Nephrotic syndrome is a kidney disorder characterized by protein in the urine, low blood protein levels, high cholesterol levels, and swelling. It is caused by damage to the glomeruli in the kidneys. The main types are minimal change disease, focal segmental glomerulosclerosis, and membranoproliferative glomerulonephritis. Nephrotic syndrome is primarily treated through dietary changes, diuretics to reduce swelling, and corticosteroids to reduce protein in the urine. The standard treatment is prednisone or prednisolone over 12 weeks, with dosage adjustments made for relapses. Complications can include infections, blood clots, and renal failure if left untreated.
Nephrotic syndrome, Characterized by heavy proteinuria>3.5g/m/day in adults,>...FarsanaM
Nephrotic syndrome, in paediatric patients(children), mainly Minimal change nephrotic syndrome (MCNS),Characterized by heavy proteinuria>3.5g/m/day in adults,>1g/m/day in children, hypoalbuminemia <2.5g/dL, oedema, hyperlipidemia 200mg/dL, Pathogenesis of MMCNS injury to the glomerular visceral epithelial cell( Podocyte) foot processes
Nephrotic syndrome made easy, it can help you a lot to learn the basics about Nephrotic Syndrome and for more information I recommend the Dr. Najeeb videos about nephrotic and nephritic syndrome.
Nephrotic syndrome, Characterized by heavy proteinuria>3.5g/m/day in adults,>...FarsanaM
Nephrotic syndrome, in paediatric patients(children), mainly Minimal change nephrotic syndrome (MCNS),Characterized by heavy proteinuria>3.5g/m/day in adults,>1g/m/day in children, hypoalbuminemia <2.5g/dL, oedema, hyperlipidemia 200mg/dL, Pathogenesis of MMCNS injury to the glomerular visceral epithelial cell( Podocyte) foot processes
Nephrotic syndrome made easy, it can help you a lot to learn the basics about Nephrotic Syndrome and for more information I recommend the Dr. Najeeb videos about nephrotic and nephritic syndrome.
This presentation was done by Dr. Julius P. Kessy,MD. An intern Doctor at Dodoma Regional Referral Hospital (DRRH) during pediatrics unit clinical meeting and supervised by Dr. Christina K. Galabawa,MD,Mmed2, Pediatrics and Child Health, University of Dodoma (UDOM) in November, 2017.
This presentation was done by Dr. Julius P. Kessy,MD. An intern Doctor at Dodoma Regional Referral Hospital (DRRH) during pediatrics unit clinical meeting and supervised by Dr. Christina K. Galabawa,MD,Mmed2, Pediatrics and Child Health, University of Dodoma (UDOM) in November, 2017.
David Snead on The use of digital pathology in the primary diagnosis of histo...Cirdan
Recent developments in digital pathology enable the rapid scanning of microscope slides at high resolution, making the digitisation of histopathology slides for routine diagnosis purposes feasible. An important initial step in the wider adoption of this technology is the establishment of validation data assessing how effective pathologists are using digital workstations in comparison to conventional light microscopes and glass slides when examining cases for primary diagnosis. I will report on the first study sufficiently powered to demonstrate a statistically valid equivalent (i.e. non-inferior) performance of digital pathology (DP) against standard glass slide (GS) microscopy. This study examined a total of 3,017 cases were included, generating 10,138 slides, which when scanned resulted in a digital archive of 2.45 terabytes. As well as demonstrating non-inferiority of digital in comparison to glass slides the study was useful in establishing rules for slide scanning and identifying areas where digital pathology has limitations and needs to be used with caution.
Finally the presentation covers the impact adopting digital pathology will have on diagnostic laboratories, the economics of these changes and where these changes are most likely to benefit patients.
Individualized Webcam facilitated and e-Classroom USMLE Step 1 Tutorials with Dr. Cray. 1 BMS Unit is 4 hr. General Principles and some Organ System require multiple units to complete in preparation for the USMLE Step 1 A HIGH YIELD FOCUS IN Biochemistry / Cell Biology, Microbiology / Immunology and the 4 P’s-Phiso, Pathophys, Path and Pharm. Webcam Facilitated USMLE Step 2 Clinical Knowledge and Clinical Skills diadactic tutorials /1 Unit is 4 hours, individualized one-on-one and group sessions, Including all Internal Medicine sub-sub-specitialities. For questions or more information.. drcray@imhotepvirtualmedsch.com
Dr. Sachin Verma is a young, diligent and dynamic physician. He did his graduation from IGMC Shimla and MD in Internal Medicine from GSVM Medical College Kanpur. Then he did his Fellowship in Intensive Care Medicine (FICM) from Apollo Hospital Delhi. He has done fellowship in infectious diseases by Infectious Disease Society of America (IDSA). He has also done FCCS course and is certified Advance Cardiac Life support (ACLS) and Basic Life Support (BLS) provider by American Heart Association. He has also done a course in Cardiology by American College of Cardiology and a course in Diabetology by International Diabetes Centre. He specializes in the management of Infections, Multiorgan Dysfunctions and Critically ill patients and has many publications and presentations in various national conferences under his belt. He is currently working in NABH Approved Ivy super-specialty Hospital Mohali as Consultant Intensivists and Physician.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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.
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
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.
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.
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.
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
2. Definition
• Manifestation of glomerular disease,
characterized by nephrotic range proteinuria
and a triad of clinical findings associated with
large urinary losses of protein :
hypoalbuminaemia , edema and
hyperlipidemia
- Nelson Textbook of Paediatrics, Vol 2, 19th Edition, page 1801
3. Why ‘nephrotic range’
• Defined as
– protein excretion of > 40 mg/m2/hr
– Spot protein : creatinine ratio of > 3 : 1
– Hypoalbuminamia <2.5g/dl
– Edema- generalised
– S cholesterol 220mg/dl
- Nelson Textbook of Paediatrics, Vol 2, 19th Edition, page 1801
4. Pathogenesis
Inherent susceptibility T CELL dysfuction
Release of lymphokines (IL 2)
Decrease in sialoprotein of glomerular basement
membrane
Loss of net negative charge of glomerulus
Increase in pore size
5. Massive proteinuria
Loss of IgG Hypoalbuminamia Loss of AT-iii
Infections
decrease in plasma oncotic pressure
Thrombotic episodes
6. hypoalbuminamia
fall in plasma oncotic pressure
hypovolumia due to fluid leak from vressels
activation of Rennin Angiotension
Aldosterone system
Retention of sodium and water
odema
8. Incidence ( paediatric ) ?
• 2 – 7 cases per 10,000 children per year
• Higher in underdeveloped countries ( South
east Asia )
• Occurs at all ages but is most prevalent in
children between the ages 1.5-6 years.
• It affects more boys than girls, 2:1 ratio
http://www.kidney.org/site/107/pdf/NephroticSyndrome.pdf
15. In children the commonest form of N.S. is
primary nephrotic syndrome
• Among these the
MCNS is the most frequent.
• Insidious onset of
• odema
• fever
• oliguria
• Many children have recurrent episodes of such transient
edema for many months.
16. • Physical examination shows
•
• Edema – The edema is initially noted around
the eyes and in the lower extremidies where it
is pitting in nature, with time edema becomes
generalized and may associate with weight gain
and the development of ascites, pleural
effusion and decreased urinal output.
• Pallor
• White nails with red bands (leukonychia)
• Normal Blood Pressure
• No evidence of Renal failure
17. NS WITH SIGNIFICANT LESIONS SUSPECTED IN
FOLLOWING CONDITIONS
Age <1y or >8y
Hypertension
Haematuria
Renal dysfuctiuon
Exta renal symptoms
Rash
Arthrlagia
Decresed c3,c4
18.
19. Complicatios of NS
A. Loss of Proteins:
Albumin Edema
Transferrin Anemia
TMG Biochemical hypothyroidism
Vit.D Binding Globulin Hypocalcemia (Along with
loss1,25diOH chole calciferol)
Immunoglobulin Infection
Coagulation factors Hypercoagulable state
20. B. Infection:
Loss of Immunoglobulin Acute
Depressed CMI Chronic
C. Hypercoagulable State:
- due to alteration in coagulation factors, associated infections,
sepsis, Hypovolemia
i) Renal Vein Thrombosis
ii) Peripheral Vein Thrombosis
iii) Cerebral Vein Thrombosis
21. D. Renal Failure:
i) Chronic renal failure
- as a part of disease process.
ii) Acute renal failure
a) Hypovolemia induced ATN
b) Septicemia leading to shock and ATN
c) Septicemia causing bacterimia and AIN
d) Other drugs causing AIN
e) Bilateral renal vein thrombosis
f) Crescentic GN on existing glomerular disease like FSGS,
MGN and MPGN.
22. E. Convulsions:
i) Hypocalcemia due to loss of Ca, 1, 25 di OH
Cholecalciferol, Vit.D, binding protein in
urine.
ii) Hypertension
iii) Renal failure – uraemic
iv) Hyponatremia
v) Cerebral Vein thrombosis
23. OTHERS
Pericardial effusion and hyrothorax
d/t fluid retention
Postural hypotension
Atherosclerosis
Loss of zn cu decrease in immunity
24. Hb %
TC
DC
Mx
Urine Examination
Urine Culture and Sensitivity
X Ray Chest
USG Abdomen
Serum Proteins
Urinary Proteins
Spot Urine Test
Serum Cholesterol
Kidney Biopsy
25. Additional Tests
• C3 and antistreptolysin O
• Chest X ray and tuberculin test
• ANA
• Hepatitis B surface antigen
Ghai Essential Paediatrics,8th edition, page 478
Indications for Biopsy
• Age below 12 months
• Gross or persistent microscopic hematuria
• Low blood C3
• Hypertension
• Impaired renal Function
• Failure of steroid therapy
26. Therefore, presence of
Proteinuria of 3+ or more
Hyline cast on microscopy
Hypercholesterolemia> 220mg/ddl
Urine spot protein creatinine ratio of >3
oliguria
Is diagnostic of NS
27. Idiopathic Lab Findings
Minimal Change Nephrotic Syndrome Raised BUN in 15 – 30 %
Highly Selective proteinuria
Focal Segmental Glomerulosclerosis Raised BUN in 20 – 40 %
Membranoproliferative
Glomerulonephritis
Type I Low C1, C4 , C3 – C9
Type II Normal C1, C4 , Low C3 – C9
- Nelson Textbook of Paediatrics, Vol 2 : page 1803, table 521-2
28. Cause Light
microscopy
Immunoflorescence Electron Microscopy
Minimal Change
Nephrotic
Syndrome
Normal Negative Foot process fusion
Focal Segmental
Glomerulosclerosis
Focal
sclerotic
lesions
IgM, C3 in lesions Foot process fusion
Membranous
Nephropathy
Thickened
GBM
Fine Granular IgG Sub epithelial deposits
Membranoprolifer
ative
Glomerulonephriti
s
Type I Thickened
GBM,
proliferation
Granular IgG, C3 Mesangial and
subendothelial deposits
Type II Lobulation C3 only Dense deposits
- Nelson Textbook of Paediatrics, Vol 2 : page 1803, table 521-2
30. Initial Episode
Ghai Essential Paediatrics,8th edition, page 476, 477
Child is admitted in hospital
Salt restriction
To decrease edema
Table salt contains 40% of Na and 60% of
chloride
So normal salt is still advised only excess
consumption of salt is stopped
31. Fluid restriction
Fluid intake is restricted to, insensible water loss
plus urine output
Insensible loss means lost through skin and
respiratory tract
Diet
Normal protien intake of 1.5-2g/kg/day is advised. .
Idli, idiyappam, rice puttu, sweet pongal, coconut
rice, curd rice, lemon rice, beet-root, chappathi,
dhall, sugar candy, boiled potato, carrot, cabbage,
tomato and onion are accepted.
32. Control of edema
It is an integral part of
supportive care. Since treatment with
corticosteroids usually leads to diuresis within
5-10 days, diuretics are avoided unless edema
is significant. Diuretics should also not be
given to patients with diarrhea,.vomiting or
hypovolemia.
33. Patients with persistent edema and weight gain of
7-10% are treated with oral frusemide (1-3 mg/kg
daily). Additional treatment with potassium sparing
diuretics is not required if frusemide is used at this
dose for less than one week. Patients requiring
higher doses and prolonged duration of treatment
with frusemide should receive potassium sparing
diuretics, e.g., spironolactone (2-4 mg/kg daily).
Blood pressure should be monitored frequently. A
gradual reduction of edema, over one week, is
preferred.
34. For patients with refractory edema, a combination
of diuretics and albumin infusion is used. Albumin
(20%) is given as an infusion at a dose of 0.5-1
g/kg over 2-4 hr, followed by administration of
frusemide (1-2 mg/kg intravenously).
While infusion of albumin results in
increased urine output, the effect is not sustained
and repeated administration might be
necessary,Albumin should be administered very
cautiously in patients with renal failure,
pneumonia or pulmonary edema due to its
potential to increase the plasma volume. Patients
receiving albumin should be observed for
respiratory distress, hypertension and congestive
heart failure
35. Examine for hypovolemia
No
Frusemide 1-3 mg/kg/day
May add spironolactone 2-4 mg/kg/day
No response` (no weight loss or diuresis in 48 h)
Double dose of frusemide until diuresis maximum
daily dose of frusemide(4-6 mg/kg/day) is reached
No response
Add hydrochlorthiazide 1-2 mg/kg/day or
metolazone 0.1-0.3 mg/kg/day
No response
Frusemide IV bolus 1-3 mg/kg/dose
infusion 0.1-1 mg/kg/h
No response
• 20% Albumin 1 g/kg IV
• followed by IV frusemide
36. drugs to control proteinuria
• The standard medication for treatment
is prednisolone or prednisone.
The use of methylprednisolone,
dexamethasone, betamethasone, triamcinolone
or hydrocortisone is not recommended.
There is also limited evidence on the efficacy
or benefits of therapy with deflazocort for
nephrotic syndrome.
37. first episode
Prednisolone is administered at a dose of 2
mg/kg/day (maximum 60 mg in single
or divided doses) for 6 weeks, followed by
1.5mg/kg(maximum 40 mg) as a single
morning dose on alternate days for the next 6
weeks; therapy is then discontinued.
Thus the duration of therapy in first episode is
12 weeks.
38. Remission
Urine albumin nil or trace (or proteinuria <4 mg/m2/h) for 3
consecutive early morning specimens.
Relapse
Urine albumin 3+ or 4+ (or proteinuria >40 mg/m2/h) for 3
consecutive early morning specimens,having been in remission
previously.
Frequent relapses
Two or more relapses in initial six months or more than three relapses
in any twelve months.
Steroid dependence
Two consecutive relapses when on alternate day steroids or within 14
days of its discontinuation.
Steroid resistance
Absence of remission despite therapy with daily prednisolone at a
dose of 2 mg/kg per day for 4 weeks
39. Treatment of Relapse
The patient should be examined for infections,
which should be treated before initiating steroid
therapy.
Appropriate therapy of an infection might rarely
result in spontaneous remission, there by
avoiding the need for treatment with
corticosteroids.
40. Prednisolone is administered at a dose of
2 mg/kg/day (single or divided doses) until urine
protein is trace or nil for three consecutive days.
Subsequently, prednisolone is given in a single
morning dose of 1.5 mg/kg on alternate days for
4 weeks, and then discontinued. The usual
duration of treatment for a relapse is thus 5-6
weeks.
41. In case the patient is not in remission despite
two weeks treatment with daily prednisolone,
the treatment is extended for 2 more weeks.
Patients showing no remission despite 4
weeks’ treatment with daily prednisolone
should be treated as steroid resistance.
Infrequent Relapsers
• Patients who have three or less relapses a year
and respond promptly to prednisolone are
managed using the aforementioned regimen
for each relapse.Such children are at a low risk
for developing steroid toxicity.
42. Frequent Relapsers and Steroid Dependence
Patients with frequent relapses or steroid
dependence should be managed in
consultation with a pediatric nephrologist.
It is usually not necessary to
perform a renal biopsy in these cases.
Following treatment of a relapse,
prednisolone is gradually tapered to maintain
the patient in remission on alternate day dose
of 0.5-0.7 mg/kg, which is administered for 9-
18 months.
43. A close monitoring of growth and blood
pressure, and evaluation for features of steroid
toxicity is essential.
If the prednisolone threshold,to maintain
remission, is higher or if features of
corticosteroid toxicity are seen, additional use
of the following immuno-modulators is
suggested.
44. • (a) Levamisole is administered at a dose of2-
2.5 mg/kg on alternate days for 12-24months.
Co-treatment with prednisolone at a dose of
1.5 mg/kg on alternate days is given for 2-4
weeks; its dose is gradually reduced by 0.15-
0.25 mg/kg every 4 weeks to a maintenance
dose of 0.25-0.5 mg/kg that is continued for
six or more months.
The chief side effect of levamisole are
leukopenia; flu-like symptoms,liver toxicity,
convulsions and skin rash . The leukocyte
count should be monitoredevery 12-16 weeks.
45. • b) Cyclophosphamide
is administered at adose of 2-2.5 mg/kg/day for
12 weeks.Prednisolone is co-administered at a
dose of1.5 mg/kg on alternate days for 4
weeks,followed by 1 mg/kg for the next 8
weeks;steroid therapy is tapered and stopped
over thenext 2-3 months. Therapy with
cyclophosphamide should be instituted
preferablyfollowing remission of proteinuria.
46. Total leukocyte counts are monitored every
2 weeks; treatment with cyclophosphamide is
temporarily discontinued if the count falls
below 4000/mm3. An increased oral fluidintake
and frequent voiding prevents the
complication of hemorrhagic cystitis;
otherside effects are alopecia, nausea and
vomiting.The risk of gonadal toxicity is limited
with a single (12 weeks) course of
cyclophosphamide. The use of more than one
course of this agent should preferably be
avoided.
47. (c) Calcineurin inhibitors: Cyclosporin (CsA) is
given at a dose of 4-5 mg/kg daily for 12-24
months. Prednisolone is co-administered at a
dose of 1.5 mg/kg on alternate days for 2-4
weeks; its dose is gradually reduced by 0.15-
0.25 mg/kg every 4 weeks to a maintenance
dose of 0.25-0.5 mg/kg that is continued for six
or more months. Occasionally, treatment
withcorticosteroids may be discontinued
48. Side effects of CsA therapy include,
hypertension, cosmetic symptoms(gum
hypertrophy, hirsutism) and
nephrotoxicity;hypercholesterolemia and
elevated transaminases may occur. Estimation
of blood levels of creatinine is required every
2-3months and a lipid profile annually. A
repeat kidney biopsy, to examine for
histologicalevidence of nephrotoxicity, should
be done iftherapy with calcineurin inhibitors is
extendedbeyond 2 years.
49. Tacrolimus is an alternative agent,
administeredat a dose of 0.1-0.2 mg/kg daily
for 12-24months.
Side effects include hyperglycemia,diarrhea
and rarely neurotoxicity (headache,seizures).
The use of tacrolimus is preferred especially in
adolescents, because of lack of
cosmetic side effects . Blood levels of creatinine
and glucose should be estimated every 2-3
months.
50. (d) Mycophenolate mofetil (MMF)is given at
dose of 800-1200 mg/m2 along with tapering
doses of prednisolone for 12-24 month.The
principal side effects include gastrointestinal
discomfort, diarrhea and leukopenia.
Leukocyte counts should be monitored every
1-2 months; treatment is withheld if count falls
below 4000/mm3.
51. Patient and parent education
Parental motivation and involvement is essential
in the long-term management of these children.
They should be provided information about
the disease, its expected course and risk of
complications. The following are emphasized
(a) Urine examination for protein at home using
dipstick, sulfosalicylic acid or boiling test. The
examination should be done every morning
during a relapse, during intercurrent infections
or if there is even mild periorbital puffiness.
52. (b) Maintain a diary showing results of urine
protein examination, medications received and
intercurrent infections.
(c) Ensure normal activity and school
attendance;the child should continue to
participate in allactivities and sports.
(d) Since infections are an important cause of
morbidity, patients should receive appropriate
immunization and other measures for
protection
53. Immunization:
Parents should be advised regarding
the need for completing the primary
immunization.Administration of some vaccines,
e.g., hepatitis B,measles-mumps-rubella or
meningococcal vaccinesmay rarely precipitate a
relapse.
Patients receiving prednisolone at a dose of 2 mg/
kg/day or greater, or total 20 mg/day or greater (for
patients weighing >10 kg) for more than 14 days are
considered immunocompromised. Such patients
should not receive live attenuated vaccines;
inactivated or killed vaccines are safe).
54. Live vaccines are administered once the child is
off immunosuppressive medications for at
least 4weeks. If there is a pressing need, these
vaccines maybe given to patients receiving
alternate day prednisolone at a dose less than
0.5 mg/kg.
All children with nephrotic syndrome should
receive immunization against pneumococcal and
chickenpox infections.
55. Complications of steroid treatment
Patients with steroid sensitive nephrotic
syndrome are at risk for certain complications,
early detection of which is necessary.
Infections
Peritonitis
Children with nephrotic syndrome are
susceptible to severe infections, which need
prompttreatment. Common infections include
peritonitis,cellulitis and pneumonia.
56. Thrombosis: Children with nephrotic syndrome
are at risk for venous and, rarely, arterial
Thrombosis. Patients with thrombotic
complications require urgent treatment.
The treatment includes correction of
dehydration and other complications, and use
of heparin (IV) or low-molecular-weight
heparin (subcutaneously) initially, followed by
oral anti-coagulants on the long-term
57. Hypertension:
This may be detected at the onset of
nephrotic syndrome or later due to steroid
toxicity.
Therapy is initiated with ACE inhibitors, calcium
channel blockers or β adrenergic antagonists,
keeping the blood pressure at less than the 90th
percentile.
58. All patients should be monitored for
cushingoid features and blood pressure; six-
monthly record of height and weight, and
yearly evaluation for cataract should be done.
Patients on prolonged (>3 months) treatment
with steroids should receivedaily supplements
of oral calcium (250-500 mgdaily) and vitamin
D (125-250 IU
59. INDICATIONS FOR REFERRAL TO A PEDIATRIC
NEPHROLOGIST
• Onset below 1-year of age;
• family history of nephroticsyndrome.
• Nephrotic syndrome with hypertension,
gross/persistent microscopic hematuria, impaired renal
function, or extrarenal features (e.g., arthritis, serositis,
rash).
• Complications: refractory edema, thrombosis, severe
infections, steroid toxicity.
• Resistance to steroid therapy.
Frequently relapsing or steroid dependent nephrotic
syndrome
60. Prognosis
85%cases NS respond to steroids.
5% cases recover spontaneously.
10%cases are steroid dependent.
In cases with significant lesions
1/3rd recover spontaneously
Another 1/3rd cases go for CRF.