The document discusses the history of dialysis and definitions of acute kidney injury. It notes that Dr. Haas invented the first dialysis machine for humans in 1928 but all 6 of his initial patients died. In 1943, Dr. Kolff created the second human dialysis machine from household items and successfully treated a patient with nephritis. It introduces the RIFLE and AKIN criteria for classifying acute kidney injury based on changes in creatinine and urine output. Studies found RIFLE and AKIN criteria effectively stratified patients by risk of poor outcomes like mortality and need for renal replacement therapy. Oliguria is highly sensitive but not very specific for predicting subsequent acute kidney injury defined by creatinine changes. There is
Sudden impairment of kidney function occurring over a period of hours to days.
AKI is present in 7% of all hospitalized patients, and up to 30% of patients in ICU
The incidence is increasing at an alarming rate
That's why we need ideal biomarker to diagnose the AKI as early as possible and deliver better treatment to the patient.
Sudden impairment of kidney function occurring over a period of hours to days.
AKI is present in 7% of all hospitalized patients, and up to 30% of patients in ICU
The incidence is increasing at an alarming rate
That's why we need ideal biomarker to diagnose the AKI as early as possible and deliver better treatment to the patient.
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
Final presentation on Acute kidney injury AKI and Chronic kidney disease CKD ...HariSedai
Approach to a patient with AKI or CKD in emergency setup and the relevant analysis of patient who visit emergency setting with the AKI and ckd a retrospective analysis in THTH emergency nepal, a developing country scenario
Objective Acute kidney injury
Know about definition of Acute kidney injury
Function of kidney
Sign and symptoms of AKI
Know about Risk factor of AKI
Understand about complication of AKI
Contents:
Introduction Of Acute kidney injury
Physiology Of Acute kidney injury
Pathophysiology Of Acute kidney injury
Clinical feature Of Acute kidney injury
Risk Factor Of Acute kidney injury
Diagnosis Of Acute kidney injury
Differential diagnosis Of Acute kidney injury
Complication Of Acute kidney injury
Management Of Acute kidney injury
Acute Kidney Injury epidemiology, pathophysiology and management based on current evidence. The presentation is suitable for internal medicine trainees and nephrology fellows.
Acute kidney injury, previously known as acute renal failure, encompasses a wide spectrum of injury to the kidneys, not just kidney failure. The definition of acute kidney injury has changed in recent years, and detection is now mostly based on monitoring creatinine levels, with or without urine output. Acute kidney injury is increasingly being seen in primary care in people without any acute illness, and awareness of the condition needs to be raised among primary care health professionals.
Acute kidney injury is seen in 13–18% of all people admitted to hospital, with older adults being particularly affected. These patients are usually under the care of healthcare professionals practising in specialties other than nephrology, who may not always be familiar with the optimum care of patients with acute kidney injury. The number of inpatients affected by acute kidney injury means that it has a major impact on healthcare resources. The costs to the NHS of acute kidney injury (excluding costs in the community) are estimated to be between £434 million and £620 million per year, which is more than the costs associated with breast cancer, or lung and skin cancer combined.
Final presentation on Acute kidney injury AKI and Chronic kidney disease CKD ...HariSedai
Approach to a patient with AKI or CKD in emergency setup and the relevant analysis of patient who visit emergency setting with the AKI and ckd a retrospective analysis in THTH emergency nepal, a developing country scenario
Objective Acute kidney injury
Know about definition of Acute kidney injury
Function of kidney
Sign and symptoms of AKI
Know about Risk factor of AKI
Understand about complication of AKI
Contents:
Introduction Of Acute kidney injury
Physiology Of Acute kidney injury
Pathophysiology Of Acute kidney injury
Clinical feature Of Acute kidney injury
Risk Factor Of Acute kidney injury
Diagnosis Of Acute kidney injury
Differential diagnosis Of Acute kidney injury
Complication Of Acute kidney injury
Management Of Acute kidney injury
Acute Kidney Injury epidemiology, pathophysiology and management based on current evidence. The presentation is suitable for internal medicine trainees and nephrology fellows.
Drs. Lena, Avery, and Davis’s CMC Abdominal Imaging Mastery Project: August C...Sean M. Fox
Dr. Kelsey Lena is an Emergency Medicine Resident and Drs. Michael Avery and Joshua Davis are Surgery Residents at Carolinas Medical Center in Charlotte, NC. They are interested in medical education. With the guidance of Drs. Kyle Cunningham and Michael Gibbs, they aim to help augment our understanding of emergent abdominal imaging. Follow along with the EMGuideWire.com team as they post these monthly educational, self-guided radiology slides. This month’s topics include:
• Splenic Rupture
• Obstructive jaundice
• Ovarian Torsion
Dr. Michael Gibbs's CMC X-Ray Mastery Project - Week #7 CasesSean M. Fox
Dr. Michael Gibbs is a Professor of Emergency Medicine and interested in educating others. Radiology is a passion of his. Follow along with the EMGuideWire.com team as they post Dr. Gibbs's weekly educational, self-guided radiology slides on: Hemopericardium, Cardiomyopathy, Heart Failure, Myocarditis, Ruptured Hemidiaphragm, Hydropneumothorax, Pneumothorax, ECMO
Grand Rounds which summarizes the data pointing to fructose and sugar intake as the chief cause of hypertension and the use of allopurinal to treat pediatric hypertension.
This demonstrates lead time bias. I do not know if lead time bias is responsible for the prolonged survival with early referral to nephrology I just know that it needs to be accounted for and most literature ignores this source of error.
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
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
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
Associate Division Director for Ambulatory Operations
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
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
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
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.
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
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
3. Dr. Haas invented the first dialysis machine designed
for humans and in 1928 he treated 6 patients.
4. Dr. Haas invented the first dialysis machine designed
for humans and in 1928 he treated 6 patients.
All of them died.
5. In 1943, Willem Kolff’s, working in Nazi
occupied Netherlands created the
second human dialysis machine from
a washing machine, juice cans and
sausage casings.
In 1943 he dialyzed his first patient, a
young man with acute nephritis.
6. In 1943, Willem Kolff’s, working in Nazi
occupied Netherlands created the
second human dialysis machine from
a washing machine, juice cans and
sausage casings.
In 1943 he dialyzed his first patient, a
young man with acute nephritis.
7. In 1943, Willem Kolff’s, working in Nazi
occupied Netherlands created the
second human dialysis machine from
a washing machine, juice cans and
sausage casings.
In 1943 he dialyzed his first patient, a
young man with acute nephritis.
8. In 1943, Willem Kolff’s, working in Nazi
occupied Netherlands created the
second human dialysis machine from
a washing machine, juice cans and
sausage casings.
In 1943 he dialyzed his first patient, a
young man with acute nephritis.
Dr. Haas
9. In 1943, Willem Kolff’s, working in Nazi
occupied Netherlands created the
second human dialysis machine from
a washing machine, juice cans and
sausage casings.
In 1943 he dialyzed his first patient, a
young man with acute nephritis.
Dr. Haas
0 for 22
10. In 1943, Willem Kolff’s, working in Nazi
occupied Netherlands created the
second human dialysis machine from
a washing machine, juice cans and
sausage casings.
In 1943 he dialyzed his first patient, a
young man with acute nephritis.
In 1945, a 67-year-old woman in
uremic coma presented to Dr Kolff.
Dr. Haas
0 for 22
11. In 1943, Willem Kolff’s, working in Nazi
occupied Netherlands created the
second human dialysis machine from
a washing machine, juice cans and
sausage casings.
In 1943 he dialyzed his first patient, a
young man with acute nephritis.
In 1945, a 67-year-old woman in
uremic coma presented to Dr Kolff.
Dr. Haas
Regained consciousness after 11
hours of hemodialysis.
0 for 22
18. Patients with primary diagnosis of AKI have
higher mortality when they are:
admitted on week-ends
admitted to smaller hospitals
James et al. Weekend Hospital Admission, Acute Kidney Injury, and Mortality.
Journal of the American Society of Nephrology (2010) vol. 21 (5) pp. 845-851
19. ICU associated AKI is
characterized by a
d e l a y b e t w e e n
a d m i s s i o n a n d
d e v e l o p m e n t o f
acute renal injury
21. Risk
Increase in Cr of 1.5-2.0 X baseline or
urine output < 0.5 mL/kg/hr for more than 6 hours.
Injury
Failure
Loss of function
End-Stage Renal disease
22. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
Injury
increase in Cr 2-3 X baseline (loss of 50% of GFR) or
urine output < 0.5 mL/kg/hr for more than 12 hours.
Failure
Loss of function
End-Stage Renal disease
23. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
Failure
increase in Cr rises > 3X baseline Cr (loss of 75% of GFR) or
an increase in serum creatinine greater than 4 mg/dL, or
urine output < 0.3 mL/kg/hr for more than 24 hours or
anuria for more than 12 hours.
Loss of function
End-Stage Renal disease
24. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr >
24 hrs or anuria for more than 12 hours
Loss of function
persistent renal failure (i.e. need for dialysis) for more than 4
weeks.
End-Stage Renal disease
25. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr >
24 hrs or anuria for more than 12 hours
Loss of function: Need for dialysis for more than 4 weeks
End-Stage Renal disease
persistent renal failure (i.e. need for dialysis) for more than 3
months.
26. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr >
24 hrs or anuria for more than 12 hours
Loss of function: Need for dialysis for more than 4 weeks
End-Stage Renal disease : Need for dialysis for more than 3
months
27. nice criteria. do they work?
20,126 consecutive
admissions to a
university hospital
Excluded kids
Kidney transplant and
dialysis patients
Patients admitted for <
24 hours
Using RIFLE:
Risk 9.1%
Injury 5.2%
Failure 3.7%
Uchino S, Bellomo R, Goldsmith D. Crit Care Med 2006 Vol 34 1913-1917.
28. nice criteria. do they work?
20,126 consecutive
admissions to a
university hospital
Excluded kids
Kidney transplant and
dialysis patients
Patients admitted for <
24 hours
Using RIFLE:
Risk 9.1%
Injury 5.2%
Failure 3.7%
No Renal failure
82%
Failure
4%
Injury
5%
Risk
9%
Uchino S, Bellomo R, Goldsmith D. Crit Care Med 2006 Vol 34 1913-1917.
32. nice criteria. do they work in the icu?
University of Pittsburgh
has 7 ICUs
5,383 patients
Excluded dialysis
Subsequent admissions
Frequency of acute
Kidney failure:
No AKD 1,766
Risk 670
Injury 1,436
Failure 1,511
Hoste E, Clermont G, Kersten A. Crit Care 2006 Vol 310
33. nice criteria. do they work in the icu?
University of Pittsburgh
has 7 ICUs
5,383 patients
Excluded dialysis
Subsequent admissions
Frequency of acute
Kidney failure:
No AKD 1,766
Risk 670
Injury 1,436
Failure 1,511
No Renal failure
33%
Failure
28%
Injury
27%
Risk
12%
Hoste E, Clermont G, Kersten A. Crit Care 2006 Vol 310
34. No AKI Risk Injury Failure
0
5
10
15
20
25
30
RRT
LOS
ICU LOS
Mortality
35. No AKI Risk Injury Failure
0
5
10
15
20
25
30
RRT
LOS
ICU LOS
Mortality
36. No AKI Risk Injury Failure
0
5
10
15
20
25
30
RRT
LOS
ICU LOS
Mortality
37. AKIN criteria
refinement of RIFLE criteria
smaller change in Cr 0.3
time constraint of 48 hours for the diagnosis of
AKI
anyone requiring dialysis is stage 3 AKI
38. RIFLE v AKIN
RIFLERIFLE
R
Cr increased by
50-100%
I
Cr increased by
100-200%
F
Cr increased by more
than 200% or Cr > 4
L
Need for dialysis for >
4 weeks
E
Need for dialysis for >
3 months
39. RIFLE v AKIN
RIFLERIFLE
R
Cr increased by
50-100%
I
Cr increased by
100-200%
F
Cr increased by more
than 200% or Cr > 4
L
E
40. RIFLE v AKIN
RIFLERIFLE AKINAKIN
R
Cr increased by
50-100%
1
Cr increased by 0.3 or
50-100%
I
Cr increased by
100-200%
2
Cr increased by
100-200%
F
Cr increased by more
than 200% or Cr > 4
3
Cr increased by more
than 200%, Cr > 4, or
renal replacement
therapyL
Cr increased by more
than 200%, Cr > 4, or
renal replacement
therapy
E
41.
42. AKIN vs RIFLE
120,123 critically ill patients in
57 ICUs in New Zealand and
Australia
43. AKIN vs RIFLE
120,123 critically ill patients in
57 ICUs in New Zealand and
Australia
64%
16%
14%
6%
RIFLE
63%
18%
10%
9%
AKIN
None
Risk / 1
Injury / 2
Failure / 3
44. AKIN vs RIFLE
120,123 critically ill patients in
57 ICUs in New Zealand and
Australia
64%
16%
14%
6%
RIFLE
63%
18%
10%
9%
AKIN
None
Risk / 1
Injury / 2
Failure / 3
2.24
3.95
5.13
2.45
4.23
5.22
Risk / 1
Injury / 2
Failure / 3
mortality odds ratio vs no AKI
45. oliguria: sensitive or specific?
oliguria is a biomarker of ARF
Used in the definition of RIFLE and AKIN
How good is it at predicting AKICreatinine
46.
47. ICU patients and tracked hourly urine
outputs
oliguria: <0.5 ml/kg/hr
primary outcome: how predictive was oliguria
for subsequent AKI as defined by creatinine
239 patients, 723 days, 23 cases of hospital
acquired AKI
48. duration of oliguria AKI the next day No AKI next day
None 5 443
≥1 hour 18 257
≥2 hours 15 194
≥3 hours 13 125
≥4 hours 12 95
≥5 hours 7 75
≥6 hours 5 50
≥12 hours 4 9
49. duration of oliguria AKI the next day No AKI next day
None 5 443
≥1 hour 18 257
≥2 hours 15 194
≥3 hours 13 125
≥4 hours 12 95
≥5 hours 7 75
≥6 hours 5 50
≥12 hours 4 9
50. duration of oliguria AKI the next day No AKI next day
None 5 443
≥1 hour 18 257
≥2 hours 15 194
≥3 hours 13 125
≥4 hours 12 95
≥5 hours 7 75
≥6 hours 5 50
≥12 hours 4 9
51. duration of oliguria AKI the next day No AKI next day
None 5 443
≥1 hour 18 257
≥2 hours 15 194
≥3 hours 13 125
≥4 hours 12 95
≥5 hours 7 75
≥6 hours 5 50
≥12 hours 4 9
52. ICU associated AKI is
characterized by a
d e l a y b e t w e e n
a d m i s s i o n a n d
d e v e l o p m e n t o f
acute renal injury
63. etiologies of arf
Seventy percent have concurrent oliguria
< 400 mL/day
< 0.5 mL/kg/hr in children
< 1 mL/kg/hr in infants
Complicates 5-7% of hospitalizations
64. Community acquired
49.7%
Hospital acquired
50.3%
Hou SH, Bushinsky DA, Wish JB. Am J Med 1983; 74: 243-8.
Nash K, Hafeez A, Hou S. Am J Kidney Dis. 2002; 39: 930-6.
Kaufman J, Dhakal M, Patel B, Et al. Am J Kidney Dis 1991; 17: 191-8.
65. Hou SH, Bushinsky DA, Wish JB. Am J Med 1983; 74: 243-8.
Nash K, Hafeez A, Hou S. Am J Kidney Dis. 2002; 39: 930-6.
Kaufman J, Dhakal M, Patel B, Et al. Am J Kidney Dis 1991; 17: 191-8.
84. Excreted Na
Filtered Na
FENa =
Urine Na x Urine Volume
Serum Na x UrCr x Urine Volume
Serum Cr
FENa =
Urine Na
Serum Na x UrCr
Serum Cr
FENa =
85. Excreted Na
Filtered Na
FENa =
Urine Na x Urine Volume
Serum Na x UrCr x Urine Volume
Serum Cr
FENa =
Urine Na
Serum Na x UrCr
Serum Cr
FENa =
Urine Na x Serum Cr
Serum Na x UrCr
FENa =
87. FENa the easy way
FENa is a small number 0.1% to 3%
88. FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
89. FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
90. Sr Na
FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
91. Sr Na
Sr Na
FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
92. Sr Na
Sr Cr
Sr Na
FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
93. Sr Na
Sr Cr
Sr Na
Sr Cr
FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
94. Sr Na
Ur Na
Sr Cr
Sr Na
Sr Cr
FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
95. Sr Na
Ur Na
Sr Cr
Sr Na
Sr Cr x Ur Na
FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
96. Sr Na
Ur Na
Ur Cr
Sr Cr
Sr Na
Sr Cr x Ur Na
FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
97. Sr Na
Ur Na
Ur Cr
Sr Cr
Sr Na
Sr Cr x Ur Na
x Ur Cr
FENa =
FENa the easy way
FENa is a small number 0.1% to 3%
So the calculation will be 0.001-0.03 prior to
converting to percent by X 100
So make the fraction small by putting the small
numbers over the big numbers
98. Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium
99. serum Na x GFR x minutes in a day
urinary Na excretion
Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium
100. Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium
140 x 0.1 x 1440
180
101. Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium
20160
180
102. Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium
0.8%
103. Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium
0.8%
So does ATN cause the tubules to fail to
reabsorb the 99%?
104. Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium
0.8%
So does ATN cause the tubules to fail to
reabsorb the 99%?
NO
105. false positive FeNa
Contrast nephropathy
Acute glomerulonephritis
ATN with heart failure
ATN with burns
ATN with cirrhosis
106. Contrast nephropathy
Acute glomerulonephritis
ATN with heart failure
ATN with burns
ATN with cirrhosis
Low FeNa not pre-renal
107. Contrast nephropathy
Acute glomerulonephritis
ATN with heart failure
ATN with burns
ATN with cirrhosis
Low FeNa not pre-renal
108. Contrast nephropathy
Acute glomerulonephritis
ATN with heart failure
ATN with burns
ATN with cirrhosis
Low FeNa not pre-renal
these are cases of ATN where the
tubules effectively hold on to sodium
109. Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules
that are undamaged. Tubules affected by
ischemia have a GFR of zero.
110. serum Na x GFR x minutes in a day
urinary Na excretion
Why is the feNa high in ATN
Normally tubules reabsorb 98-99% of the
filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules
that are undamaged. Tubules affected by
ischemia have a GFR of zero.
111. Why is the feNa high in ATN
140 x 0.03 x 1440
180
Normally tubules reabsorb 98-99% of the
filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules
that are undamaged. Tubules affected by
ischemia have a GFR of zero.
112. Why is the feNa high in ATN
6048
180
Normally tubules reabsorb 98-99% of the
filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules
that are undamaged. Tubules affected by
ischemia have a GFR of zero.
113. Why is the feNa high in ATN
2.9%
Normally tubules reabsorb 98-99% of the
filtered sodium but now the GFR is 30 not 100
The fena reflects the behavior of the tubules
that are undamaged. Tubules affected by
ischemia have a GFR of zero.
114. Acute renal success
GFR is normally 100
mL/min
Total plasma volume
is only 3 liters
without massive
fluid reabsorption,
30 minutes to filter
all the plasma
115. Acute renal success
GFR is normally 100
mL/min
Total plasma volume
is only 3 liters
without massive
fluid reabsorption,
30 minutes to filter
all the plasma
116. Acute renal success
GFR is normally 100
mL/min
Total plasma volume
is only 3 liters
without massive
fluid reabsorption,
30 minutes to filter
all the plasma
117. Acute renal success
GFR is normally 100
mL/min
Total plasma volume
is only 3 liters
without massive
fluid reabsorption,
30 minutes to filter
all the plasma
Tubuloglomerular feedback
118.
119. Kaplan, Kohn. American J Nephrol, 1992; 12: 49-54.
fractional excretion of urea
Based on the physiologic increase in urea
reabsorption with pre-renal azotemia
Normal FE Urea is 50-65% in well hydrated
individuals
In prerenal azotemia this falls below 35%
Not affected by diuretics
Sr Na
Sr Cr x Ur Na
x Ur Cr
FENa =
120. Kaplan, Kohn. American J Nephrol, 1992; 12: 49-54.
fractional excretion of urea
Based on the physiologic increase in urea
reabsorption with pre-renal azotemia
Normal FE Urea is 50-65% in well hydrated
individuals
In prerenal azotemia this falls below 35%
Not affected by diuretics
Sr Urea
Sr Cr x Ur Urea
x Ur Cr
FEurea =
121. Kaplan, Kohn. American J Nephrol, 1992; 12: 49-54.
fractional excretion of urea
Based on the physiologic increase in urea
reabsorption with pre-renal azotemia
Normal FE Urea is 50-65% in well hydrated
individuals
In prerenal azotemia this falls below 35%
Not affected by diuretics
Sr Urea
Sr Cr x Ur Urea
x Ur Cr
FEurea =
122.
123.
124.
125.
126.
127. Carvounis, Sabeeha, Nisar, Et al. Kidney Int, 2002 Vol 62. p 2223-2229
FEurea in the differential diagnosis
of atn
102 patients with ARF
Gold standard was consultants full analysis
and retrospective analysis of response to
treatment.
Divided the cases into:
ATN
Prerenal without diuretic
Prerenal treated with diuretics
135. Acute kidney injury
as a cause of CKD
3,679 diabetic veterans
baseline creatinine 1.1, average age 61
primary outcome: development of CKD 4
secondary outcome: all-cause mortality
1,822 hospitalized
530 developed AKI at least once
88% AKIN 1
12% AKIN 2, 3
136.
137.
138.
139. 39,805 Kaiser Permanente
Hospitalized 1996-2003
all had pre-hospitalization GFR <45
among those who developed ARF (50%
increase in Cr and dialysis)
26% died in the hospital
among survivors:
GFR 30-44 42% required permanent dialysis within a
month of discharge
GFR 15-29 63% required permanent dialysis within a
month of discharge
151. Patient empowerment
talk to patients about what to do if they
become acutely ill
increase fluid intake
decrease diuretics
monitor blood pressure
172. Ronco’s landmark dialysis dose
study
425 patients with dialysis dependent acute
renal failure were randomized to one of three
doses of CVVH
20 mL/kg/hr of effluent
35 mL/kg/hr
45 mL/kg/hr
174. Ronco
425 CVVH 20/h vs. 35-45 ml/kg/h*
Bouman
106 CVVH 20ml/kg/h* vs. 48 ml/kg/h
Schiffl
160 Alternate day vs. daily hemodialysis
Saudan
206 CVVH 25 ml/kg/h vs. CVVHDF 42 ml/kg/h
Total (fixed effects)
Total (random effects)
1 10
Odds ratio
Study
n
treatment groups
*For purposes of analysis the two high-dose arms in Ronco were combined, as were the two low-dose arms in
Bouman. If these groups are removed the odds ratio is unchanged (1.94; P <0.001).
Kellum J. Nature Clin Practice Nephrol 2007 3: 128-9.
175. Ronco
425 CVVH 20/h vs. 35-45 ml/kg/h*
Bouman
106 CVVH 20ml/kg/h* vs. 48 ml/kg/h
Schiffl
160 Alternate day vs. daily hemodialysis
Saudan
206 CVVH 25 ml/kg/h vs. CVVHDF 42 ml/kg/h
Total (fixed effects)
Total (random effects)
1 10
Odds ratio
Study
n
treatment groups
*For purposes of analysis the two high-dose arms in Ronco were combined, as were the two low-dose arms in
Bouman. If these groups are removed the odds ratio is unchanged (1.94; P <0.001).
Kellum J. Nature Clin Practice Nephrol 2007 3: 128-9.
179. endpoint
Primary Endpoint:
All-cause mortality at day 60.
Secondary endpoints:
In-hospital death
Recovery of renal function (CrCl>20)
defined as complete if Cr was <0.5 over the baseline
Duration of renal replacement therapy
Dialysis free at 60 days
Duration of ICU stay
Return to previous home at day 60
193. Patients stratified by net fluid gain from
admission to initiation of CRT
Fluid in – fluid out
ICU admit weight X 100
194. longer ICU stay
higher mortality
more multi-organ
dysfunction
more likely to be
intubated
more inotropes
more sepsis
higher PRISM score
More fluid. More sick.
195. Worse fluid overload severity remained
independently associated with mortality (OR,
1.03; 95% CI, 1.01-1.05). The relationship
was satisfactorily linear and the OR suggests a
3% increase in mortality
for each 1% increase
in degree of fluid overload
at CRRT initiation.
196. 80 kg adult
Is and Os: 2,400 mL in (100 mL/hr) and
1,600 mL of urine (67 mL/hr)
Positive balance of 800 mL. If after 3 days the
patient becomes oliguric with 200 mL of
urine output for two days (2,200 mL positive
per day) before initiating CRT.
That patient would be up 6,800 mL or 8% of
bodyweight
24% increase in mortality compared to
someone with matched ins and outs
197.
198. observational data from SOAP study of ICU
care in Europe
198 ICUs
24 countries
147 patients
1120 had AKI
ARF defined as a Cr >3.5 or urine output <
500 mL
199.
200.
201.
202. Moreover, this would suggest that
prevention or management of
fluid overload is evolving as a
primary trigger/indicator for
extra-corporeal fluid
removal, and this may be
independent of dose delivery or solute
clearance.
Critical Care 2008, 12:169
203. summary
Prognosis is grim
We have two validated, consensus definitions
R isk
I njury
F ailure
L oss of function
E srd
Outpatient and inpatient acquired ARF differ in
etiology
Hospital acquired disease is your fault
AKIN
Stage 1
Stage 2
Stage 3
204. summary
FE of Urea is a validated way to separate pre-renal
from AKI even in the presence of diuretics
Use of high dose dialysis regardless of methodology
offers no survival benefit
Do not fluid overload your patient
Dopamine doesn’t work
205. Acute kidney injury is not a
specialist’s emergency; it is seen
commonly in acute medicine
and, as such, it is essential
that all physicians have the
confidence and skills to
identify and manage it.