This document discusses acute kidney injury (AKI) in intensive care unit patients. It provides definitions and criteria for AKI, including RIFLE and AKIN classifications. Mortality rates increase significantly with more severe AKI, from 5-10% with no renal dysfunction to 26-40% with renal failure. While decreased urine output can indicate decreased kidney function, urine output alone is a less severe marker. Multiple factors influence the relationship between renal blood flow, perfusion pressure, and glomerular filtration rate. Early markers like neutrophil gelatinase-associated lipocalin and cystatin C may help predict AKI and prognosis better than creatinine. Fluid management must balance resuscitation with avoiding overload,
Renal Replacement Therapy: modes and evidenceMohd Saif Khan
Renal replacement therapy is a supportive care often required in critically ill patients who develop acute renal failure and its complications. Complexity arises when such patients become hemodynamically unstable and pose special challenge to critical care clinicians in ICU to carefully choose dialytic modality to tackle volume and solute overload. This presentation is about short description of modalities of RRT and current evidence regarding initiation, dose and type of modality.
Renal Replacement Therapy: modes and evidenceMohd Saif Khan
Renal replacement therapy is a supportive care often required in critically ill patients who develop acute renal failure and its complications. Complexity arises when such patients become hemodynamically unstable and pose special challenge to critical care clinicians in ICU to carefully choose dialytic modality to tackle volume and solute overload. This presentation is about short description of modalities of RRT and current evidence regarding initiation, dose and type of modality.
Renal Replacement therapy (Dialytic Management) in AKI - Dr.GawadNephroTube - Dr.Gawad
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/NN9vyWjIPbE
Arabic Language version of this lecture is available at:
https://youtu.be/i-Qlf31Vd-Y
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Renal Replacement therapy (Dialytic Management) in AKI - Dr.GawadNephroTube - Dr.Gawad
- Recorded videos of this lecture:
English Language version of this lecture is available at:
https://youtu.be/NN9vyWjIPbE
Arabic Language version of this lecture is available at:
https://youtu.be/i-Qlf31Vd-Y
- Visit our website for more lectures: www.NephroTube.com
- Subscribe to our YouTube channel: www.youtube.com/NephroTube
- Join our facebook group: www.facebook.com/groups/NephroTube
- Like our facebook page: www.facebook.com/NephroTube
- Follow us on twitter: www.twitter.com/NephroTube
Good overview of acute renal failure but this was written before the most recent ATN data which negates one of the premises of the lectuer that higher doses of dialysis are beneficial in patients in ARF.
Acute kidney injury is important topic for students.
the presentation covers all aspects including guidelines from KDIGO, harrison 20th edition and relevant articles.
COURTSEY - DEPARTMENT OF CRITICAL CARE
ABVIMS & DR RML HOSPITAL NEW DELHI.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
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.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
2. Why should we be concerned?
• Increased risk of death
• Marker of severity
3. Outcomes in AKI
• BEST study* (Beginning and Ending Supportive
Therapy for the Kidney)
– The prevalence of AKI requiring renal replacement therapy
(RRT) ~ 4%
– 28 days in-hospital mortality in patients with AKI was ~
60%
• RIFLE criteria
– In-hospital mortality with AKI is in the range of
•
•
•
•
5 to 10% with no renal dysfunction
9 to 27% in patients classified as at risk
11 to 30% with injury
26 to 40% with failure
*Clin J Am Soc Nephrol. 2007 May;2(3):431-9. Septic acute kidney injury in critically ill patients: clinical characteristics and outcomes.
5. AKIN criteria
1. Increase the sensitivity of the RIFLE criteria by
recommending that a smaller change in serum
creatinine (≥26.2 µmol/L) be used as a threshold to
define the presence of AKI and identify patients with
Stage 1 AKI (analogous to RIFLE-Risk)
2. A time constraint of 48 h for the diagnosis of AKI was
proposed.
3. Any patients receiving renal replacement therapy
(RRT) were to now be classified as Stage 3 AKI (RIFLEFailure)
Bagshaw SM, George C, Bellomo R; ANZICS Database Management Committe. A comparison of
the RIFLE and AKIN criteria for acute kidney injury in critically ill patients. Nephrol Dial
Transplant. 2008 May;23(5):1569-74. Epub 2008 Feb 15.
6. Is ↓UO= renal failure?
• Does ↓UO = ↓GFR?
• May be physiological to preserve body volume
or electrolyte homeostasis.
• Severe tubular dysfunction can lead to
increased urine output despite low GFR.
• Bottom line: urine output alone is less severe
marker if used alone.
7. Normal GFR
GFR = Kf[(PGC-PBS) –(ΠGC-ΠPB)]
Kf = filtration coefficient
ΠPB = zero, since no protein
A higher renal plasma flow will induce a
reduction in filtration fraction (i.e., ratio
of ultrafiltration to renal plasma flow)
with a lesser increase of capillary plasma
protein concentration along the
glomerular capillaries.
When the renal plasma flow is reduced,
the glomerular filtration rate decreases
but with an increase in the filtration
fraction
9. What if renal perfusion pressure increases?
• the ultrafiltrate will be
mainly generated on the first
portion of the afferent side
of the capillary network and
to cease when hydraulic and
oncotic pressures become
equal along the glomerular
capillary network
• Therefore the oncotic
pressure becomes the
limiting factor of glomerular
filtration
10. Clinical implication
• When you resuscitate patient with crystalloids
you are diluting the serum proteins thereby
decreasing the plasma oncotic pressure.
• Hence the urine response you may be seeing
is simply due to decreased oncotic pressure !!!
12. What happens in chronic kidney
disease?
• Decreased glomerular surface area
• Glomerular hydraulic pressure becomes major
determinant of GFR.
13. Relation between renal blood flow and
GFR
• the renal blood flow is autoregulated, which
means that it remains unchanged when
arterial blood pressure varies
• Mediated by
– Myogenic mechanism: FAST
– Tubuloglomerular feedback: SLOW
14. How long can kidneys suffer low
perfusion?
• Interruption of blood flow x >30min followed
by reperfusion tubular and microvascular
damage
• But this scenario is not what we encounter.
• This is seen in supra renal aortic surgery
where aorta has to be clamped for some time!
15. How long can kidneys suffer low
perfusion?
• Prolonged period of renal hypo-perfusion
does not always results in renal histological
damage and renal failure.
• Reduced renal blood flow by 80% x 2 hrs no
kidney damage
16. In five sheep: renal blood flow (RBF) was reduced by 25, 50 and 75%, respectively, by
acute vascular occlusion for 30 min at weekly intervals.
In another six sheep: RBF was reduced by 80% for 2 h.
Release of occlusion induced brief hyperemia before all measured variables returned
to normal within 8 h and remained normal for the following 72 h.
At autopsy, the kidneys were histopathologically normal
17.
18. • Rats with LPS infusion
to reduce blood flow by
50%
• Decrease in cortical
PO2 from
6852mHg
• Rats with mechanical
reduction of blood flow
to 50% anuria
• No decrease in PO2
seen
• Fluid resuscitation in
LPS rats with
normalized blood flow
• No decrease in
cortical Po2
19. Conclusions
• Severe transient hypoperfusion is able to reduce
GFR and urine output but is not sufficient to
induce persistent AKI.
• Superimposition of renal hypoperfusion episodes
in relation to other insults, such as sepsis or
ischemia may induce renal failure
• It is expected that preventing a decrease of renal
blood flow may prevent or limit the occurrence of
AKI in ICU patients
21. • Review of all studies in
literature do not show a
correlation between TRPF
and GFR, implying
uncoupling between
perfusion(TRPF) and
function (GFR), such that
‘for a given decrease in
decreased perfusion,
there is an unpredictable
and much greater loss in
function’.
22. Possible explanations for uncoupling
between RBF and GFR.
1. Raised bowman’s space
pressure secondary to tubular
obstruction
2. Failure of active reabsorption
of ultrafiltrate
3. Back-leak of tubular
ultrafiltrate into the
interstitium and circulation
4. Tubulo-glomerular feedbackinduced afferent arteriolar
vasoconstriction
5. Decreased efferent arteriolar
tone
23. Intra renal blood flow distribution
• normal kidneys receive ~20% of cardiac output
• medulla receives less than 10% of renal blood flow
• In contrast to the cortical microcirculation, the medulla
microcirculation appears to be poorly autoregulated,
i.e., pressure-dependent.
– Regulation of diuretics and natriuresis and, therefore, the
response of the kidney to the body fluid composition and
volume status
– in mammalians kidneys, the ability of the medulla
circulation to regulate its own blood flow depends largely
on the body volume status
24. • With changes in
RPP, the only
detectable change
in intra-renal
perfusion occurs
in the inner
medulla
25. • In contrast, both renal cortical and
medulla are well autoregulated in
hydropenic rats.
• Because the descending vasa recta
provide blood flow to the medulla
emerge from efferent arterioles of
juxtamedullary glomerules, these
data suggest that changes in
resistance in the postglomerular
circulation of juxtamedullary
nephrons might be responsible for
the lack of autoregulation of
medullary blood flow in volume
expended animals
26. Pressure induced diuresis
• Increase in renal medullary blood flow
– decreases the outer-inner medullar osmotic gradient
– increases renal interstitial hydrostatic pressure
• which both impair the ability to concentrate urine
and participate in the natriuresis response to
hypertension in well-hydrated mammalians.
• In hydropenic animals, this response is blunted
preventing further loss of water and sodium
27. Hypothesis for developing AKI in sepsis
• Increased vascular response of the renal
microcirculation to vasoconstrictors elicit
intense renal vasoconstriction induces AKI
• Endogenous vasoconstrictors, including
angiotensin II
– decrease GFR due to decrease in renal blood flow
– blunt the natriuresis response after the renal
perfusion pressure has been restored
• Endotoxemia also can increase urine output and
water clearance despite decrease in GFR due to
tubular aquaporin-2 dysfunction
28.
29. Tubulo-glomerular feedback
• Higher [NaCl] in tubular fluids in macula densa
adenosine release increase of the glomerular
afferent arteriole vascular tone decreases GFR
– Operates for few seconds to minutes
– It resets in 30-60 min
– Prevents rapid loss of water and electrolytes in condition of
tubular dysfunction
• Na+ absorption network has the major renal oxygen
consumption.
• So decrease in GFR lesser amount of Na reaching
distal tubules decreased oxygen consumption.
30. • In ischemic kidneys:
– Diversion of oxygen consumption from Na+
reabsorption to other oxygen-consuming
pathways illustrated by an increase of the ratio
oxygen consumption/Na Reabsorp +
31. Postcardiac surgery patients with (n = 12) and without (n = 37) acute kidney injury were compared with
respect to renal blood flow, glomerular filtration, RVO2, and renal oxygenation.
In the acute kidney injury group, GFR (-57%), renal blood flow (-40%), filtration fraction (-26%), and
sodium resorption (-59%) were lower, renal vascular resistance (52%) and renal oxygen extraction (68%)
were higher, whereas there was no difference in renal oxygen consumption between groups.
Renal oxygen consumption for one unit of reabsorbed sodium was 2.4 times higher in acute kidney
injury
32. • Oxygen consumption to absorptive work mismatch is
not well understood and may result from:
– higher production of reactive oxygen species by infiltrative
immune cells
– high level of NO, which regulates the renal oxygen
consumption
• This may partially explain why strategies designed to
inhibit renal oxygen consumption (e.g., loops diuretics)
have failed to improve the prognosis of patients
suffering from AKI
33. Distant effects of renal
ischemia/reperfusion injury
J Am Soc Nephrol 14: 1549–1558, 2003
34. Acute renal failure leads to dysregulation
of lung salt and water channels
Kidney International, Vol. 63 (2003), pp. 600–606
35. Summary
• Decrease urine output can mirror a decrease
in creatinine clearance.
• Although a decrease in renal blood flow
and/or a decrease in renal perfusion pressure
is a major determinant of GFR, plasma oncotic
pressure appears to be central in the
glomerular hydrodynamic forces.
• Colloids increase the oncotic pressure and
may reduce filtration rate
36. Summary
• Fluid administration may be found inappropriate
and even harmful in numerous situations due to
the inconstant relationship between renal blood
flow or renal perfusion pressure and
diuresis/natriuresis due to complex
neurohormonal control.
• systemic inflammation can induce natriuresis and
diuresis changes due to functional changes
unrelated to hypoperfusion, histological, or
tubular damage
37. How to identify early AKI ?
• Is creatinine good enough?
• Use it with Urine output
• What about prediction equations: MDRD or
Cockroft & Gault.
– In critical care where creatinine is changing
rapidly, these formulas cannot be used to predict
GFR.
– Cannot be used in oliguric/anuric patients.
– These are used only for steady states
39. Is FeNa useful?
• Although a low UNa or FeNa (e.g., FeNa <1%) suggest a
preserved renal tubular reabsorptive capacity, there is
NO evidence for a correlation between urinary
biochemical modifications and tissue damage.
• Control of urinary Na+ excretion results from a complex
neurohumoral regulation and is influenced by
• fluid resuscitation
• arterial pressure
• infusion of diuretics
40. How do I predict renal prognosis?
• FeNa and FeUrea are not helpful
• Neutrophil Gelatinase associated lipocalin (NGAL)
41. Neutrophil Gelatinase associated
lipocalin (NGAL)
• Plasma NGAL had an area under the ROC curve of 0.71
(95% confidence interval (CI), 0.55-0.88) for predicting
AKI progression and of 0.78 (95% CI, 0.61-0.95) for
need for renal replacement therapy
• Area under the ROC curve of 0.82 (95% CI, 0.7-0.95) for
predicting the use of renal replacement therapy
• Urine NGAL remains low in patients admitted in the
emergency department with prerenal azotemia versus
AKI
42. Cystatin-C
• 13 kD endogenous cysteine-proteinase
inhibitor that is produced by all cells.
• Freely filtered across the glomerulus and, in
contrast to creatinine, it is not secreted by
renal epithelial cells.
• Rises earlier than creatinine in ICU patients
with AKI
Kidney Int. 2004 Sep;66(3):1115-22.
43. Conclusions
• These urinary markers have been poorly studied among
critically ill patients.
• Recent reviews of experimental and human sepsis have
highlighted the paucity of available studies and their
design heterogeneity regarding urinary findings in septic
AKI
• there is no evidence that these urinary biochemical
findings can predict the response to hemodynamic
optimization in terms of renal injury and renal function
44. How should we assess renal perfusion
in ICU patient?
• Doppler-based determination of resistive
index
• Problems
– Need data with respect to GFR, Crclearance, FeNa
and oxygen consumption
– Need baseline data before the insult
– Difficult technically and in obese persons
45. Can We Predict Which Patient in the
ICU Will Develop AKI ?
• There are risk factors but no prediction score.
– Age
– Sepsis
– Cardiac surgery
– Infusion of contrast
– Diabetes
– Rhabdomyolysis
– Preexisting renal disease
– Hypovolemia and shock
46. How do we protect kidneys?
• Improve Renal perfusion
1. Volume status – fluid resuscitation
2. Pressors
48. FACTT trial
• Selected patients with acute lung injury, conservative fluid
management may not be detrimental to kidney function.
• Fluid balance over 7 days was -136 ml in the conservative
group versus +6,992 ml in the liberal fluid strategy group
• Not associated with an increase in the frequency of RRT,
which occurred in 10% of the conservative-strategy group and
14% of the liberal-strategy group
49. Fluid resuscitation in AKI
• Although fluid
resuscitation and
optimization of renal
perfusion pressure are
central to the prevention
and treatment of AKI,
excessive fluid
resuscitation may be
harmful in some
critically ill patients
50. Problems with fluid overload
• Aggressive fluid resuscitation increases renal blood
flow but can be ineffective in restoring renal
microvascular oxygenation due to hemodilution with
no increase in blood-oxygen carriage capacities.
• Positive fluid balance can deteriorate cell oxygenation
and prolong mechanical ventilation.
• Fluid overload may lead to central venous congestion
and decrease of renal perfusion pressure, which will
promote the development of AKI in patients with acute
heart failure or sepsis
52. • Hyperosmotic colloids can be associated with
development of renal dysfunction
Schortgen F et al. Effects of hydroxyethylstarch and gelatin on renal function in severe
sepsis: a multicentre randomised study. Lancet 2001;357:911–916.
53. Brunkhorst FM et al. Intensive insulin therapy and pentastarch resuscitation in severe
sepsis. N Engl J Med 2008;358:125–139
54. SAFE study
• No differences between
the groups in
– Patients who required RRT
(1.3% and 1.2%)
– the mean number of days
of RRT (0.5 ±2.3 and 0.4 ±
2.0; P =0.41)
– number of days of
mechanical ventilation (4.5
± 6.1 and 4.3 ± 5.7; P =
0.74).
N Engl J Med. 2004 May 27;350(22):2247-56
55. • Fuid resuscitation with
crystalloids or gelatin is
associated with a lower
incidence of AKI than
resuscitation with artificial
hyperoncotic colloids
• Dextran in 3% of patients
and starches in 98% of
patients (adjusted odds
ratio, 2.48) or
• Hyperoncotic albumin
(adjusted odds ratio, 5.99)
Schortgen F, Girou E, Deye N, Brochard L. The risk
associated with hyperoncotic colloids in patients with
shock. Intensive Care Med 2008;34:2157–2168.
56. Recommendations*
• Consider fluid resuscitation with crystalloids to be as
effective and safe as fluid resuscitation with
hypooncotic colloids (gelatins and 4% albumin)
• Based on current knowledge, hyperoncotic solutions
(dextrans, hydroxyethyl starches, or 20–25%
albumin) not be used for routine fluid resuscitation
because they carry a risk for renal dysfunction.
*An Official ATS/ERS/ESICM/SCCM/SRLF Statement:Prevention and Management of
Acute Renal Failure in the ICU Patient. Am J Respir Crit Care Med Vol 181. pp 1128–
1155, 2010
57. Role of vasoactive drugs
• Titrate to what ?
• What pressors should I use?
• Don’t the vasopressors cause renal afferents
to vasoconstrict and worsen renal blood flow?
58. How much MAP is sufficient ?
• Unknown whether the current
recommendation to maintain a mean arterial
pressure (MAP) at or above 65 mm Hg in
patients who are critically ill is adequate for
preventing AKI.
• It is likely that some patients—especially
those with history of hypertension and the
elderly—may require higher MAP to maintain
adequate renal perfusion.
59. • Twenty-eight patients with a
diagnosis of septic shock who
required fluid resuscitation and
pressor agents
• to achieve and maintain a mean
arterial pressure of 65 mm Hg.
• Then they were randomized in
two groups:
– In the first group (control group,
n 14), mean arterial pressure
was maintained at 65 mm Hg
– in the second group (n 14),
mean arterial pressure was
increased to 85 mm Hg by
increasing the dose of
norepinephrine
60.
61. • Increasing the CI to a supra normal level > 4.5 (cardiac-index group)
• Increasing mixed venous oxygen saturation to a normal level (oxygen-saturation
group)
62. Conclusions
• Higher MAP is associated with increased cardiac
output but no difference in urine output or
creatinine clearance
• Normalization of mixed venous oxygen saturation or
by increasing oxygen delivery to supranormal levels
does not decrease rate of AKI
• Resuscitation should be titrated to end points of
oxygen metabolism and organ function.
63. Does type of vasopressor has any
role?
• You would expect NE to cause afferent vessel
vasoconstriction and decrease renal blood
flow.
66. • Twelve post-cardiac
surgery patients with NEdependent vasodilatory
shock and AKI were
studied
• 2–6 days after surgery.
• NE infusion rate was
randomly and
sequentially titrated to
target MAPs of 60, 75 and
90 mmHg.
67. Vasopressin
• Binding to the V2-receptors in the inner
medullary collecting ducts activates the UTA1 molecules
• increases the urea permeability of
collecting duct
• increase the ability to concentrate urine
68. Vasopressin
• Increase of plasma
vasopressin concentration
(independently of any
increase of systemic arterial
pressure) also influences
the pressure-natriuresis/
diuresis relationship in
decreasing the medullary
blood flow through
receptor V1a
Crit Care Med. 2004 Sep;32(9):1891-8.
69. • Vasopressin may reduce the progression to severe AKI only in a
prespecified subgroup of patients with less severe septic shock
(norepinephrine dose ,15 mg/minute)
• No difference was observed in the need for RRT in any subgroup.
Holmes CL, Mehta S, Granton JT, Storms MM, et al. Vasopressin versus norepinephrine infusion in patients with septic shock. N Engl
JMed2008;358:877–887.
70. What about dopamine? Low dose?
7 sheep
6 h of placebo (saline solution) or
drugs (MD-NE at 0.4 micro g/kg/min or LDD
at 2 micro g/kg/min),
Outcomes: cardiac output (CO), and flow to
vital organs, lactate, creatinine, and
creatinine clearances
Chest. 2004 Jun;125(6):2260-7.Increasing renal blood flow: low-dose dopamine or medium-dose norepinephrine.
71.
72. In patients with or at risk for AKI, low-dose dopamine may increase diuresis on the first
day of use but it does not protect against the development of AKI
74. Fenoldopam
• Short-acting dopamine receptor-1 agonist
• Fenoldopam did not affect the need for RRT
and survival at 21 days.
• In secondary analysis, however, fenoldopam
reduced the need for RRT and the incidence of
death in patients without diabetes and in
postoperative patients who have undergone
cardiothoracic surgery
75.
76.
77. Anything else?
• Angiotensin II
• In the absence of angiotensin II, volume
expansion with no increase in MAP induces
natriuresis, whereas the increase in MAP by
angiotensin II infusion did not induce a
natriuresis response
78. Summary
• Norepinephrine and vasopressin may induce, in septic
states, an increase of renal blood flow through a
combined
– increase of renal perfusion pressure (i.e., prerenal mechanism)
and
– an increase of renal vascular conductance (i.e., intrarenal
mechanism)
• Increase of renal blood flow does not necessarily
translate into GFR increase
• Current clinical data are insufficient to conclude that one
vasoactive agent is superior to another in preventing
development of AKI
79. Renal support
• Introduce early
• Traditional thresholds used in stable patients may not be
appropriate in ICU patients with AKI
– impact of renal failure on other failing organs such as the lungs (ARDS,
pulmonary edema) and brain (encephalopathy) should be considered
in the timing of RRT
– the increased catabolism associated with critical illness and the need
to administer adequate nutritional protein will lead to increased urea
generation
– Often difficult to limit fluid intake in these patients, in part due to the
administration of intravenous medications (antibiotics, vasopressors,
etc.)
– patients who are critically ill may be more sensitive to metabolic
derangements, and swings in their acidbase and electrolyte status may
be poorly tolerated.
80. Program to Improve Care in Acute
Renal Disease (PICARD) study
• Timing: early vs. late
• Odds ratio for adverse outcome of 1.97 (95%
confidence interval *CI+ 1.21– 3.20) was
associated with late start of RRT (BUN ,76
mg/dl versus BUN .76 mg/dl)
Clin J Am Soc Nephrol 1: 915–919, 2006
81. RRT dose
• Acute Renal Failure Trial Network study: no
difference between CVVHD(22ml/kg/hr) and
IHD (>3.9Kt/Vd/Wk) – OR 0.92 (0.73-1.16)
• Randomized Evaluation of Normal versus
Augmented Level [RENAL] Replacement
Therapy Study: CVVHD @ 25 and 40ml/kg/hr.
– OR for mortality 1.00 (0.81-1.23)
82.
83. Recommendations
• Timing
– In patients who are critically ill with AKF we suggest initiating RRT
before the development of extreme metabolic derangements or other
life-threatening events.
• Intensity
– For IHD and SLED, we recommend clearances at least equal to
minimum requirements for chronic renal failure (3.6 Kt/Vd/wk)
– For CRRT (CVVH or CVVHD), we recommend clearance rates for small
solutes of 20 m/kg/h (actual delivered dose).
– Higher doses of CRRT cannot be generally recommended and should
only be considered by teams that can administer them safely
*An Official ATS/ERS/ESICM/SCCM/SRLF Statement:Prevention and Management of Acute Renal
Failure in the ICU Patient. Am J Respir Crit Care Med Vol 181. pp 1128–1155, 2010