically ill patients with a clear and hard indication, such as severe acidosis,
pulmonary edema, and hyperkalemia, could benefit from early initiation of RRT.
clinical outcomes were comparable between the two groups. In addition, results showed that
delayed RRT initiation could reduce the incidence of RRT-associated adverse events.
Undoubtedly, unnecessary RRT will increase the workload of medical staff, augment
treatment costs, and waste health resources. Therefore, it is reasonable to assume that
delayed initiation of RRT is a preferable approach for critically ill patients with AKI.
Bagshaw, S.M., Hoste, E.A. & Wald, R. When should we start renal-replacement therapy in critically ill patients with acute kidney injury: do we finally have the answer?. Crit Care 25, 179 (2021).
Whenshould we start renal replacement therapy in critically ill patients with acute
kidney injury: do we finally have the answer?
OUTLINE :
1 2 3
Q4
Which ……..
form of RRT?
4
Renal Replacement Therapy for AKI
peritoneal
dialysis
intermittent
hemodialysis
continuous
blood purification
• rarely used
• if no vascular
access can be
obtained
• equipment identical
to chronic renal
failure
• standard HD
treatments
• appropriate for
isolated AKI
NO other organs
involved
• dedicated
equipment
• mostly
hemofiltration
• therapy of choice
for complicated
ARF
WHICH modality of RRT IN AKI :
PIRRT
• prolonged
treatments with
(modified) HD
monitors
• appropriate for
severely ill patients
also
daily, intermittent haemodialysis
continuous haemodialysis
Therapy:
Continuous or Intermittent?
Key messages (when)
1.Early initiation of RRT was not associated with survival benefit in
critically ill patients with AKI.
2.Early initiation of RRT could lead to unnecessary RRT exposure
in some patients, resulting in a waste of health resources and a
higher incidence of RRT-associated adverse events, including
hypotension and infection.
3.Delayed initiation of RRT might be safe in the absence of life-
threatening conditions, such as acute pulmonary edema, severe
acidosis, and severe hyperkalemia.
Thank You
APPENDIX FOR FURTHER
READINGS
Prevention and Treatment of AKI
3.1.1: In the absence of hemorrhagic shock, we suggest
using isotonic crystalloids rather than colloids (albumin or
starches) as initial management for expansion of
intravascular volume in patients at risk for AKI or with AKI.
(2B)
3.1.2: We recommend the use of vasopressors in
conjunction with fluids in patients with vasomotor shock
with, or at risk for, AKI. (1C)
3.1.3: We suggest using protocol-based management of
hemodynamic and oxygenation parameters to prevent
development or worsening of AKI in high-risk patients in
the perioperative setting (2C) or in patients with septic
shock (2C).
KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1 138.
Prevention and Treatment
of AKI
3.3.1: In critically ill patients, we suggest insulin therapy
targeting plasma glucose 110–149mg/dl (6.1–8.3mmol/l).
(2C)
3.3.2: We suggest achieving a total energy intake of 20–30
kcal/kg/d in patients with any stage of AKI. (2C)
3.3.3: We suggest to avoid restriction of protein intake with
the aim of preventing or delaying initiation of RRT. (2D)
3.3.4: We suggest administering 0.8–1.0 g/kg/d of protein in
non catabolic AKI patients without need for dialysis (2D),
1.0–1.5 g/kg/d in patients with AKI on RRT (2D), and up to a
maximum of 1.7 g/kg/d in patients on (CRRT) and in hyper
catabolic patients. (2D)
3.3.5: We suggest providing nutrition preferentially via the
enteral route in patients with AKI. (2C)
3.4.1: We recommend not using diuretics to prevent AKI. (1B)
3.4.2: We suggest not using diuretics to treat AKI, except in the
management of volume overload. (2C)
3.5.1: We recommend not using low-dose dopamine to prevent or treat
AKI. (1A)
3.5.2: We suggest not using fenoldopam to prevent or treat AKI. (2C)
3.5.3: We suggest not using atrial natriuretic peptide (ANP) to prevent
(2C) or treat (2B) AKI.
3.6.1: We recommend not using recombinant human (rh)IGF-1 to
prevent or treat AKI. (1B)
3.7.1: We suggest that a single dose of theophylline may be given in
neonates with severe perinatal asphyxia, who are at high risk of AKI.
(2B)
3.8.1: We suggest not using aminoglycosides for the treatment of infections
unless no suitable, less nephrotoxic, therapeutic alternatives are available.
(2A)
3.8.2: We suggest that, in patients with normal kidney function in steady state,
aminoglycosides are administered as a single dose daily rather than multiple-
dose daily treatment regimens. (2B)
3.8.3: We recommend monitoring aminoglycoside drug levels when treatment
with multiple daily dosing is used for more than 24 hours. (1A)
3.8.4: We suggest monitoring aminoglycoside drug levels when treatment with
single-daily dosing is used for more than 48 hours. (2C)
3.8.5: We suggest using topical or local applications of aminoglycosides (e.g.,
respiratory aerosols, instilled antibiotic beads), rather than i.v. application,
when feasible and suitable. (2B)
3.8.6: We suggest using lipid formulations of amphotericin B rather than
conventional formulations of amphotericin B. (2A)
3.8.7: In the treatment of systemic mycoses or parasitic infections, we
recommend using azole antifungal agents and/or the echinocandins
(caspofungin ) rather than conventional amphotericin B, if equal therapeutic
efficacy can be assumed. (1A)
KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1 138.
KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1 138.
3.9.1: We suggest that off-pump coronary artery bypass
graft surgery not be selected solely for the purpose of
reducing perioperative AKI or need for RRT. (2C)
3.9.2: We suggest not using NACETYL CYSTEINE to
prevent AKI in critically ill patients with hypotension.
(2D)
3.9.3: We recommend not using oral or i.v. NAC for
prevention of postsurgical AKI. (1A)
Risk factors for AKI :
Biomarkers of AKI
American Journal of Kidney Diseases 2020 76710-719DOI: (10.1053/j.ajkd.2020.03.016)
Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021).
Severity of AKI and long-term kidney outcome
Certain biomarkers indicate early kidney injury or subclinical acute kidney injury (AKI) as a risk
factor for proceeding to AKI according to the Kidney Disease Improving Global Outcomes
(KDIGO) definitions. AKI itself is indicated by injury markers in blood and urine before any
impairment of kidney function (as measured by serum creatinine levels and urine output)
occurs.
The three stages of AKI are defined by the extent of renal function impairment. Patients with
AKI in which structural damage causing irreversible nephron loss does not occur may fully
recover. AKI with structural damage frequently lasts >7 days, which is classified as acute kidney
disease (AKD), and the irreversible nephron loss precludes restoration of the baseline
glomerular filtration rate (GFR), resulting in chronic kidney disease (CKD) or persistent kidney
failure.
Cys-C, cystatin C; IGFBP-7, insulin-like growth factor-binding protein 7; IL-18, interleukin 18;
KIM-1, kidney injury molecule; sCr, serum creatinine level; TIMP-2, metalloproteinase inhibitor.

More Related Content

Similar to Renal Replacement Therapy in Acute Kidney Injury -time modality -Dr Ayman Seddik.pptx final 1.pptx

Prevention of AKI
Prevention of AKIPrevention of AKI
Prevention of AKI
DrAnkitPurohit
 
Aki icu
Aki icuAki icu
IM-II-Lec-5-Acute-Kidney-Injury-Dr.-D.-Arco.pdf
IM-II-Lec-5-Acute-Kidney-Injury-Dr.-D.-Arco.pdfIM-II-Lec-5-Acute-Kidney-Injury-Dr.-D.-Arco.pdf
IM-II-Lec-5-Acute-Kidney-Injury-Dr.-D.-Arco.pdf
ChristianLancelot1
 
Lra que hay de nuevo
Lra que hay de nuevoLra que hay de nuevo
Lra que hay de nuevo
Aivan Lima
 
CARDIORENAL SYNDROME
CARDIORENAL SYNDROMECARDIORENAL SYNDROME
CARDIORENAL SYNDROME
drvasudev007
 
Atn
AtnAtn
Entendendo a oliguria do doente critico
Entendendo a oliguria do doente criticoEntendendo a oliguria do doente critico
Entendendo a oliguria do doente critico
Ana Nataly
 
Acute Kidney Injury
Acute Kidney InjuryAcute Kidney Injury
Acute Kidney Injury
Viquas Saim
 
Prof. a. el sebaeii.fluid management in patients with aki
Prof. a. el sebaeii.fluid management in patients with akiProf. a. el sebaeii.fluid management in patients with aki
Prof. a. el sebaeii.fluid management in patients with aki
wessam1071
 
Ckd prevention
Ckd preventionCkd prevention
Ckd prevention
darsh 1980
 
Chronic renal failure(2010505)
Chronic renal failure(2010505)Chronic renal failure(2010505)
Chronic renal failure(2010505)
internalmed
 
Chronic renal failure(2010505)
Chronic renal failure(2010505)Chronic renal failure(2010505)
Chronic renal failure(2010505)
internalmed
 
AKIforResidentsInternalMedicine2022.pptx
AKIforResidentsInternalMedicine2022.pptxAKIforResidentsInternalMedicine2022.pptx
AKIforResidentsInternalMedicine2022.pptx
hcahoustonim
 
Acute kidney injury asa guidelines
Acute kidney injury   asa guidelinesAcute kidney injury   asa guidelines
Acute kidney injury asa guidelines
MohamedKhamis77
 
Chronic Kidney Disease - Definition , Risk Factors , Causes & Staging.pdf
Chronic Kidney Disease - Definition , Risk Factors , Causes & Staging.pdfChronic Kidney Disease - Definition , Risk Factors , Causes & Staging.pdf
Chronic Kidney Disease - Definition , Risk Factors , Causes & Staging.pdf
Jim Jacob Roy
 
MCDP_Renal.pdf
MCDP_Renal.pdfMCDP_Renal.pdf
MCDP_Renal.pdf
HanaDalila
 
Aki dr osama el shahat 2017
Aki  dr osama el shahat  2017Aki  dr osama el shahat  2017
Aki dr osama el shahat 2017
FarragBahbah
 
kidney Transplant in lupus nephritis
kidney Transplant in lupus nephritiskidney Transplant in lupus nephritis
kidney Transplant in lupus nephritis
Pediatric Nephrology
 
17 CKD Hanif diagnosis and treatmentpptx
17 CKD Hanif diagnosis and treatmentpptx17 CKD Hanif diagnosis and treatmentpptx
17 CKD Hanif diagnosis and treatmentpptx
arahmanzai5
 
CKD(1).pptx
CKD(1).pptxCKD(1).pptx
CKD(1).pptx
DrYaqoobBahar
 

Similar to Renal Replacement Therapy in Acute Kidney Injury -time modality -Dr Ayman Seddik.pptx final 1.pptx (20)

Prevention of AKI
Prevention of AKIPrevention of AKI
Prevention of AKI
 
Aki icu
Aki icuAki icu
Aki icu
 
IM-II-Lec-5-Acute-Kidney-Injury-Dr.-D.-Arco.pdf
IM-II-Lec-5-Acute-Kidney-Injury-Dr.-D.-Arco.pdfIM-II-Lec-5-Acute-Kidney-Injury-Dr.-D.-Arco.pdf
IM-II-Lec-5-Acute-Kidney-Injury-Dr.-D.-Arco.pdf
 
Lra que hay de nuevo
Lra que hay de nuevoLra que hay de nuevo
Lra que hay de nuevo
 
CARDIORENAL SYNDROME
CARDIORENAL SYNDROMECARDIORENAL SYNDROME
CARDIORENAL SYNDROME
 
Atn
AtnAtn
Atn
 
Entendendo a oliguria do doente critico
Entendendo a oliguria do doente criticoEntendendo a oliguria do doente critico
Entendendo a oliguria do doente critico
 
Acute Kidney Injury
Acute Kidney InjuryAcute Kidney Injury
Acute Kidney Injury
 
Prof. a. el sebaeii.fluid management in patients with aki
Prof. a. el sebaeii.fluid management in patients with akiProf. a. el sebaeii.fluid management in patients with aki
Prof. a. el sebaeii.fluid management in patients with aki
 
Ckd prevention
Ckd preventionCkd prevention
Ckd prevention
 
Chronic renal failure(2010505)
Chronic renal failure(2010505)Chronic renal failure(2010505)
Chronic renal failure(2010505)
 
Chronic renal failure(2010505)
Chronic renal failure(2010505)Chronic renal failure(2010505)
Chronic renal failure(2010505)
 
AKIforResidentsInternalMedicine2022.pptx
AKIforResidentsInternalMedicine2022.pptxAKIforResidentsInternalMedicine2022.pptx
AKIforResidentsInternalMedicine2022.pptx
 
Acute kidney injury asa guidelines
Acute kidney injury   asa guidelinesAcute kidney injury   asa guidelines
Acute kidney injury asa guidelines
 
Chronic Kidney Disease - Definition , Risk Factors , Causes & Staging.pdf
Chronic Kidney Disease - Definition , Risk Factors , Causes & Staging.pdfChronic Kidney Disease - Definition , Risk Factors , Causes & Staging.pdf
Chronic Kidney Disease - Definition , Risk Factors , Causes & Staging.pdf
 
MCDP_Renal.pdf
MCDP_Renal.pdfMCDP_Renal.pdf
MCDP_Renal.pdf
 
Aki dr osama el shahat 2017
Aki  dr osama el shahat  2017Aki  dr osama el shahat  2017
Aki dr osama el shahat 2017
 
kidney Transplant in lupus nephritis
kidney Transplant in lupus nephritiskidney Transplant in lupus nephritis
kidney Transplant in lupus nephritis
 
17 CKD Hanif diagnosis and treatmentpptx
17 CKD Hanif diagnosis and treatmentpptx17 CKD Hanif diagnosis and treatmentpptx
17 CKD Hanif diagnosis and treatmentpptx
 
CKD(1).pptx
CKD(1).pptxCKD(1).pptx
CKD(1).pptx
 

More from Ayman Seddik

PD THE ROAD LESS TRAVELLED Dr Ayman Seddik 2.pdf
PD THE ROAD LESS TRAVELLED Dr Ayman Seddik 2.pdfPD THE ROAD LESS TRAVELLED Dr Ayman Seddik 2.pdf
PD THE ROAD LESS TRAVELLED Dr Ayman Seddik 2.pdf
Ayman Seddik
 
CKD MBD & osteoporosis in elderly the management dilemma
CKD MBD  &  osteoporosis in elderly the management dilemmaCKD MBD  &  osteoporosis in elderly the management dilemma
CKD MBD & osteoporosis in elderly the management dilemma
Ayman Seddik
 
صحة الكلي للجميع في كل مكان ... درهم وقاية خير من قنطار علاج
 صحة الكلي للجميع في كل مكان ... درهم وقاية خير من قنطار علاج صحة الكلي للجميع في كل مكان ... درهم وقاية خير من قنطار علاج
صحة الكلي للجميع في كل مكان ... درهم وقاية خير من قنطار علاج
Ayman Seddik
 
SGLT2 inhibitors and RISK OF necrotizing fasciitis
SGLT2  inhibitors and RISK OF necrotizing fasciitis SGLT2  inhibitors and RISK OF necrotizing fasciitis
SGLT2 inhibitors and RISK OF necrotizing fasciitis
Ayman Seddik
 
Pregabalin and gabapentin use in HD patients
Pregabalin and gabapentin use in HD patients Pregabalin and gabapentin use in HD patients
Pregabalin and gabapentin use in HD patients
Ayman Seddik
 
Patient selection and training for PERITONEAL DIALYSIS
Patient selection and training for PERITONEAL DIALYSIS Patient selection and training for PERITONEAL DIALYSIS
Patient selection and training for PERITONEAL DIALYSIS
Ayman Seddik
 
Onconephrology shield the kidney while fighting cancer , dr ayman seddik
Onconephrology shield the kidney while fighting cancer , dr ayman seddikOnconephrology shield the kidney while fighting cancer , dr ayman seddik
Onconephrology shield the kidney while fighting cancer , dr ayman seddik
Ayman Seddik
 
Hepatitis c treatment in ESRD patients , update Dr Ayman Seddik
Hepatitis c treatment in ESRD patients , update  Dr Ayman Seddik  Hepatitis c treatment in ESRD patients , update  Dr Ayman Seddik
Hepatitis c treatment in ESRD patients , update Dr Ayman Seddik
Ayman Seddik
 
Brain kidney cross talk final 2016
Brain   kidney cross talk final 2016Brain   kidney cross talk final 2016
Brain kidney cross talk final 2016
Ayman Seddik
 
Patient selection and training for peritoneal dialysis
Patient selection  and training for peritoneal dialysisPatient selection  and training for peritoneal dialysis
Patient selection and training for peritoneal dialysis
Ayman Seddik
 
كليتك تتقدم في العمر مثلك تماما .... حافظ عليها )
كليتك تتقدم في العمر مثلك تماما .... حافظ عليها )كليتك تتقدم في العمر مثلك تماما .... حافظ عليها )
كليتك تتقدم في العمر مثلك تماما .... حافظ عليها )
Ayman Seddik
 
Extracorporeal liver support therapies
Extracorporeal liver support therapies Extracorporeal liver support therapies
Extracorporeal liver support therapies
Ayman Seddik
 
Aging kidney-structural-and-functional-changes ayman seddik
Aging kidney-structural-and-functional-changes ayman seddikAging kidney-structural-and-functional-changes ayman seddik
Aging kidney-structural-and-functional-changes ayman seddik
Ayman Seddik
 
Dr Ayman Seddik , The top 10 facts nephrologists wish every physician knew
Dr Ayman Seddik , The top 10 facts  nephrologists wish every physician knew Dr Ayman Seddik , The top 10 facts  nephrologists wish every physician knew
Dr Ayman Seddik , The top 10 facts nephrologists wish every physician knew
Ayman Seddik
 
Kidney transplantation from myth to reality , ajman meeting 2013 may
Kidney transplantation from myth to reality , ajman meeting 2013 mayKidney transplantation from myth to reality , ajman meeting 2013 may
Kidney transplantation from myth to reality , ajman meeting 2013 may
Ayman Seddik
 
Ckd-MBD & osteoporosis the management dilemma
Ckd-MBD  & osteoporosis the management dilemma Ckd-MBD  & osteoporosis the management dilemma
Ckd-MBD & osteoporosis the management dilemma
Ayman Seddik
 
Dr ayman seddik plasmapheresis why when and how
Dr ayman seddik plasmapheresis why when and how  Dr ayman seddik plasmapheresis why when and how
Dr ayman seddik plasmapheresis why when and how
Ayman Seddik
 
Acute kidney injury prevention new microsoft power po.int presentation
Acute kidney injury prevention new microsoft power po.int presentationAcute kidney injury prevention new microsoft power po.int presentation
Acute kidney injury prevention new microsoft power po.int presentation
Ayman Seddik
 
World kidney day arabic final2015
World kidney day arabic final2015World kidney day arabic final2015
World kidney day arabic final2015
Ayman Seddik
 
Kidney transplantation from myth to reality , ajman meeting 2013 may
Kidney transplantation from myth to reality , ajman meeting 2013 mayKidney transplantation from myth to reality , ajman meeting 2013 may
Kidney transplantation from myth to reality , ajman meeting 2013 may
Ayman Seddik
 

More from Ayman Seddik (20)

PD THE ROAD LESS TRAVELLED Dr Ayman Seddik 2.pdf
PD THE ROAD LESS TRAVELLED Dr Ayman Seddik 2.pdfPD THE ROAD LESS TRAVELLED Dr Ayman Seddik 2.pdf
PD THE ROAD LESS TRAVELLED Dr Ayman Seddik 2.pdf
 
CKD MBD & osteoporosis in elderly the management dilemma
CKD MBD  &  osteoporosis in elderly the management dilemmaCKD MBD  &  osteoporosis in elderly the management dilemma
CKD MBD & osteoporosis in elderly the management dilemma
 
صحة الكلي للجميع في كل مكان ... درهم وقاية خير من قنطار علاج
 صحة الكلي للجميع في كل مكان ... درهم وقاية خير من قنطار علاج صحة الكلي للجميع في كل مكان ... درهم وقاية خير من قنطار علاج
صحة الكلي للجميع في كل مكان ... درهم وقاية خير من قنطار علاج
 
SGLT2 inhibitors and RISK OF necrotizing fasciitis
SGLT2  inhibitors and RISK OF necrotizing fasciitis SGLT2  inhibitors and RISK OF necrotizing fasciitis
SGLT2 inhibitors and RISK OF necrotizing fasciitis
 
Pregabalin and gabapentin use in HD patients
Pregabalin and gabapentin use in HD patients Pregabalin and gabapentin use in HD patients
Pregabalin and gabapentin use in HD patients
 
Patient selection and training for PERITONEAL DIALYSIS
Patient selection and training for PERITONEAL DIALYSIS Patient selection and training for PERITONEAL DIALYSIS
Patient selection and training for PERITONEAL DIALYSIS
 
Onconephrology shield the kidney while fighting cancer , dr ayman seddik
Onconephrology shield the kidney while fighting cancer , dr ayman seddikOnconephrology shield the kidney while fighting cancer , dr ayman seddik
Onconephrology shield the kidney while fighting cancer , dr ayman seddik
 
Hepatitis c treatment in ESRD patients , update Dr Ayman Seddik
Hepatitis c treatment in ESRD patients , update  Dr Ayman Seddik  Hepatitis c treatment in ESRD patients , update  Dr Ayman Seddik
Hepatitis c treatment in ESRD patients , update Dr Ayman Seddik
 
Brain kidney cross talk final 2016
Brain   kidney cross talk final 2016Brain   kidney cross talk final 2016
Brain kidney cross talk final 2016
 
Patient selection and training for peritoneal dialysis
Patient selection  and training for peritoneal dialysisPatient selection  and training for peritoneal dialysis
Patient selection and training for peritoneal dialysis
 
كليتك تتقدم في العمر مثلك تماما .... حافظ عليها )
كليتك تتقدم في العمر مثلك تماما .... حافظ عليها )كليتك تتقدم في العمر مثلك تماما .... حافظ عليها )
كليتك تتقدم في العمر مثلك تماما .... حافظ عليها )
 
Extracorporeal liver support therapies
Extracorporeal liver support therapies Extracorporeal liver support therapies
Extracorporeal liver support therapies
 
Aging kidney-structural-and-functional-changes ayman seddik
Aging kidney-structural-and-functional-changes ayman seddikAging kidney-structural-and-functional-changes ayman seddik
Aging kidney-structural-and-functional-changes ayman seddik
 
Dr Ayman Seddik , The top 10 facts nephrologists wish every physician knew
Dr Ayman Seddik , The top 10 facts  nephrologists wish every physician knew Dr Ayman Seddik , The top 10 facts  nephrologists wish every physician knew
Dr Ayman Seddik , The top 10 facts nephrologists wish every physician knew
 
Kidney transplantation from myth to reality , ajman meeting 2013 may
Kidney transplantation from myth to reality , ajman meeting 2013 mayKidney transplantation from myth to reality , ajman meeting 2013 may
Kidney transplantation from myth to reality , ajman meeting 2013 may
 
Ckd-MBD & osteoporosis the management dilemma
Ckd-MBD  & osteoporosis the management dilemma Ckd-MBD  & osteoporosis the management dilemma
Ckd-MBD & osteoporosis the management dilemma
 
Dr ayman seddik plasmapheresis why when and how
Dr ayman seddik plasmapheresis why when and how  Dr ayman seddik plasmapheresis why when and how
Dr ayman seddik plasmapheresis why when and how
 
Acute kidney injury prevention new microsoft power po.int presentation
Acute kidney injury prevention new microsoft power po.int presentationAcute kidney injury prevention new microsoft power po.int presentation
Acute kidney injury prevention new microsoft power po.int presentation
 
World kidney day arabic final2015
World kidney day arabic final2015World kidney day arabic final2015
World kidney day arabic final2015
 
Kidney transplantation from myth to reality , ajman meeting 2013 may
Kidney transplantation from myth to reality , ajman meeting 2013 mayKidney transplantation from myth to reality , ajman meeting 2013 may
Kidney transplantation from myth to reality , ajman meeting 2013 may
 

Recently uploaded

Helminthiasis or Worm infestation in Children for Nursing students
Helminthiasis or Worm infestation in Children for Nursing studentsHelminthiasis or Worm infestation in Children for Nursing students
Helminthiasis or Worm infestation in Children for Nursing students
RAJU B N
 
Gene Expression System-viral gene delivery Mpharm(Pharamaceutics)
Gene Expression System-viral gene delivery Mpharm(Pharamaceutics)Gene Expression System-viral gene delivery Mpharm(Pharamaceutics)
Gene Expression System-viral gene delivery Mpharm(Pharamaceutics)
MuskanShingari
 
Ageing, the Elderly, Gerontology and Public Health
Ageing, the Elderly, Gerontology and Public HealthAgeing, the Elderly, Gerontology and Public Health
Ageing, the Elderly, Gerontology and Public Health
phuakl
 
Pharmacology of Drugs for Congestive Heart Failure
Pharmacology of Drugs for Congestive Heart FailurePharmacology of Drugs for Congestive Heart Failure
Pharmacology of Drugs for Congestive Heart Failure
Dr. Nikhilkumar Sakle
 
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) Cosmetics
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) CosmeticsStoryboard on Acne-Innovative Learning-M. pharm. (2nd sem.) Cosmetics
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) Cosmetics
MuskanShingari
 
Hemodialysis: Chapter 6, Hemodialysis Adequacy and Dose - Dr.Gawad
Hemodialysis: Chapter 6, Hemodialysis Adequacy and Dose - Dr.GawadHemodialysis: Chapter 6, Hemodialysis Adequacy and Dose - Dr.Gawad
Hemodialysis: Chapter 6, Hemodialysis Adequacy and Dose - Dr.Gawad
NephroTube - Dr.Gawad
 
Tele Optometry (kunj'sppt) / Basics of tele optometry.
Tele Optometry (kunj'sppt) / Basics of tele optometry.Tele Optometry (kunj'sppt) / Basics of tele optometry.
Tele Optometry (kunj'sppt) / Basics of tele optometry.
Kunj Vihari
 
2nd-generation Antihistaminic Part I.pptx
2nd-generation Antihistaminic Part I.pptx2nd-generation Antihistaminic Part I.pptx
2nd-generation Antihistaminic Part I.pptx
Madhumita Dixit
 
Call Girls Goa (india) +91-7426014248 Goa Call Girls
Call Girls Goa (india) +91-7426014248 Goa Call GirlsCall Girls Goa (india) +91-7426014248 Goa Call Girls
Call Girls Goa (india) +91-7426014248 Goa Call Girls
sagarvarma453
 
Cervical Disc Arthroplasty ORSI 2024.pptx
Cervical Disc Arthroplasty ORSI 2024.pptxCervical Disc Arthroplasty ORSI 2024.pptx
Cervical Disc Arthroplasty ORSI 2024.pptx
LEFLOT Jean-Louis
 
Giloy in Ayurveda - Classical Categorization and Synonyms
Giloy in Ayurveda - Classical Categorization and SynonymsGiloy in Ayurveda - Classical Categorization and Synonyms
Giloy in Ayurveda - Classical Categorization and Synonyms
Planet Ayurveda
 
Selective α1-Blocker.pptx
Selective α1-Blocker.pptxSelective α1-Blocker.pptx
Selective α1-Blocker.pptx
Madhumita Dixit
 
RESPIRATORY DISEASES by bhavya kelavadiya
RESPIRATORY DISEASES by bhavya kelavadiyaRESPIRATORY DISEASES by bhavya kelavadiya
RESPIRATORY DISEASES by bhavya kelavadiya
Bhavyakelawadiya
 
Call Girls In Mumbai +91-7426014248 High Profile Call Girl Mumbai
Call Girls In Mumbai +91-7426014248 High Profile Call Girl MumbaiCall Girls In Mumbai +91-7426014248 High Profile Call Girl Mumbai
Call Girls In Mumbai +91-7426014248 High Profile Call Girl Mumbai
Mobile Problem
 
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
MuskanShingari
 
Can Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptx
Can Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptxCan Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptx
Can Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptx
FFragrant
 
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
shruti jagirdar
 
anatomy of submandibular region presentation
anatomy of submandibular region presentationanatomy of submandibular region presentation
anatomy of submandibular region presentation
MalaM67
 
Call Girls Lucknow 9024918724 Vip Call Girls Lucknow
Call Girls Lucknow 9024918724 Vip Call Girls LucknowCall Girls Lucknow 9024918724 Vip Call Girls Lucknow
Call Girls Lucknow 9024918724 Vip Call Girls Lucknow
nandinirastogi03
 
Nano-gold for Cancer Therapy chemistry investigatory project
Nano-gold for Cancer Therapy chemistry investigatory projectNano-gold for Cancer Therapy chemistry investigatory project
Nano-gold for Cancer Therapy chemistry investigatory project
SIVAVINAYAKPK
 

Recently uploaded (20)

Helminthiasis or Worm infestation in Children for Nursing students
Helminthiasis or Worm infestation in Children for Nursing studentsHelminthiasis or Worm infestation in Children for Nursing students
Helminthiasis or Worm infestation in Children for Nursing students
 
Gene Expression System-viral gene delivery Mpharm(Pharamaceutics)
Gene Expression System-viral gene delivery Mpharm(Pharamaceutics)Gene Expression System-viral gene delivery Mpharm(Pharamaceutics)
Gene Expression System-viral gene delivery Mpharm(Pharamaceutics)
 
Ageing, the Elderly, Gerontology and Public Health
Ageing, the Elderly, Gerontology and Public HealthAgeing, the Elderly, Gerontology and Public Health
Ageing, the Elderly, Gerontology and Public Health
 
Pharmacology of Drugs for Congestive Heart Failure
Pharmacology of Drugs for Congestive Heart FailurePharmacology of Drugs for Congestive Heart Failure
Pharmacology of Drugs for Congestive Heart Failure
 
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) Cosmetics
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) CosmeticsStoryboard on Acne-Innovative Learning-M. pharm. (2nd sem.) Cosmetics
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) Cosmetics
 
Hemodialysis: Chapter 6, Hemodialysis Adequacy and Dose - Dr.Gawad
Hemodialysis: Chapter 6, Hemodialysis Adequacy and Dose - Dr.GawadHemodialysis: Chapter 6, Hemodialysis Adequacy and Dose - Dr.Gawad
Hemodialysis: Chapter 6, Hemodialysis Adequacy and Dose - Dr.Gawad
 
Tele Optometry (kunj'sppt) / Basics of tele optometry.
Tele Optometry (kunj'sppt) / Basics of tele optometry.Tele Optometry (kunj'sppt) / Basics of tele optometry.
Tele Optometry (kunj'sppt) / Basics of tele optometry.
 
2nd-generation Antihistaminic Part I.pptx
2nd-generation Antihistaminic Part I.pptx2nd-generation Antihistaminic Part I.pptx
2nd-generation Antihistaminic Part I.pptx
 
Call Girls Goa (india) +91-7426014248 Goa Call Girls
Call Girls Goa (india) +91-7426014248 Goa Call GirlsCall Girls Goa (india) +91-7426014248 Goa Call Girls
Call Girls Goa (india) +91-7426014248 Goa Call Girls
 
Cervical Disc Arthroplasty ORSI 2024.pptx
Cervical Disc Arthroplasty ORSI 2024.pptxCervical Disc Arthroplasty ORSI 2024.pptx
Cervical Disc Arthroplasty ORSI 2024.pptx
 
Giloy in Ayurveda - Classical Categorization and Synonyms
Giloy in Ayurveda - Classical Categorization and SynonymsGiloy in Ayurveda - Classical Categorization and Synonyms
Giloy in Ayurveda - Classical Categorization and Synonyms
 
Selective α1-Blocker.pptx
Selective α1-Blocker.pptxSelective α1-Blocker.pptx
Selective α1-Blocker.pptx
 
RESPIRATORY DISEASES by bhavya kelavadiya
RESPIRATORY DISEASES by bhavya kelavadiyaRESPIRATORY DISEASES by bhavya kelavadiya
RESPIRATORY DISEASES by bhavya kelavadiya
 
Call Girls In Mumbai +91-7426014248 High Profile Call Girl Mumbai
Call Girls In Mumbai +91-7426014248 High Profile Call Girl MumbaiCall Girls In Mumbai +91-7426014248 High Profile Call Girl Mumbai
Call Girls In Mumbai +91-7426014248 High Profile Call Girl Mumbai
 
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)
 
Can Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptx
Can Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptxCan Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptx
Can Traditional Chinese Medicine Treat Blocked Fallopian Tubes.pptx
 
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
STUDIES IN SUPPORT OF SPECIAL POPULATIONS: GERIATRICS E7
 
anatomy of submandibular region presentation
anatomy of submandibular region presentationanatomy of submandibular region presentation
anatomy of submandibular region presentation
 
Call Girls Lucknow 9024918724 Vip Call Girls Lucknow
Call Girls Lucknow 9024918724 Vip Call Girls LucknowCall Girls Lucknow 9024918724 Vip Call Girls Lucknow
Call Girls Lucknow 9024918724 Vip Call Girls Lucknow
 
Nano-gold for Cancer Therapy chemistry investigatory project
Nano-gold for Cancer Therapy chemistry investigatory projectNano-gold for Cancer Therapy chemistry investigatory project
Nano-gold for Cancer Therapy chemistry investigatory project
 

Renal Replacement Therapy in Acute Kidney Injury -time modality -Dr Ayman Seddik.pptx final 1.pptx

  • 1. RRT in AKI Time & Modality Dr Ayman Seddik, MD, ECNeph, FASN Prof. OF Nephrology Ain Shams University Nephrology consultant Diaverum KSA
  • 2. OUTLINE : Definition of AKI ( what is new ) 1 Q2 PATHOPHYSIOLOGY of severe AKI requiring RRT? 2 Q3 When ….. TIME TO START RRT IN AKI? 3 Q4 Which …….. form of RRT? 4 Q1
  • 3. OUTLINE : Definition of AKI ( what is new ) 1 2 Q3 3 4 Q1
  • 4.
  • 5.
  • 7.
  • 8. OUTLINE : 1 Q2 PATHOPHYSIOLOGY of severe AKI requiring RRT? 2 Q3 3 4
  • 9. Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021). Main principles of the pathophysiology of AKI. A) Mild acute kidney injury (AKI), defined by a transient decline in urinary output or excretory function, involves no or minimal kidney cell necrosis or loss. Precedent and subsequent nephron numbers remain identical and no persistent adaptive cellular responses are necessary. In the long term, the risk of cardiovascular disease (CVD) is somewhat increased, which may also depend on the underlying cause of AKI.
  • 10. Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021). Main principles of the pathophysiology of AKI. B) Whenever AKI is associated with kidney cell or tubule necrosis, the affected cells are irreversibly lost during the phase of acute necroinflammation, as indicated by activated immune cells in the interstitial compartment. Renal progenitor cells are more resistant to death and their clonal expansion may facilitate the structural and functional recovery of some injured nephrons. Nephrons in which injured segments do not recover undergo atrophy, are irreversibly lost, and are replaced by fibrous tissue that stabilizes the structural integrity of remnant nephrons. Resulting hyperfiltration requires an increase of the functional capacity of remnant nephrons achieved through an increase in their dimensions, with tubular epithelial cells (TECs) undergoing polyploidization, indicated by an increased size of cytoplasm and cell nuclei. Depending on the number of remnant nephrons, their capacity for adaption (kidney reserve), and filtration load (dependent on body weight, fluid intake, diet, and others), glomerular filtration rate (GFR) can return to baseline. This status already qualifies as CKD, even if GFR returns to baseline. The adaptive changes of CKD imply a higher risk of CVD and possibly kidney cancer, and the irreversible loss of nephrons reduces kidney lifespan.
  • 11. Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021). Main principles of the pathophysiology of AKI. C) When severe AKI involves extensive tubule necrosis, the consequences on nephron number are substantial. Tubule recovery occurs only in those nephrons with surviving progenitor cells. Adaptation to filtration and metabolic demands results in large increases in the dimensions of the few surviving nephrons (megalonephrons). Such adaptations frequently exceed the adaptive capacity of podocytes, leading to secondary focal segmental glomerulosclerosis and subsequent loss of the remnant nephrons (that is, progressive CKD). Cellular adaptation-related polyploidization and senescence, as well as nephron loss-related scarring, drive interstitial fibrosis and progressive kidney atrophy. These adaptive changes strongly increase the risk of CVD and possibly kidney cancer. Kidney lifespan is drastically reduced and some patients remain on kidney replacement therapy.
  • 12. Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021). Systemic consequences of AKI.
  • 13. The kidneys maintain homeostasis; hence, acute kidney injury (AKI) affects almost all systems of the body, albeit in different ways. 1- Fluid retention affects especially the lungs and the heart, frequently with clinical signs of respiratory or circulatory failure. Fluid retention also compromises the gastrointestinal system, for example, the liver or the intestine, promoting intestinal barrier dysfunction and translocation of bacteria and bacterial toxins. 2- Impaired uremic toxin excretion affects the function of the brain, the heart, the bone marrow, and the immune system, leading to neurocognitive defects, anemia, and acquired immunodeficiency accompanied by persistent systemic inflammation. 3-Kidney cell necrosis releases debris into the venous circulation, which accumulates in the lungs and causes direct microvascular injury, thrombosis, and, sometimes, acute respiratory distress syndrome.
  • 14. OUTLINE : 1 2 Q3 When ….. TIME TO START RRT IN AKI? 3 4
  • 15. Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021). Management of AKI.
  • 16. Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021). Fluid management in acute kidney injury.
  • 17. Joannidis, M., Meersch-Dini, M. & Forni, L.G. Acute kidney injury. Intensive Care Med 49, 665–668 (2023). https://doi.org/10.1007/s00134-023-07061-4
  • 18. Both hypovolaemia (kidney hypoperfusion) and hypervolaemia (kidney congestion) compromise kidney function. Impaired cardiac function adds to both problems as renal and cardiac dysfunction aggravate each other, referred to as cardiorenal syndromes. An injured kidney or heart increases the likelihood of developing clinical symptoms of hypovolaemia or hypervolaemia compared with healthy organs. An increasing severity of symptoms requires escalating therapeutic interventions. Hypotension frequently indicates kidney hypoperfusion despite clinically apparent hypervolaemia whenever fluid redistributes to the venous system, into tissue interstitium or third compartments, for example, in hepatorenal syndrome, congestive heart failure or capillary leakage during sepsis. Kidney and/or heart failure drastically decrease both organs’ capacity to maintain function during hypovolaemia or hypervolaemia. In a euvolemic patient with AKI, a single bolus of buffered crystalloid fluid can indicate the presence of subclinical hypovolaemia and hypoperfusion of the kidney (prerenal AKI). Prolonged administration of balanced crystalloids should be handled with caution in order not to promote oedema or congestion and not to decrease tissue oxygenation. Patients with hypervolaemia should not receive fluids for AKI but loop natriuretics. In patients who are critically ill with suppressed vasomotor response, vasopressors are frequently needed to improve cardiac output.
  • 19.
  • 21.
  • 22.
  • 23.
  • 24.
  • 25.
  • 26. hospital mortality and 90-day RRT dependence rates were higher in the early RRT group than in the delayed RRT group. HOWEVER WITHOUT STATISTICAL SIGNIFICANCE
  • 27. Hemodynamic instability is a common complication during RRT, which can increase hospital mortality and limit kidney recovery. Many factors contribute to hemodynamic instability, including excessive ultrafiltration, rapid osmotic/oncotic shifts, decreased cardiac output, and decreased peripheral resistance. The incidence of hypotension was 15.7% and 11.0% in the early-strategy group and in the delayed- strategy group, respectively. studies that reported hypotension events all involved intermittent hemodialysis (IHD), which was more likely to result in hemodynamic instability than CRRT.
  • 28. A remarkable higher incidence of RRT-associated infection events was also found in the early RRT group. Patients treated with RRT are more susceptible to infection, as they are exposure to catheters and invasive treatments Moreover, RRT may enhance the elimination of antibiotics, leading to suboptimal antibiotic concentrations
  • 29. Conclusions • This meta-analysis suggested that early initiation of RRT was not associated with survival benefit in critically ill patients with AKI. • In addition, early initiation of RRT could lead to unnecessary RRT exposure in some patients, resulting in a waste of health resources and a higher incidence of RRT-associated adverse events. • Maybe, only critically ill patients with a clear and hard indication, such as severe acidosis, pulmonary edema, and hyperkalemia, could benefit from early initiation of RRT. clinical outcomes were comparable between the two groups. In addition, results showed that delayed RRT initiation could reduce the incidence of RRT-associated adverse events. Undoubtedly, unnecessary RRT will increase the workload of medical staff, augment treatment costs, and waste health resources. Therefore, it is reasonable to assume that delayed initiation of RRT is a preferable approach for critically ill patients with AKI.
  • 30.
  • 31. Bagshaw, S.M., Hoste, E.A. & Wald, R. When should we start renal-replacement therapy in critically ill patients with acute kidney injury: do we finally have the answer?. Crit Care 25, 179 (2021). Whenshould we start renal replacement therapy in critically ill patients with acute kidney injury: do we finally have the answer?
  • 32. OUTLINE : 1 2 3 Q4 Which …….. form of RRT? 4
  • 33. Renal Replacement Therapy for AKI peritoneal dialysis intermittent hemodialysis continuous blood purification • rarely used • if no vascular access can be obtained • equipment identical to chronic renal failure • standard HD treatments • appropriate for isolated AKI NO other organs involved • dedicated equipment • mostly hemofiltration • therapy of choice for complicated ARF WHICH modality of RRT IN AKI : PIRRT • prolonged treatments with (modified) HD monitors • appropriate for severely ill patients also
  • 34.
  • 35. daily, intermittent haemodialysis continuous haemodialysis Therapy: Continuous or Intermittent?
  • 36.
  • 37.
  • 38.
  • 39.
  • 40.
  • 41.
  • 42.
  • 43. Key messages (when) 1.Early initiation of RRT was not associated with survival benefit in critically ill patients with AKI. 2.Early initiation of RRT could lead to unnecessary RRT exposure in some patients, resulting in a waste of health resources and a higher incidence of RRT-associated adverse events, including hypotension and infection. 3.Delayed initiation of RRT might be safe in the absence of life- threatening conditions, such as acute pulmonary edema, severe acidosis, and severe hyperkalemia.
  • 44.
  • 45.
  • 48. Prevention and Treatment of AKI 3.1.1: In the absence of hemorrhagic shock, we suggest using isotonic crystalloids rather than colloids (albumin or starches) as initial management for expansion of intravascular volume in patients at risk for AKI or with AKI. (2B) 3.1.2: We recommend the use of vasopressors in conjunction with fluids in patients with vasomotor shock with, or at risk for, AKI. (1C) 3.1.3: We suggest using protocol-based management of hemodynamic and oxygenation parameters to prevent development or worsening of AKI in high-risk patients in the perioperative setting (2C) or in patients with septic shock (2C). KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1 138.
  • 49. Prevention and Treatment of AKI 3.3.1: In critically ill patients, we suggest insulin therapy targeting plasma glucose 110–149mg/dl (6.1–8.3mmol/l). (2C) 3.3.2: We suggest achieving a total energy intake of 20–30 kcal/kg/d in patients with any stage of AKI. (2C) 3.3.3: We suggest to avoid restriction of protein intake with the aim of preventing or delaying initiation of RRT. (2D) 3.3.4: We suggest administering 0.8–1.0 g/kg/d of protein in non catabolic AKI patients without need for dialysis (2D), 1.0–1.5 g/kg/d in patients with AKI on RRT (2D), and up to a maximum of 1.7 g/kg/d in patients on (CRRT) and in hyper catabolic patients. (2D) 3.3.5: We suggest providing nutrition preferentially via the enteral route in patients with AKI. (2C)
  • 50. 3.4.1: We recommend not using diuretics to prevent AKI. (1B) 3.4.2: We suggest not using diuretics to treat AKI, except in the management of volume overload. (2C) 3.5.1: We recommend not using low-dose dopamine to prevent or treat AKI. (1A) 3.5.2: We suggest not using fenoldopam to prevent or treat AKI. (2C) 3.5.3: We suggest not using atrial natriuretic peptide (ANP) to prevent (2C) or treat (2B) AKI. 3.6.1: We recommend not using recombinant human (rh)IGF-1 to prevent or treat AKI. (1B) 3.7.1: We suggest that a single dose of theophylline may be given in neonates with severe perinatal asphyxia, who are at high risk of AKI. (2B)
  • 51. 3.8.1: We suggest not using aminoglycosides for the treatment of infections unless no suitable, less nephrotoxic, therapeutic alternatives are available. (2A) 3.8.2: We suggest that, in patients with normal kidney function in steady state, aminoglycosides are administered as a single dose daily rather than multiple- dose daily treatment regimens. (2B) 3.8.3: We recommend monitoring aminoglycoside drug levels when treatment with multiple daily dosing is used for more than 24 hours. (1A) 3.8.4: We suggest monitoring aminoglycoside drug levels when treatment with single-daily dosing is used for more than 48 hours. (2C) 3.8.5: We suggest using topical or local applications of aminoglycosides (e.g., respiratory aerosols, instilled antibiotic beads), rather than i.v. application, when feasible and suitable. (2B) 3.8.6: We suggest using lipid formulations of amphotericin B rather than conventional formulations of amphotericin B. (2A) 3.8.7: In the treatment of systemic mycoses or parasitic infections, we recommend using azole antifungal agents and/or the echinocandins (caspofungin ) rather than conventional amphotericin B, if equal therapeutic efficacy can be assumed. (1A) KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1 138.
  • 52. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1 138. 3.9.1: We suggest that off-pump coronary artery bypass graft surgery not be selected solely for the purpose of reducing perioperative AKI or need for RRT. (2C) 3.9.2: We suggest not using NACETYL CYSTEINE to prevent AKI in critically ill patients with hypotension. (2D) 3.9.3: We recommend not using oral or i.v. NAC for prevention of postsurgical AKI. (1A)
  • 54.
  • 55. Biomarkers of AKI American Journal of Kidney Diseases 2020 76710-719DOI: (10.1053/j.ajkd.2020.03.016)
  • 56. Kellum, et al. Acute kidney injury. Nat Rev Dis Primers 7, 52 (2021). Severity of AKI and long-term kidney outcome
  • 57. Certain biomarkers indicate early kidney injury or subclinical acute kidney injury (AKI) as a risk factor for proceeding to AKI according to the Kidney Disease Improving Global Outcomes (KDIGO) definitions. AKI itself is indicated by injury markers in blood and urine before any impairment of kidney function (as measured by serum creatinine levels and urine output) occurs. The three stages of AKI are defined by the extent of renal function impairment. Patients with AKI in which structural damage causing irreversible nephron loss does not occur may fully recover. AKI with structural damage frequently lasts >7 days, which is classified as acute kidney disease (AKD), and the irreversible nephron loss precludes restoration of the baseline glomerular filtration rate (GFR), resulting in chronic kidney disease (CKD) or persistent kidney failure. Cys-C, cystatin C; IGFBP-7, insulin-like growth factor-binding protein 7; IL-18, interleukin 18; KIM-1, kidney injury molecule; sCr, serum creatinine level; TIMP-2, metalloproteinase inhibitor.

Editor's Notes

  1. CRRT IN AKI , DR AYMAN SEDDIK