Acute kidney injury (AKI) is a major public health problem associated with high mortality and morbidity. It can occur in 1-2% of hospitalized patients and up to 50-65% of patients in the ICU. AKI is defined based on changes in serum creatinine and urine output using the RIFLE, AKIN, and KDIGO criteria. The causes of AKI include sepsis, surgery, cardiogenic shock, nephrotoxins, obstruction and hepatorenal syndrome. The pathology involves tubular injury, endothelial dysfunction, inflammation and vasoconstriction. Evaluation of AKI includes assessing volume status, potential causes, urine analysis and imaging. Management involves treating the underlying cause, fluid
Acute Kidney Injury.
ARF is defined as a decrease in glomerular filtration rate (GFR), generally occurring over hours to days, sometimes over the week that is associated with an accumulation of waste products, including urea and creatinine.
Presence of proteinuria/albuminuria for at least 3 months
A decrease in urine output.
Normal urine output of ≥1,200 ml/day
Patients with ARF are often categorized as being anuric (urine output <50 ml/day), oliguric (urine output <500 ml/day), or nonoliguric (urine output >500 ml/day).
Clinicians use a combination of the serum creatinine(Scr) value with change in either Scr or urine output(UOP) as the primary criteria for diagnosing ARF.
Acute Kidney Injury.
ARF is defined as a decrease in glomerular filtration rate (GFR), generally occurring over hours to days, sometimes over the week that is associated with an accumulation of waste products, including urea and creatinine.
Presence of proteinuria/albuminuria for at least 3 months
A decrease in urine output.
Normal urine output of ≥1,200 ml/day
Patients with ARF are often categorized as being anuric (urine output <50 ml/day), oliguric (urine output <500 ml/day), or nonoliguric (urine output >500 ml/day).
Clinicians use a combination of the serum creatinine(Scr) value with change in either Scr or urine output(UOP) as the primary criteria for diagnosing ARF.
Acute Kidney Failure is a sudden reduction in kidney function that results in nitrogenous wastes accumulating in the blood.
Chronic renal failure is a Progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic, fluid and electrolyte balance fails resulting in Uremia and Azotemia.
Definition, Etiology, Risk Factors, Stages, Clinical Manifestations, Management, Surgical Management, Prevention, Complications. Nursing Management
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
Acute Kidney Failure is a sudden reduction in kidney function that results in nitrogenous wastes accumulating in the blood.
Chronic renal failure is a Progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic, fluid and electrolyte balance fails resulting in Uremia and Azotemia.
Definition, Etiology, Risk Factors, Stages, Clinical Manifestations, Management, Surgical Management, Prevention, Complications. Nursing Management
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
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
- 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
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!
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.
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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.
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
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.
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
2. OUTLINE
• Epidemiology
• Definition - RIFLE , AKIN ,KDIGO
• Causes
• Pathology and Pathophysiology
• Nephrotoxins and AKI
• Approach to AKI
• Investigative modalities
3. EPIDEMIOLOGY
• A major public health problem globally associated with high
mortality,morbidity and long term risk of CKD
• CA-AKI/HA-AKI
• Relatively younger patients in India ( 40 to 50 years)
• 1 % at the time of admission to hospital
• 2 to 5 % indidence during hospitalization
• 1% in one month of post operative period for general surgery
cases.
• 50% to 65% in ICU patients
5. RIFLE CRITERIA
• The acronym RIFLE denotes increasing severity classes Risk, Injury,
and Failure; and the two outcomes,Loss and End-stage renal
disease (ESRD).
• The three severity grades are defined on the basis of changes in
serum creatinine (SCr) or urine output where the worst of each
criterion is used, whereas the two outcome criteria, Loss and
ESRD, are defined by the duration of kidney failure.
6.
7. AKIN CLASSIFICATION
Modification of RIFLE Criteria
1. Broadening of the ‘Risk’ category of RIFLE to include an increase in absolute SCr
concentration of at least 0.3 mg/dL (26.4 μmol/L) even if this does not reach the 50%
threshold as long as it is documented to occur within a 48-hour window .
2. Categorizing patients as ‘Failure’ if they are treated with renal replacement therapy
(RRT), regardless of what their SCr or urine output is at the point of initiation of RRT .
3. GFR was discarded as a criteria
8. KDIGO
• The KDIGO criteria only utilize changes in SCr and urine output, and
not changes in GFR for staging, with the exception of children under
the age of 18 years, for whom an acute decrease in estimated GFR
to < 35 mL/min per 1.73 m2 is included in the criteria for stage 3
AKI .
9.
10. Caveats in using the serum creatinine
Reduction in creatinine production.
- Reduction in GFR canoccur in critically ill patients with unchanged
creatinine levels because of a reduction in creatinine generation
rate correlating with the degree of illness severity .
- Thus in sicker patients, increases in creatinine concentration could
be smaller and occur more slowly than in less sick patients with
the same AKI severity.
11. Risk factors for development of acute
kidney injury
AKI is most often a consequence of another severe disease. In
the large, international, multicentre BEST Kidney study in
Critically ill patients,
-Sepsis (47.5%)
-Major surgery (34.3%)
-Cardiogenic shock (26.9%)
-Hypovolaemia (25.6%)
-Drug-induced causes (19.0%)
- Hepatorenal syndrome (5.7%)
- Obstruction (2.6%)
12. Risk factors for development of acute
kidney injury
- Gene polymorphisms for a number of factors (ACE, cytokines,
hypoxia-inducible factor 1α and others)
- Older patients and men
- Multiple co-morbidities, including diabetes mellitus,
cardiovascular disease, chronic liver disease, malignancy.
18. Common morphologic findings
- Dilation of the tubules
- Flattening and desquamation of tubular epithelium
- Presence of granular and brownish-reddish casts
- Focal infiltration and oedema of the proximal tubular epithelium and the
interstitium.
- Mitotic figures in the proximal and distal epithelial cells; and occasional
tubular Necrosis
- Although glomerular abnormalities are rare, a common finding is that of
glomerular tubularization substitution of parietal epithelia of Bowman’s
capsule with proximal tubular epithelia
19. Renal blood flow and glomerular filtration rate
Proximal tubular pressure-
• Hydrostatic pressure more than doubles within the first 1–2 hours
post ischaemia, then slowly declines.
• Desquamation of tubular epithelium into the lumen
• Reason for lack of efficacy of treatments based solely on enhancing
RBF.
• Interstitial pressure – Tubulorrhexis leads to decline in proximal
tubular pressure and restoration of glomerular filtration, on the one
hand, and elevation of interstitial pressure (as discussed below), on
the other.
20.
21. Epithelial and endothelial cell injury as a basis for
tubular and hemodynamic abnormalities
Epithelial cell injury
↓
Cell stress
↓
Elevation of cytosolic calcium concentration and activation of cysteine
proteases calpains.
↓
Calpastatin, which dissociates upon elevation of cytosolic calcium,
↓
Hydrolysis of plasma membrane and cytoskeletal proteins, especially
ankyrin and α-fodrin
↓
Activation of calpain results in proteolytic cleavage and disassembly of
focal adhesions, and collapse of the membrane-anchored cytoskeleton
22. Consequences of the hydrolysis of cytoskeletal
proteins
- Epithelial desquamation
- Desquamation from the basement membrane take place in
endothelial cells and result in the appearance of detached
cells in the circulation.
- Denuded patches of basement membrane become sites of
platelet aggregation, portals for leucocyte infiltration, and
foci of vasoconstriction
23. Endothelial cell injury
• Blood flow in glomerular and peritubular capillaries becomes
stagnant, retrograde, or oscillatory (alternating forward and
retrograde).
• The pro-inflammatory phenotype of endothelial cells is
activated when subjected to oscillatory shear stress .
1)Reduced bioavailable nitric oxide (NO) .
2)Downregulation of antioxidative peroxiredoxin and induction of
mitochondrial superoxide production and NADPH oxidase.
- Lead to endothelial cell activation and dysfunction.
25. Pathophysiologic consequences of
oscillating shear stress
- Laminar fluid shear stress is a physiological stimulus for
endothelial production of autocoids, nitric oxide synthase (NOS)
activation, and generation of NO .
- Stagnation of blood flow and oscillatory pattern ofblood flow, as
mentioned above, produce opposite effects, thus predisposing to
prevailing vasoconstriction.
27. Role of Endothelin
- Ischaemic, endotoxic,and nephrotoxic (ciclosporin, contrast media,
tumour necrosis factor(TNF), thrombin, epinephrine) insults
stimulate production and release of ET-1 from the activated
endothelial cells
- The coordination of this functional coupling between ET-1 and NO
systems is lost in AKI.
- eNOS - prevention of platelet aggregation and leucocyte–
endothelial cell adhesion and transmigration, the key anti-
inflammatory effects of NO.
28. Cellular actions of endotoxins:
Pathogenesis of sepsis induced AKI
• In endotoxic shock,renal ischaemia secondary to the fall of RBF
is no longer valid .
• Predominant vasodilatation of the efferent rather than afferent
arterioles imbalance in intraglomerular vasomotor control is
probably only one step in the development of the sepsis-
induced AKI.
29. Microcirculatory changes in Sepsis
• All septic patients demonstrated acute tubular lesions, intense glomerular
and interstitial infiltration by leucocytes, and presence of tubular cell
apoptosis (3% of tubular cells).
• LPS and TNF-ALFA induce apoptotic cell death.
• Upregulation of complement and coagulation cascade.
• Breach in the endothelial barrier.
30. Cellular actions of nephrotoxins
• The severity of critical illness requires the administration of
several therapeutics, increasing the risk of a drug-related
nephrotoxicity
• The role of drugs in the development of AKI is a major
contributing factor in 19–25% of AKI
31. • NSAIDS
• The NSAIDs block cyclooxygenase (COX), the enzyme that converts
arachidonicacid into the proinflammatory and afferent vasodilatory
prostaglandin.
• Calcineurin inhibitors-
- Acute (haemodynamically mediated) or chronic (interstitial damage) renal
side effects.
- Calcineurin inhibitors induce afferent arteriolar vasoconstriction due to an
increased endothelin and thromboxane A2 production and to reduction of
vasodilatory prostaglandins and nitric oxide production.
- This will provoke a reduction of RBF and GFR.
32. Aminoglycosides
• Proximal tubular damage-Rupture of lysosomes
• Production of ROS
• Stimulate production of ET-1 , PAF , TXA2
Cisplatin
• Cell cycle dysregulation,mitochondrial toxicity
• Acute phase-reversible renal vasoconstriction
• Chronic-Tubular atrophy,TI fibrosis
• Down regulation of TRPM6 and NCC in DCT-Loss of
Magnesium and sodium
33. Vancomycin –
• Proximal tubular cells
• Mitochondrial dysfunction,superoxide production,cell
apoptosis
Amphotericin B
• In upto 80% of patients
• Increased tubular permeability-Sodium,potassium and
Magnesium wasting
• Afferent arteriolar vasoconstriction
34. Radio contrast dyes (CM)
• Iodide ion-cytotoxic-Disrupts the cell membrane
• CM generates ROS/oxidative stress/vaso constriction
• Vasa recta in renal medulla is very sensitive to CM
Acute tubulointerstitial nephritis-
Hypersensivity reaction to drugs/infections/systemic disease
35. Osmotic Nephrosis –
• IVIg,Radiocontrast media,HES
• Renal failure appears 2-4 days after the drug
administration and is usually reversible
36.
37. Post obstructive AKI –
• Intratubular precipitation of drugs and metabolites, or increased
resistance to urine flow in the lower urinary tract.
• The obstruction results in dilatation of the urinary tract above the site
of obstruction, increase of hydrostatic pressure, and a decrease of
GFR.
• Bilateral obstruction and hydronephrosis can lead to renal failure
• Intravenous high doses of aciclovir, methotrexate, sulfadiazine,
and foscarnet are some of the drugs leading to tubular precipitation
and potential obstructive nephropathy
38. • From injury to regeneration
• In clinical practice, a typical case of recovery from oliguric AKI is
seen as conversion to the diuretic phase accompanied by a
progressive increase in urine volume
• It is followed by recovery phase, characterized by a gradual
restoration of GFR, the process that may last 3–12 months and
rarely results in a complete functional Recovery
• The final result of AKI in a typical case is a variable combination of
tissue scarring and regeneration, shifted more towards scarring in
elderly individuals and towards regeneration in younger ones.
41. Clinical evaluation of the patient with AKI
This evaluation should at least address six questions:
1. Is there immediate need for therapeutic intervention because of a life
threatening complication?
2. Is the renal dysfunction acute, acute-on-chronic, or chronic?
3. Is there evidence of true hypovolaemia or reduced effective arterial
blood volume, that is, is the AKI prerenal or renal and can renal
dysfunction be corrected by improving kidney perfusion?
4. Is there a major vascular occlusion?
5. Is there evidence of renal parenchymal disease other than ATN?
6. Is the cause of AKI urinary tract obstruction, that is, ‘post-obstructive’
AKI?
42. Differentiating acute from chronic
kidney disease
• Anaemia,hyperphosphataemia,hypocalcaemia,hyperparathyroidism,
neuropathy, band keratopathy, and imaging evidence of renal
osteodystrophy or of small scarred kidneys are useful pointers to a
chronic process.
• In CKD, the kidneys will usually be small (< 10 cm longitudinally in a
person of normal stature) and echogenic; however, normal-sized
kidneys on ultrasound do not absolutely exclude CKD.
• It should be remembered that anaemia, hyperphosphataemia, and
hypocalcaemia may also complicate prolonged AKI.
43. Urine volume in the diagnosis of AKI
• Urine volume in AKI can vary from oliguria (i.e. < 500 mL/24 hours
or < 20 mL/hour) and even anuria (i.e. < 100 mL/24 hours) to
polyuria.
• Achieve euvolemia
• Monitor hourly urine output to assess the initial response to fluid
resuscitation
• Incresed urine flow should not be regarded as primary treatment
goal.
• Oliguric vs Non oliguric AKI
44. • Anuria - RPGN,Acute cortical necrosis,Total arterial/venous
obstruction,complete urinary tract obstruction.
• Prerenal forms of AKI nearly always present with oliguria.
45. Physical examination in the differential
diagnosisof intrinsic AKI
• Blood pressure – Hypotension/Relative hypotension / Higher
than normal BP
• Skin examination-Vasculitis/Hypersensitivity/Athero emboli
• Neck - JVP
• CVS
• Pharyngeal examination
• Abdominal examination
46. Abdominal hypertension
• IAH- 12mmhg
• ACS- 20mmhg with new organ dysfunction / failure
• Primary vs Secondary ACS
• Assessment of the patient’s volume status/the effect
of a fluid challenge
• The general and renal response to a fluid challenge is often an
important diagnostic test in differentiating ‘transient’ AKI
from ‘established’ AKI, mostly ATN.
47. • When performing a fluid challenge, four items must be
defined in advance, which can be summarized by the
acronym, TROL:
1. Type of fluid (e.g. Ringer’s lactate or isotonic saline)
2. Rate of infusion (e.g. 500 mL in 30 min)
3. Objective (e.g. increase in arterial pressure to 75 mmHg or
urine output > 20 mL in 30 min)
4. Limits (e.g. a maximal increase in CVP of 3 mmHg from a
baseline of 12 mmHg).
48.
49. EXCEPTIONS
• High FENa despite the presence of prerenal AKI occurs during
diuretic treatment, including mannitol,glycosuria,excretion of
alkaline urine.
• ATN in the setting of rhabdomyolysis and myoglobinuria,
haemolysis, cirrhosis, heart failure, sepsis , obstruction, acute
glomerulonephritis and radiocontrast nephropathy may be
associated with a low UNa (e.g. < 10 mmol/L) and FENa of
< 1 % .
• A urinary osmolality value > 500mOsm/kg indicates thus an
intact tubular function and is to be expected in prerenal AKI.
50. Urine dipstick
• The presence of > 1–2 g/day of urine protein suggests a glomerular
cause of AKI but in many cases of ATN significant proteinuria may
be present, due to disturbances of tubular albumin reabsorption.
The urine sediment
• Gross or microscopic haematuria, particularly with dysmorphic red
cells or red cell casts in the urinary sediment, suggests a glomerular
disease.
• Macroscopic Haematuria -vascular, interstitial, or other structural
renal cause of AKI (e.g. stone, tumour, infection, or trauma) and is
rarely seen with ATN.
• Eosinophiluria (> 1% of urine WBCs) - Allergic interstitial nephritis,
cholesterol embolism,or in some forms of glomerulonephritis.
51. The furosemide stress test
• 2-hour urine output after a standardized high-dose FST (1
mg/kg of furosemide in naïve patients or 1.5 mg/kg in those
with prior exposure to furosemide) in clinically euvolaemic
patients with early AKI has the predictive capacity to identify
those with severe and progressive AKI .
• The ideal cut-off for predicting progressive AKI during these first 2
hours was a urine volume of 200 mL (100 mL/hour) with a
sensitivity of 87.1% and a specificity of 84.1%.
53. Renal ultrasonography
• Mandatory in patients with AKI if obstructive nephropathy is
suspected - Hydronephrosis
• Other sensitive ultrasonographic findings to rule out postrenal
AKI are a post–void residual bladder urine < 50 mL and
absence of pelvicalyceal dilatation.
• Increased cortical echogenicity can be seen in nephrotoxic
ATN where as enlarged hypoechoic cortex may be more
typical of ischemic ATN.
54. Renal Doppler Ultrasonography
• RRI-Renal resistivity index
• Differentiate transient AKI from established AKI
• RRI more than 0.74.
• The RRI predicted delayed AKI with high sensitivity and specificity
(0.85 and 0.94) respectively.
55. IVU AND CT SCAN
• Intravenous urography is nowadays largely abandoned in patients
with AKI given the need for potentially nephrotoxic contrast media.
• A plain radiograph of the abdomen is a mandatory investigation .
• CT is superior in the evaluation of ureteral obstruction, since it
can delineate the level of obstruction and define retroperitoneal
inflammatory tissue (in retroperitoneal fibrosis) or a retroperitoneal
malignant mass
56. MRI
• MR angiography can be useful for detecting abnormalities in the
renal artery and vein.
• The diagnosis of acute renal cortical necrosis in particular becomes
more reliable with gadolinium-enhanced MRI. The ‘rim sign’ is
characteristic for this infrequent cause of AKI.
• Increasingly reported incidence of the syndrome of nephrogenic
systemic fibrosis
• It is not recommended to use gadolinium-containing compounds
unless unavoidable, in patients with a GFR < 30–40 mL/min.
58. Role of Renal Biopsy
• RPGN, vasculitis, and AIN.
• In patients diagnosed with AKI and normal-sized kidneys, who
do not recover kidney function after 3–4 weeks, a kidney biopsy
may be indicated to confirm the cause of AKI, to exclude other
treatable causes, and determine the prognosis.
• AKI after transplantation when it is often essential for
distinguishing between ischaemic AKI, acute rejection, and
calcineurin inhibitor toxicity.
59. SUMMARY-PATHOGENESIS
• The combination of haemodynamic and tubular dysfunction is
responsible for the pathogenesis of the syndrome of AKI.
• Haemodynamic compromise is in most cases a result of excessive
vasoconstriction and defective vasorelaxation, except for the
endotoxaemia-induced AKI.
• Tubulopathy, on the other hand, is manifested by the desquamation of
proximal tubular epithelia and obstruction of the distal nephron, leading
to the elevation of tubular hydrostatic pressure and equilibration of
glomerular filtration pressure, culminating in cessation of glomerular
filtration.
• Clinical AKI is a ‘tip of the iceberg’, whereas an asymptomatic, subclinical
response to various insults, including medications, represents an as yet
obscure and uninvestigated much larger proportion of cases.
60. SUMMARY-PATHOGENESIS
• AKI is an example example of localized and systemic inflammatory disease.
• The systemic inflammatory response, when sufficiently intense and/or
prolonged, may not only exacerbate the local disease, but can also involve
other organs (heart, lungs, liver, etc.) accounting for the increased
mortality even in cases of a mild AKI.
• This explains the old dictum that patients die not from AKI but with AKI.
• While therapies for ameliorating AKI per se are limited, an additional
potentially powerful strategy that could reap significant benefits in the
future is to tackle the intensity of the systemic inflammatory response.