This document defines nephrotic syndrome and describes its causes, clinical features, investigations, and management. Nephrotic syndrome is characterized by proteinuria, hypoalbuminemia, edema, and hyperlipidemia. It is usually caused by damage to the glomeruli, which allows protein to leak from the blood into the urine. Primary nephrotic syndrome of unknown cause is most common in children. Complications include edema, hypertension, infection risk, and thrombosis. Investigations help determine the underlying cause, and management focuses on treating symptoms, complications, and any identified causes.
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, 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
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
This presentation focuses on main and most common oncological emergencies that are required by any stagiaire or junior doctor.
This presentation based on three books mainly, Davison’s principles and practice of medicine, pocket guide to oncological emergencies and ESMO hand book of oncological emergencies, in addition to some researches.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
This presentation focuses on main and most common oncological emergencies that are required by any stagiaire or junior doctor.
This presentation based on three books mainly, Davison’s principles and practice of medicine, pocket guide to oncological emergencies and ESMO hand book of oncological emergencies, in addition to some researches.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
- 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
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
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
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
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
2. DEFINITION
Is a clinical syndrome of massive proteinuria defined by
-oedema
-hypoalbuminemia (<25g/L)
-proteinuria (>1g/m2/day) (>40mg/m2/hour) or
early morning urine protein creatinine index of >200mg/mmol (>3.5
mg/mg)
-hypercholesterolemia
3. • The kidneys are made up of about a
million filtering units called nephrons.
Each nephron includes a filter, called
the glomerulus, and a tubule.
The glomerulus filters the blood, and
the tubule returns needed substances
to the blood and removes wastes and
extra water, which become urine.
Nephrotic syndrome usually happens
when the glomeruli are damaged,
allowing too much protein to leak from
the blood into the urine.
4. AETIOLOGY
• Primary or idiopathic (of unknown cause) nephrotic
syndrome is the commonest type of nephrotic syndrome in
children.
• Secondary causes of nephrotic syndrome include post-
streptococcal glomerulonephritis and systemic lupus
erythematosus (SLE).
5. Clinical Features
1. Marked edema
-periorbital pitting edema
2. Weight gain
3. Frothy urine
4. Hypertension
5. Hypercoagulable state with increased risk of thrombosis/embolic
event
6. Increased risk of infection
6. Causes of nephrotic syndrome
• Primary or idiopathic
(of unknown cause) nephrotic syndrome is the commonest type
• Secondary causes of nephrotic syndrome such as
• Henoch–Schönlein purpura and SLE (systemic lupus erythematosus),
• Malignancy—lymphoma, leukaemia
• Infections (e.g. malaria, hepatitis B, CMV, infective endocarditis) or
• allergens (e.g. bee sting)
• post-streptococcal glomerulonephritis
• Congenital nephrotic syndrome in the first 3 months of life. It is rare.
• The most common kind is recessively inherited and the gene frequency is particularly high in
Finns.
7. Investigations at initial presentation
-Full blood count
-Renal profile: Urea, electrolyte, creatinine
-Serum cholesterol
-Liver function tests, particularly serum albumin
-Urinalysis, urine culture
-Quantitative urinary protein excretion
(spot urine protein: creatinine ratio or 24 hour urine protein)
Other investigations would depend on the age of the patient, associated
renal impairment, hematuria, hypertension or features to suggest an
underlying secondary cause for the nephrotic syndrome.
These tests include:
-Antinuclear factor / anti-dsDNA to exclude SLE.
-Serum complement (C3, C4) levels to exclude SLE, post-infectious
glomerulonephritis.
-ASOT titres to exclude Post-streptococcal glomerulonephritis.
-Other tests as indicated.
8. COMPLICATION
• 1 Hypovolaemia
• Clinical features: Abdominal pain, cold peripheries, poor pulse volume,
hypotension, and haemoconcentration.
• Treatment: Infuse Human Albumin at 0.5 to 1.0 g/kg/dose fast. If human albumin
is not available, other volume expanders like human plasma can be used. Do not
give Frusemide.
9. • 2. Primary Peritonitis
• Clinical features: Fever, abdominal pain and tenderness in children with newly diagnosed or relapse nephrotic
syndrome.
• Investigations: Blood culture, peritoneal fluid culture (not usually done)
• Treatment: Parenteral penicillin and a third generation cephalosporin
3. Thrombosis
• Thorough investigation and adequate treatment with anticoagulation is usually needed. Please consult a
Paediatric Nephrologist.
10. Genaral managemant
• A normal protein diet with adequate calories is recommended.
• No added salt to the diet when child has oedema.
• Penicillin V 125 mg BD (1-5 years age), 250 mg BD (6-12 years), 500 mg BD (> 12
years) is recommended at diagnosis and during relapses, particularly in the
presence of gross oedema.
• Careful assessment of the haemodynamic status. Check for signs and symptoms
which may indicate
- Hypovolaemia: Abdominal pain, cold peripheries, poor capillary refill, poor pulse
volume with or without low blood pressure; OR
- Hypervolaemia: Basal lung crepitations, rhonchi, hepatomegaly, hypertension.
11. • Fluid restriction - not recommended except in chronic oedematous states.
• Diuretics (e.g. frusemide) are not necessary in steroid responsive nephrotic
syndrome but use with caution if required, as may precipitate hypovolaemia.
• Human albumin (20-25%) at 0.5 - 1.0 g/kg can be used in symptomatic grossly
oedematous states together with IV frusemide at 1-2 mg/kg to produce a diuresis.
• Caution: fluid overload and pulmonary oedema can occur with albumin infusion
especially in those with impaired renal function. Urine output and blood pressure
should be closely monitored.
12. Intinial treatment
• Once a diagnosis of idiopathic nephrotic syndrome has been established, oral Prednisolone should be started at:
- Initial Prednisolone therapy of 60 mg/m2 per day for 4 weeks
(maximum dose of 60 mg/day), followed by
-Alternate-day prednisolone of 40 mg/m2 per day for 4 weeks
(maximum dose of 40 mg/day), then taper over 4 weeks and stop.
• With this corticosteroid regime, 80% of children will achieve remission (defined as urine dipstix trace or nil for 3
consecutive days) within 28 days.
• Children with Steroid resistant nephrotic syndrome, defined by failure to achieve response to an initial 4 weeks
treatment with prednisolone at 60 mg/m²/ day, should be referred to a Paediatric Nephrologist
13. Treatment of relapses
• The majority of children with nephrotic syndrome will relapse.
• A relapse is defined by urine albumin excretion > 40 mg/m²/hour or urine dipstix of
≥ 2+ for 3 consecutive days.
• These children do not need admission unless they are grossly oedematous or have
any of the complications of nephrotic syndrome.
Treatment of Initial or Infrequent Relapse
• Induction with Prednisolone at dose of 60 mg/m2 per day (maximum dose of 60 mg/day)
until remission
• then 40mg/m2/EOD (maximum dose 40mg /day) for 4 weeks then stop.
14. Treatment of frequent relapses
• Defined as ≥ 2 relapses within 6 months of initial diagnosis or ≥ 4 relapses within
any 12 month period.
• Induction of relapse is with oral Prednisolone as follows:
1. 60 mg/m²/day ( maximum 60 mg/day ) until remission followed by
2. 40 mg/m²/EOD (maximum 40 mg) for 4 weeks only.
• Taper Prednisolone dose every 2 weeks and keep on as low an alternate day dose
as possible for 6 months. Should a child relapse while on low dose alternate day
Prednisolone, then re-induce with Prednisolone as for relapse.
15. Treatment of steroid dependent nephrotic syndrome
• Defined as ≥ 2 consecutive relapses occurring during steroid taper or
within 14 days of the cessation of steroids.
• If the child is not steroid toxic, re-induce with steroids and maintain
on as low a dose of alternate day prednisolone as possible. If the child
is steroid toxic (short stature, striae, cataracts, glaucoma, severe
cushingoid features) consider steroid-sparing agents.
16.
17. Breakthrough proteinuria/ Intercurrent infections
• Most common relapse trigger is intercurrent infection.
• In patients on weaning or maintenance alternate day prednisolone: Risk of
relapse can be reduced by temporarily increasing the dose from alternate to
every day for 3-5 days.
• Usually does not require corticosteroid induction if the child has no oedema,
remains well and the proteinuria remits with resolution of the infection.
However, if proteinuria persists, treat as a relapse.
18. • Age <12 months or >12 years.
• Persistent hypertension +/- persistent microscopic hematuria.
• Elevated creatinine despite correction of any hypovolemia.
• C3 or C4 below normal range.
• Unclear if nephrotic versus mixed nephritic-nephrotic (e.g. macroscopic
• haematuria, intravascular fluid overload with hypertension, renal
• impairment).
• Steroid resistance.
• Needing steroid sparing agents beyond oral Cyclophosphamide/Levamisole.
A Paediatric nephrology consultation is recommended if:
19. Steroid resistant nephrotic syndrome
• Refer for renal biopsy. Specific treatment will depend on the histopathology. General management of the
Nephrotic state:
Control of edema:
Restriction of dietary sodium.
Diuretics e.g. Frusemide, Spironolactone.
• ACE inhibitor e.g. Captopril or Angiotensin II receptor blocker (AIIRB). e.g. Losartan, Irbesartan, to reduce
proteinuria.
• Monitor BP and renal profile 1-2 weeks after initiation of ACE inhibitor or AIIRB.
20. • Control of hypertension: antihypertensive of choice - ACE inhibitor/AIIRB.
• Penicillin prophylaxis.
• Monitor renal function.
• Nutrition: normal dietary protein content, salt-restricted diet.
• Evaluate calcium and phosphate metabolism.
21. Acute glomerulonephritis (AGN) is an abrupt onset of one or
more features of an Acute Nephritic Syndrome:
• Oedema e.g. facial puffiness
• Microscopic /macroscopic haematuria (urine: tea-coloured
or smoky)
• Decreased urine output (oliguria)
• Hypertension
• Azotemia
Definition OF ACUTE GLOMERULONEPHRITIS
22. CAUSES OF ACUTE NEPHRITIS
• Post streptococcal AGN
• Post-infectious acute glomerulonephritis
(other than Grp A ß-Haemolytic Streptococci )
• Subacute bacterial endocarditis
• Henoch-Schoenlein purpura
• IgA nephropathy
• Hereditary nephritis
• Systemic lupus erythematosus
• Systemic vasculitidis
23. POST STREPTOCOCCAL AGN
• The commonest cause of an acute nephritic syndrome is
post-infectious AGN, mainly due to post-streptococcal
pharynx or skin infection.
• Post streptococcal AGN is commonest at 6 – 10 years age.
26. Investigation findings in Post-Streptococcal AGN
• Urinalysis and culture
Haematuria – present in all patients.
Proteinuria (trace to 2+, but may be in
the nephrotic range; usually associated
with more severe disease.)
Red blood cell casts (pathognomonic of
acute glomerulonephritis).
Other cellular casts.
Pyuria may also be present.
Bacteriological and serological evidence
of an antecedent streptococcal
infection:
Raised ASOT ( > 200 IU/ml )
Increased anti-DNAse B (if available) –
a better serological marker of
preceding streptococcal skin infection
Throat swab or skin swab
27. Renal function test
Blood urea, electrolytes
and serum creatinine
Full blood count
• Anaemia (mainly dilutional)
• Leucocytosis may be
present
Complement levels
C3 level – low at onset of
symptoms, normalises by 6 weeks
C4 is usually within normal limits in
post-streptococcal AGN
Ultrasound of the kidneys
• Not necessary if patient has clear cut
acute nephritic syndrome
28. MANAGEMENT
• Strict monitoring - fluid intake, urine output, daily weight, BP (Nephrotic chart)
• Penicillin V for 10 days to eliminate β - haemolytic streptococcal infection (give
erythromycin if penicillin is contraindicated)
• Fluid restriction to control oedema and circulatory overload during the oliguric
phase until child diureses and blood pressure is controlled
• Day 1 : up to 400 mls/m²/day. Do not administer intravenous or oral fluids
if child has pulmonary oedema.
• Day 2 : till patient diureses – 400 mls/m²/day
(as long as patient remains in circulatory overload)
• When child is in diuresis – free fluid is allowed
29. • Diuretics (e.g. Frusemide) should be given in children with pulmonary
oedema. It is also usually needed for treatment of hypertension.
• Diet – no added salt to diet. Protein restriction is unnecessary
• Look out for complications of post-streptococcal AGN:
• Hypertensive encephalopathy usually presenting with seizures
• Pulmonary oedema (acute left ventricular failure)
• Acute renal failure
30. Management of severe
complications of post-
streptococcal AGN
• HYPERTENSION
-treatment goal is
reduction of SBP and DBP
to <90th percentile and
<130/80 mmHg in
adolescents >13 years old
31. • Acute kidney injury
1. Metabolic acidosis
-treat if pH<7.2 or symptomatic
-bicarbonate deficit: 0.3xbody weight (kg)x base excess (BE)
-replace half the deficit with IV 8.4% sodium bicarbonate (1:1 dilution)
-ensure patient’s serum calcium is >1.8 mmol/L to prevent hypocalcemic seizure with
sodium bicarbonate therapy
2. Hypocalcemia
-treat if symptomatic (ca<1.8mmol/L) or if sodium bicarbonate is required for
hyperkalemia
-with IV 10% calcium gluconate 0.5mL/kg, given over 10-20 minutes
3. Hyperkalemia
-serum K>6 in neonate, >5.5 in children
-cardiac toxicity when K>7mmol/L
-ECG changes: tall tented T wave, prolonged PR interval, widened QRS complex,
flattened P wave, sine wave (QRS complex merges with peaked T wave), VF, asystole
32. Treatment of hyperkalemia
IV 10% calcium gluconate 0.5-1.0 mL/kg (1:1 dilution) over 5-15 mins
IV dextrose 0.5g/kg (2mL/kg of 25%) over 15-30 mins
IV insulin 0.1 unit/kg
IV 8.4% sodium bicarbonate 1mL/kg (1:1 dilution) over 10-30 minutes
Neb 0.5% salbutamol 2.5-5mg (0.5-1mL:3mL 0.9% saline)
Calcium polystyrene sulphonate 0.25g/kg oral or rectally 4x/day (max 10g/dose)
Neonates: per rectal 0.125-0.25g/kg 4x/day
Or
Sodium polysterene sulphonate 1g/kg oral or rectally 4x/day (max 15g/day)
33. 4. Dialysis
-fluid overload manifesting as pulmonary oedema, congestive cardiac
failure, refractory hypertension
-electrolyte/acid-base imbalances: hyperkalemia K>7, symptomatic hypo
or hypernatremia, refractory metabolic acidosis
-symptomatic uraemia
-oliguria preventing adequate nutrition
-oliguria following recent cardiac surgery
34. Reference
• Paediatric protocols for Malaysian Hospitals 4th Edition
• Tom Lissauer, Will Carroll - Illustrated Textbook of Paediatrics-Elsevier
(2018)
• www.usmle.org