This document discusses acute kidney injury (AKI), including its definition, classification systems, causes, biomarkers, treatment and management. It provides a brief history of terms used to describe AKI. It summarizes the RIFLE and AKIN classification systems used to stage AKI severity. Treatment options discussed include conservative non-dialytic support, dialytic support, and avoiding interventions like diuretics that may worsen outcomes. The document emphasizes early detection of AKI using biomarkers and early nephrology consultation to optimize outcomes.
‘Think Kidneys': Improving the management of acute kidney injury in the NHS Renal Association
‘Think Kidneys': Improving the management of acute kidney injury in the NHS
Presented by Dr Richard Fluck, National Clinical Director (Renal) – NHS England
Hepatorenal Syndrome is one of major complication of Liver Cirhosis.......Early detection & Accurate Treatment....26/6/2016 at Kafrelsheik University ( Resident Lectures).
‘Think Kidneys': Improving the management of acute kidney injury in the NHS Renal Association
‘Think Kidneys': Improving the management of acute kidney injury in the NHS
Presented by Dr Richard Fluck, National Clinical Director (Renal) – NHS England
Hepatorenal Syndrome is one of major complication of Liver Cirhosis.......Early detection & Accurate Treatment....26/6/2016 at Kafrelsheik University ( Resident Lectures).
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Acute kidney injury (AKI) is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days.It's most common in those who are critically ill and already hospitalized.
Acute kidney injury is important topic for students.
the presentation covers all aspects including guidelines from KDIGO, harrison 20th edition and relevant articles.
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
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The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
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1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
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CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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4. By AKI we actually mean “loss of small solute
clearance” (urea/creatinine increase in
blood)
This implies loss of GFR
So…clinically we actually mean
“acute decrease in GFR”
What do we mean by AKI?
5. Lameire N, Van BW, Vanholder R. Nat Clin Pract Nephrol 2006; 2: 364–377.
Can we do staging for AKI?
7. What is the advantages of RIFLE Criteria?
Applying the RIFLE criteria revealed new insights.
Firstly, the RIFLE classification is feasible and
fairly straightforward.
Secondly, the patients categorized as RIFLE-F had a
far higher mortality than RIFLE-I and -R patients.
Max Bell et al; Nephrol Dial Transplant 2005 20:354 –360
8. Number of ARF Hospitalizations: 1979 to 2002
Rates per 1,000 persons
0.0
0.5
1.0
1.5
2.0
2.5
1980 1982 1984 1986 1988 1990 1992 1994 1996 1998 2000 2002
Source: National Center for Health Statistics, National Hospital Discharge Survey
10. Causes of AKI
Pre renal Intrinsic renal Post renal
Decrease in
effective
blood volume.
Arterial
occlusion
Or
stenosis.
Homodynamic
Form.
Vascular
Vasculitis.
Malignant
hypertension
Acute
Glomerulo
nephritis
Acute
Interstitial
nephritis
Acute
Tubular
necrosis
Ischemic. Nephrotoxic.
Obstruction
Of
Collecting
System
Or
Extra renal
drainage
Exogenous
Antibiotic
Radio contrast
cisplatin
Endogenous
Intra tubular pigment
Intra tubular protein.
Intra tubular crystal.
12. Timing nephrology consultation
(Mehta,Am J Med 2002)
In-hospital mortality
Early
consult
Delayed
consult
P
40% 67% <0,001
Early nephrologist involvement in patients with
AKI may reduce the risk of a further decrease in
kidney function.
Am J Kidney Dis. 2011;57(2):228-234
14. Biomarkers are foot prints of actual
organ damage
Creatinine Not A Biomarker
The creatinine level is influenced by multiple non-
renal factors, such as age, gender, muscle mass, muscle
metabolism, diet, medications, and hydration status
In AKI, the serum creatinine level can take several
hours or days to reach a new steady state and thus does
not reflect the actual decrease in GFR in the acute
setting
Because of renal reserve, the serum creatinine level
may not rise until more than half of the kidney
function has been lost
16. New urinary biomarkers for the early detection of
acute kidney disease
Han, Bonventre,Current Opin Crit Care 2004, 10:476–482
Neutrophil gelatinase associated lipocalin
17. Early detection of AKI by Cystatin C
Definition of AF
Area under the ROC
Day - 2 Day - 1 Day 0
≥ 50 % increase 0.82 0.97 0.99
≥ 100 % increase 0.92 0.98 0.98
≥ 200 % increase 0.97 0.99 0.99
•Changes in cystatin C were able to detect the onset of AKI
one to two days earlier than comparable changes in serum creatinine
1. RIFLE- R ( ≥ 50 % increase ): 1.5 ± 0.6 days earlier
2. RIFLE- I ( ≥ 100 % increase): 1.2 ± 0.9 days earlier
3. RIFLE- F ( ≥ 200 % increase): 1.0 ± 0.6 days earlier
Herget-Rosenthal et al, Kidney Int 2004, 66: 1115- 1122
18. Indications of Renal Biopsy
1
Urine
No cast
FENa<1%
Muddy
brown cast
FENa>1%
Red cell
cast
White cell
cast
eosinophil
Pre-renal
ATN Glomerular Interstitial
Biopsy
2. Unknown cause
3. Prolonged ATN
19. Loop diuretics in AKI
Diuretics, particularly high doses of loop diuretics, are frequently
administered to patients with acute renal failure. This is done in part
in an attempt to convert oliguric to nonoliguric acute renal failure.
However, a retrospective observational report found that the use of
diuretics in this setting may increase the risk of death and no
recovery of renal function.
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 )
20. There is insufficient evidence that the low-dose dopamine
improves survival or obviates the need for dialysis in persons with
acute renal failure. The routine use of low-dose dopamine should be
discouraged until a prospective, randomized, placebo-controlled trial
establishes its safety and efficacy.
Is the administration of dopamine associated with adverse or
favorable outcomes in acute renal failure? Auriculin Anaritide
Acute Renal Failure Study Group.
Low Dose Dopamine in AKI
3.5.1: We recommend not using low-dose dopamine to prevent or
treat AKI. (1A)
21. IV Fluids in 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)
22. Contrast Induced AKI
isotonic sodiumwith eitherexpansionvolume.i.v:We recommend4.4.1
. volume expansion,i.v, rather than nochloride or sodium bicarbonate solutions
)A1AKI. (-in patients at increased risk for CI
or)IHD(hemodialysisnot using prophylactic intermittent:We suggest4.5.1
hemofiltration (HF) for contrast-media removal in patients at increased risk for
)C2AKI. (-CI
, incrystalloidsisotonic.i.vwithtogether,NACoral:We suggest using4.4.3
)D2AKI. (-patients at increased risk of CI
4.3.2:We recommend using either iso-osmolar or low-osmolar iodinated
contrast media, rather than high-osmolar iodinated contrast media in patients
at increased risk of CI-AKI. (1B)
23. Bicarbonate or Saline
Among the large
randomized trials there
was no evidence of benefit
for hydration with sodium
bicarbonate compared
with sodium chloride for
the prevention of CI-AKI.
Contrast Induced AKI
24. Stage-based management
General Principles
Stage 1 (Risk)
Risk for more severe AKI
Monitor (prevent
progression)
Stage 2 (Injury)
Risk of AKI-related
mortality/morbidity high
Conservative therapy)
Stage 3 (Failure)
Highest risk of death
Consider RRT
Avoid subclavian catheters if possible
Discontinue all nephrotoxic agents when possible
Consider invasive diagnostic workup
Consider Renal Replacement Therapy
1 2 3
Non-invasive diagnostic workup
Ensure volume status and perfusion pressure
Check for changes in drug dosing
AKI Stage
Consider functional hemodynamic monitoring
Monitoring Serum creatinine and urine output
Consider ICU admission
Avoid hyperglycemia
Consider alternatives to radiocontrast procedures
25. Indications for RRT in critically ill AKI patients
Renal Indications
Life-threatening indications
Hyperkalemia
Metabolic Acidosis
Pulmonary edema
Uremic omplications
26. Dialysis Interventions forTreatment of AKI
5.1.1: Initiate RRT emergently when life-threatening
changes in fluid, electrolyte, and acid-base balance
exist.(Not Graded)
5.1.2: Consider the broader clinical context, the presence
of conditions that can be modified with RRT, and trends
of laboratory tests—rather than single BUN and
creatinine thresholds alone—when making the decision
to start RRT. (Not Graded)
27. Conclusions
Early detection and treatment of AKI may improve
outcomes.
Even a minor acute reduction in kidney function has
an adverse prognosis.
Hunting AKI in ICU….use a RIFLE .
Early referral will improve outcome in AKI