The document discusses acute kidney injury (AKI). It defines AKI and outlines its causes including pre-renal, intrinsic renal, and post-renal etiologies. Diagnosis involves evaluating history, examination for volume status, and investigations such as blood tests, urinalysis, and imaging. Urinalysis can provide clues to the etiology such as presence of red blood cells or casts. Ultrasound is useful for assessing kidney size and detecting obstruction. Managing the underlying cause and treating complications are important in AKI.
Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.
Acute kidney injury is common among hospitalized patients. It affects some 3–7% of patients admitted to the hospital and approximately 25–30% of patients in the intensive care unit.
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 (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 renal failure (ARF) is a common and serious problem in clinical medicine. It is characterized by an abrupt reduction (usually within a 48-h period) in kidney function.
This results in an accumulation of nitrogenous waste products and other toxins. Many patients become oliguric (low urine output) with subsequent salt and water retention. In
patients with pre-existing renal impairment, a rapid decline
in renal function is termed ‘acute on chronic renal failure’.
The nomenclature of ARF is evolving and the term acute
kidney injury (AKI) is being increasingly used in clinical
practice.
The Aloe vera plant has been known and used for centuries for its, beauty health, medicinal, skin care and other various properties. It has a vast traditional role in the indigenous system of medicine like Ayurveda, Siddha, Unani and homeopathy. Aloe barbadensis miller is the botanical name of Aloe vera. Aloe vera, commonly known as Barbados, considered as a magical plant. The arborescent, perennial, xerophytic, succulent plant mainly grows in subtropical areas. Aloe vera is considered to be a storehouse of phytochemicals. The plant leaves contain lots of chemical constituents such as anthraquinones, carbohydrates, vitamins, steroids, mineral, other inorganic and organics substances. Bioactive compounds from Aloe vera are very effective in various treatments, such as burns, allergic reactions, rheumatoid arthritis, rheumatic fever, acid indigestion, ulcers, skin diseases, diabetes, dysentery, diarrhoea, piles and inflammatory conditions of the digestive system and other internal organs, including the stomach, small intestine, liver, kidney, and pancreas. The active ingredients from Aloe vera have been shown to have analgesic, anti-inflammatory, antioxidant and anticancer agent. The plant also contains a lot of enzymes that regulate different types of reaction in our body. The cosmetics value of the plant is high from other plants.
Acute Kidney Injury epidemiology, pathophysiology and management based on current evidence. The presentation is suitable for internal medicine trainees and nephrology fellows.
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.
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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
Study Resources:
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
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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
7. Renal function
• Kidney has many roles:
- Excretory function
- Osmolality regulation
- Acid base balance
- BP regulation through
Salt and water balance
- Hormone secretion ( Erythropoietin, Vit D3)
8. Definition of Acute Kidney Injury
AKI has variably been defined as an abrupt
deterioration in parenchymal renal function, which is
usually but not invariably, reversible over a period of
days or weeks.
Oliguria is usually but not invariably, a feature of AKI.
Urine volume can be variable :
Anuria < 50 ml/day
Oliguria 100 – 400 ml/day
Non-oliguria > 400 ml/day
9. Definition of Acute Kidney Injury
Acute usually reversible decline in renal function*
• Rapid time course( < 48 hrs)
• Reduction of kidney function:
A) Rise in serum creatinine, defined by either:
1. absolute increase in serum creatinine of >0.3mg/dl
( >26µmol/l)
2. % increase in serum creatinine of > 50%
B) Reduction in urine output, defined as < 0.5ml/kg/hr for
more than 6 hrs
• The diagnostic criteria should only be applied after volume status has been optimized.
• Urinary tract obstruction needs to be excluded if oliguria is used as the sole criterion.
• Only one criterion (creatinine or urine output) has to be fulfilled to qualify for a stage.
11. AKI is staged for severity according to the
following criteria
12. Comparison of RIFLE and AKIN criteria for
diagnosis and classification of AKI
13. Acute kidney disease(AKD)
• Strict adherence to definitions of both AKI and
CKD may miss individuals with functional or
structural abnormalities present for < 3 months
but may benefit from active intervention to
restore kidney function.
• For this reason KDIGO have proposed the term
AKD to include not only those with AKI ,but also
those with GFR<60ml/min/1.73m2 for < 3
months or a decrease by ≥ 35% or an increase in
s.cr by>50% for <3 months.
14. Incidence of AKI
• Approximately 7% of all hospitalized patient ( 65% of
intensive care admission)
• 20% of acutely ill patient developed AKI
• Incidence of AKI needing dialysis 200/pm/year
• Pre renal and acute tubular necrosis (ATN) accounts for
75% of the cases of AKI
Mortality:
• 5-10% in uncomplicated AKI
• 50-70% in AKI secondary to other organ failure,infections
• > 50% in dialysis requiring AKI
22. Etiology and Pathophysiology
• Hypovolemia leads to glomerular hypoperfusion, but
filtration rate are preserved during mild
hypoperfusion through several compensatory
mechanisms.
• During states of more severe hypoperfusion, these
compensatory responses are overwhelmed and GFR
falls, leading to prerenal AKI.
24. Etiology and Pathophysiology
II. Low cardiac output
• Diseases of - myocardium, valves, and
pericardium; arrhythmias; tamponade
• Other: pulmonary hypertension, massive
pulmonary embolus
III. Altered renal systemic vascular resistance
ratio
• Systemic vasodilatation: sepsis, anaphylaxis IV.
Renal hypoperfusion with impairment of renal
autoregulatory responses
25. Etiology and Pathophysiology
IV. NSAIDS- they reduce affarent renal
vasodilation
V. ACEIs and ARBs- limit renal efferent vasoconstriction
Prerenal AKI can complicate any disease that
induces :
hypovolemia,
low cardiac output,
systemic vasodilatation, or
selective renal vasoconstriction.
28. Diagnosing pre-renal AKI
• Is the patient volume depleted?
• Is cardiac function good?
• Is the patient septic?
29. Diagnosing pre-renal AKI
• Is the patient volume depleted?
• Is cardiac function good?
• Is the patient septic?
History
Examination
Investigation
30. Diagnosing pre renal AKI
• History
• Examination :
1. Signs of Hypovolaemia:
a) Low BP( and reduced pulse pressure)
b) Postural BP drop ( a fall in systolic BP > 10mmHg)
c) Sinus tachycardia and postural increase in heart
rate ( increase in HR > 15 beat/min).
d) Low JVP even when the patient is supine
e) Cool peripheries and vasoconstriction
f) Poor urine output
31. Diagnosing pre-renal AKI
2. Sings of hypervolaemia( high extracellular fluid):
a) Increased circulating volume:
- High BP
- Elevation of the JVP
b) Increased interstitial fluid:
- Peripheral or generalized oedema
- Pulmonary oedema (tachypnoea, tachycardia,
third heart sound)
- Pleural effusion
- Ascites
32. Diagnosing Intrinsic Renal AKI
• Has pre-renal and post renal been excluded?
• History
- Drug, Rash, joints, nose bleed, haemoptysis, hearing loss, claudication,
IHD, diabetes, fever or night sweat, Recent infection
• Examination
- Oedema, rash, mouth ulcer, hearing loss, uveitis, ischaemic toe, bruits,
evidence of scleroderma, prosthetic valve or stigmata of Endocarditis
• Laboratory investigations
- Urine including microscopy for dysmorphic RBC, Protein, Bence Jones
protein, protein/creatinine ratio or 24hr protein excretion
- Blood – nephritic screen – ANA, dsDNA, ANCA, antiGBM,
Immunoglobulines
protein electrophoresis, Rh-factor, HBV, HCV, HIV, cryoglobulins, blood
film, CK,
C3,C4, ASO-titre , ESR and CRP
• US kidneys
. Renal biopsy
33. Diagnosing post renal AKI
• History
- pain, anuria, haematuria, prostatism
• Examination
- palpable bladder, central abdo mass, PR, PV
• Observation
• Laboratory investigations
- Urine
- Blood
- Imaging – US, CT
34. Pathophysiology of postrenal AKI
• It involves hemodynamic alterations triggered
by an abrupt increase in intratubular pressures
• An initial period of hyperemia from afferent
arteriolar dilation is followed by intrarenal
vasoconstriction from the generation of
angiotensin II, thromboxane A2, and
vasopressin, and a reduction in NO production.
35. Nature of Obstruction
• Outside
- Tumours, prostate, retroperitoneal fibrosis, cervical Ca
• Within wall
- Tumours, strictures
• Within lumen
- Stones, tumours
36. Investigations:
FBC : Hb% ↓- Haemolysis, GI bleeding
↑/ ↓ WCC: infection
↓platelets and altered coagulation : DIC, thrombotic
microangiopathy
Pancytopenia : marrow infiltration, others malignancy
PBF : fragmented RBC : send LDH,haptoglobulin,reticulocyte
count
Biochemistry :
U & E: raised s.ur,Cr ratio indicate pre-renal AKI
↑ K: needed urgent management
Na :usually normal, ↓ in case of volume overload and diuretics
↓HCO3 : metabolic acidosis
37. Investigations :
• LFT : ↓ albumin- imply proteinuria and GN
↑ billirubin : hepatorenal syndrome,
• Calcium and phosphates :
↑ Ca ++: myeloma, sarcoidosis, malignancy
• CRP : for infection/ inflammation,
(procalcitonin if available)
• Ck: rhabdomyolysis,
• Urate : tumour lysis/ pre-eclampsia
• Lactate : to asses underperfusion and tissue ischemia
Minimum AKI panel:
Urine dipstick, FBC, U&E, Ca, PO4, Albumin, LFT, CK,
CRP, ABG/ venous HCO3
40. • Dipstick test: trace or no proteinuria with pre-renal
and post-renal AKI;
• mild to moderate proteinuria with ATN and moderate
to severe proteinuria with glomerular diseases.
• RBCs and RBC casts in glomerular diseases
• Crystals, RBCs and WBCs in post-renal ARF.
41.
42. 3. Radiography/imaging
• Ultrasonography: helps to see the presence of two
kidneys, for evaluating kidney size and shape, and
for detecting hydronephrosis or hydroureter.
• It also helps to see renal calculi, and renal vein
thrombosis.
• Retrograde pyelography: is done when
obstructive uropathy is suspected
44. Cystatin-C
• Superior to serum creatinine, as a surrogate
marker of early and subtle changes of
kidney function.
• It identifies kidney injury while creatinine
levels remain in the normal range.
• Allows detection of AKI, 24-48 hours earlier
than serum creatinine
45. Kidney Injury Molecule-1 (KIM-1)
• KIM-1 is a type 1 trans-membrane
glycoprotein
• Served as a marker of severity of AKI
• Can be used to predict adverse outcomes in
hospitalized patients better than conventionally
used severity markers.
46. Neutrophil gelatinase-associated
lipocalin(NGAL)
• NGAL is highly upregulated after
inflammation and kidney injury and can be
detected in the plasma and urine within 2 hours
of cardiopulmonary bypass–associated AKI.
• Considered equivalent to troponin in acute
coronary syndrome.
47. Diuretic
• Renoprotective : Potentially lessening ischemic injury.
• Can also be harmful, by worsening established AKI.
• No evidence of incidence reduction.
• KDIGO recommend not using diuretics to prevent AKI.
(1B)
• KDIGO suggest not using diuretics to treat AKI, except in
the management of volume overload. (2C)
• Indicated only for management of fluid balance,
hyperkalemia, and hypercalcemia.
48. Clinical Approach to patient with AKI
Step Item Evaluation process & Response
1 Evaluate volume status Physical Exam, weight, CVP, PCWP.
Fluid challenge.
49. Clinical Approach to patient with AKI
Step Item Evaluation process & Response
1 Evaluate volume status Physical Exam, weight, CVP, PCWP.
Fluid challenge.
2 Rule out Obstruction Physical Exam, patency of catheters, Renal
ultrasound.
Foley catheterization.
50. Clinical Approach to patient with AKI
Step Item Evaluation process & Response
1 Evaluate volume status Physical Exam, weight, CVP, PCWP.
Fluid challenge.
2 Rule out Obstruction Physical Exam, patency of catheters, Renal
ultrasound.
Foley catheterization.
3 Renal function tests BUN, creatinine & electrolytes.
Hemoglobin, calcium & phosphorus.
51. Clinical Approach to patient with AKI
Step Item Evaluation process & Response
1 Evaluate volume status Physical Exam, weight, CVP, PCWP.
Fluid challenge.
2 Rule out Obstruction Physical Exam, patency of catheters, Renal
ultrasound.
Foley catheterization.
3 Renal function tests BUN, creatinine & electrolytes.
Hemoglobin, calcium & phosphorus.
4 Probable cause for renal
dysfunction
Evaluate nephrotoxic (drug) exposure –
NSAIDs, aminoglycosides, hypotension,
etc.
52. Clinical Approach to patient with AKI
Step Item Evaluation process & Response
1 Evaluate volume status Physical Exam, weight, CVP, PCWP.
Fluid challenge.
2 Rule out Obstruction Physical Exam, patency of catheters, Renal
ultrasound.
Foley catheterization.
3 Renal function tests BUN, creatinine & electrolytes.
Hemoglobin, calcium & phosphorus.
4 Probable cause for renal
dysfunction
Evaluate nephrotoxic (drug) exposure –
NSAIDs, aminoglycosides, hypotension,
etc.
5 Urine Routine &
Microscopy
Specific gravity, protein, glucose, blood,
casts – granular &/or cellular, cells &
crystals.
53. Clinical Approach to patient with AKI
Step Item Evaluation process & Response
1 Evaluate volume status Physical Exam, weight, CVP, PCWP.
Fluid challenge.
2 Rule out Obstruction Physical Exam, patency of catheters, Renal
ultrasound.
Foley catheterization.
3 Renal function tests BUN, creatinine & electrolytes.
Hemoglobin, calcium & phosphorus.
4 Probable cause for renal
dysfunction
Evaluate nephrotoxic (drug) exposure –
NSAIDs, aminoglycosides, hypotension,
etc.
5 Urine Routine &
Microscopy
Specific gravity, protein, glucose, blood,
casts – granular &/or cellular, cells &
crystals.
6 Urinary Indices
Fractional Excreation of
sodium (FeNa)
Obtain spot urine sodium & creatinine.
60. General Issues
1. Optimization of systemic and renal
hemodynamic through volume resuscitation and
judicious use of vasopressors
2. Elimination of nephrotoxic agents (e.g., ACE
inhibitors, ARBs, NSAIDs, aminoglycosides) if
possible
3. Initiation of renal replacement therapy when
indicated
61.
62. Dietary measure
• Adequate nutritional support should be ensured
• High protein intake should be avoided
• Enteral/ parenteral nutrition may be required.
• providing nutrition preferentially via
the enteral route in patients with AKI
63. Nutritional and glycaemic control
• Insulin therapy targeting plasma glucose 110–149
mg/dl
• Total energy intake of 20–30 kcal/kg/d in patients
with any stage of AKI. We suggest administering
• 0.8–1.0 g/kg/d of protein in noncatabolic AKI
patients without need fordialysis (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 hypercatabolic patients. (2D)
64. FLUIDS
• KDIGO suggest using isotonic crystalloids in absence of
haemorrhagic shock rather than colloids (albumin or
starches) .
• Colloids may be chosen in some patients to avoid excessive
fluid administration in patients requiring large volume
resuscitation, or in specific patient subsets (e.g., a cirrhotic
patient with spontaneous peritonitis, or in burns).
• Colloids- Albumin is renoprotective and
Hyperoncotic starch shows nephro- toxicity.
65. Vasopressors
• The Work Group emphasized that vasoactive
agents should not be withheld from patients with
vasomotor shock over concern for kidney
perfusion.
• Indeed, appropriate use of vasoactive agents can
improve kidney perfusion in volume-resuscitated
patients with vasomotor shock.
• The use of dopamine was associated with a greater
number of adverse events than Nor-epinephrine.
66. Low Dose Dopamine
• Its use has been abandoned by most subsequent
to negative results of various studies .
• KDIGO recommends not using low-dose
dopamine to prevent or treat AKI. (1A)
67. Cirrhosis and Hepatorenal Syndrome
• Albumin may prevent AKI in those treated with
antibiotics for spontaneous bacterial peritonitis.
• Bridge therapies that have shown promise include
terlipressin (a vasopressin analog), combination therapy
with octreotide (a somatostatin analog) and midodrine
(an α 1-adrenergic agonist), and norepinephrine, all in
combination with intravenous albumin (25–50 mg per
day, maximum 100 g/d).
69. Diuretic
• Reno protective : Potentially lessening ischemic injury.
• Can also be harmful, by worsening established AKI.
• No evidence of incidence reduction.
• KDIGO recommend not using diuretics to prevent AKI. (1B)
• KDIGO suggest not using diuretics to treat AKI, except in the
management of volume overload. (2C)
• Indicated only for management of fluid balance,
hyperkalemia, and hypercalcemia.
70. FENOLDOPAM
• Fenoldopam mesylate is a pure dopamine type-1
receptor agonist Without systemic adrenergic
stimulation.
• For critically ill patients with impaired renal function,
a continuous infusion of fenoldopam 0.1mg/kg/min
improves renal function when compared to low dose
dopamine.
• KDIGO suggest not using it to treat AKI
71. Erythropoietin
• Recent animal studies suggest a potential clinical benefit of
erythropoietin in AKI.
• The renoprotective action of erythropoietin may be related to
pleomorphic properties including antiapoptotic and
antioxidative effects, stimulation of cell proliferation, and stem-
cell mobilization.
• Although one recent RCT in the prevention of human AKI
was negative, the usefulness of erythropoietin in human AKI
should be further tested in RCTs.
72. Growth factor intervention
• IGF-1 is a peptide with renal vasodilatory,
mitogenic and anabolic properties.
• KDIGO Work Group recommends against its use in
patients with AKI.
73. Rhabdomyolysis
• Aggressive volume repletion (may require 10 L of fluid per day).
• Alkaline fluids are beneficial.
• Diuretics may be used if fluid repletion is adequate and there is no
urinary output.
• Dialysis.
• Focus on calcium and phosphate status because of precipitation in
damaged tissue.
74. Glomerulonephritis or Vasculitis
• May respond to immunosuppressive agents and/or
plasmapheresis .
• Allergic interstitial nephritis due to medications
requires discontinuation of the offending agent.
• Glucocorticoids have been used, but not tested in
randomized trials.
• AKI due to scleroderma (scleroderma renal crisis)
should be treated with ACE inhibitors.
75. Aminoglycoside Induced AKI
• KDIGO suggest not using aminoglycosides for the treatment
of infections unless no suitable, less nephro - toxic, therapeutic
alternatives are available.
• Avoid in high risk patients age more than 65 years, DM,
cases of septic shock.
• KDIGO suggests using single dose daily rather than multiple-
dose daily treatment regimens.
• It also suggest using topical or local applications of
aminoglycosides (e.g., respiratory aerosols, instilled antibiotic
beads), rather than i.v. application, when feasible .
76. AMPHOTERICIN B NEPHROTOXICITY
• KDIGO suggest using lipid formulations of amphotericin
B rather than conventional formulations of amphotericin B.
• KDIGO recommend using azole antifungal agents and/or
the echinocandins rather than conventional amphotericin B,
if equal therapeutic efficacy can be assumed.
• Some studies indicate that the liposomal form of
amphotericin B is less nephrotoxic than amphotericin B
lipid complex or amphotericin B colloidal dispersion.
77. Treatment of intrinsic renal AKI
• ATN
-aim of treatment is to keep the patient alive until
spontaneous recovery
- In-hospital mortality 19-37%*
- Recovery could take up to 6 weeks**
- Self correcting (full 60%, some 30%, dialysis 5-10%)
- Very severe – permanent cortical necrosis
* Oxford handbook of Nephrology and Hypertension 2009
** Kumar and Clark/ Clinical Medicine July 2012
78. Post-renal
• Prompt relief of urinary tract obstruction by
catheterization in urethral obstruction,
correction of ureteric obstruction by ureteric
stent or percutaneous nephrostomy
• Relief of obstruction is usually followed by an
appropriate diuresis and may require continued
administration of intravenous fluids and
electrolytes for a period of time.
79. Indications for Dialysis
A – Acidosis(pH<7.25)
E – Electrolyte disturb., usually hyperkalemia
( k>6 mmol/lt despite medical treatment
I – Intoxications (lithium, ethylene glycol, etc)
O – Overload (volume overload-pulmonary oedema)
U – Uremia (urea> 180-210 mg/dl,cr> 6.78 mg/dl)
& complications(pericarditis)
S- sepsis
81. Prognosis
• Pre-renal and Post- renal better prognosis.
• Kidneys may recover even after dialysis requiring
AKI.
• 10% of cases requiring dialysis develop CKD.
• Die early even after kidney function recovers
completely.
82. Complications of AKI
• Hyperkalaemia
• Pulmonary oedema
• Acidosis
• Uremia
• Other electrolyte disturbance such as
hyperphosphataemia and hypocalcaemia
83. Who is a risk?
Many cases of AKI should never occur in the first place
1- Elderly
2- Pre-existing renal disease
3- Surgery, trauma, sepsis or myoglobinuria
4- Diabetes
5- Volume depletion( Nil By Mouth, bowel obstruction,
burn)
6- LV dysfunction
7- Nephrotoxic drugs
8- Cirrhosis (reduce arterial volume)
84. Reducing risk perioperatively
• Three principles:
1- Avoid dehydration
2- Avoid nephrotoxins
3- Review clinical status and renal function those
at risk
• Optimize volume status
1- No patient should go to theatre dehydrated
2- Review daily weight, input and output chart
3- Calculate losses especially those NBM ( use
0.9% N saline and NOT 5% Dextrose)
85. Reducing risk perioperatively
• Optimize blood sugar control in DM ( use
sliding scale
• Catheterize those with prostate disease
• Avoid surgery if possible immediately after a
contrast procedure
• Stop nephrotoxic drugs 24-48hrs
preoperatively
• Review the patient EARLY postoperatively
86. Summary
• 3 categories of AKI
• Simple clinical assessment will define which
• Be aware of life threatening complications and
emergency treatment
• Recognise those at risk
87. Resource materials
• Davidson’s Principles & Practice of Medicine
• Kumar & Clark Clinical Medicine
• Oxford textbook of Clinical Nephrology
• Oxford handbook of Nephrology and
hypertension
• Renal Association website( www.renal.org)
• KDIGO guideline (www.kidney.org)
• AKI network ( www.akinet.org)