This document outlines the objectives and content for two pathology lectures on renal glomerular syndromes including nephrotic syndrome and nephritic syndrome. The lectures will cover the clinical presentation and pathological findings of key renal diseases like minimal change disease, focal segmental glomerulosclerosis, membranous glomerulonephritis, acute post-streptococcal glomerulonephritis, lupus nephritis, IgA nephropathy, and rapidly progressive glomerulonephritis. The lectures will discuss kidney biopsy techniques and the role of light microscopy, immunofluorescence and electron microscopy in the diagnosis of renal diseases. Key pathological mechanisms like the location of immune deposits and pathogenesis of glomerular
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration.
lupus nephritis is a autoimmune disease, commonly seen in adult and child and the medical or nursing care is also very important for this type of disease condition.
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration.
Nephrotic syndrome happens when damage to your kidneys causes these organs to release too much protein into your urine.
Nephrotic syndrome isn’t itself a disease. Diseases that damage blood vessels in your kidneys cause this syndrome.
Nephrotic syndrome is characterized by the following:
A high amount of protein present in the urine (proteinuria)
high cholesterol and triglyceride levels in the blood (hyperlipidemia)
Low levels of a protein called albumin in the blood (hypoalbuminemia)
Swelling (edema), particularly in your ankles and feet, and around your eyes.
Pathology of Ectopic pregnancy, spontaneous abortion and gestational trophobl...Sufia Husain
DISORDERS OF PREGNANCY AND PLACENTA.
Pathology of ECTOPIC PREGNANCY, SPONTANEOUS ABORTION AND GESTATIONAL TROPHOBLASTIC DISEASE for medical and health care students
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
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!
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.
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.
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 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
1. April 2020
Reference: Robbins & Cotran Pathology and Rubin’s Pathology
Sufia Husain
Associate Professor
Pathology Department
College of Medicine
KSU, Riyadh
Renal Pathology
Nephrotic Syndrome
&
Nephritic Syndrome
2. Objectives for pathology lectures 5 & 6:
Rapid Progressive Glomerulonephritis, Chronic kidney Disease,
AND
Nephrotic and Nephritic Syndrome:
At the end of the activity (2 lectures) the students will be able to:
Recognize the five major renal glomerular syndromes.
Describe the main differential pathological diagnosis for each syndrome.
Perform a clinico-pathological correlation.
Describe the patterns of injury of each syndrome.
Key Outlines:
The nephrotic syndrome: (Minimal change, FSGS, membranous, diabetes).
The nephritic syndrome: (Acute post streptococcal Glomerulonephritis GN, Lupus nephritis).
Asymptomatic Hematuria: IgA Nephropathy.
Rapidly progressive GN: (Crescentic GN)
The Chronic Renal Failure.
3. Outline for lecture 5
Introduction, kidney biopsy
Location of electron dense immune deposits
Pathogenesis of glomerular disease
Common markers of renal diseases
Clinical manifestation of kidney disease
Nephrotic Syndrome
Minimal change disease
Focal segmental glomerulosclerosis
Membranous GN
Diabetes mellitus
Nephritic Syndrome
Acute post-streptococcal GN
Introduction to lupus nephritis
Hematuria
IgA Nephropathy
8. The tissue obtained is used to make slides for
1. Light microscopy (LM) to study renal histology.
2. Immunofluorescence (IF) study is to detect
the presence of immunoglobulins (IgA, IgG, IgM) and complements (C3 and C1q) in the
glomeruli (in the mesangium or in the glomerular capillary loop wall.
3. Electron microscopy (EM) (ultrastructural) study is to detect the
presence or absence of
effacement of the epithelial cell (podocytes)foot processes.
electron dense immune complex deposits
And if deposits are present then to identify the location of the deposits in the glomeruli
(mesangial/paramesangial, subepithelial, subendothelial).
Kidney biopsy
10. Deposits (depicted in black)Normal glomerular capillary loop
Common locations of electron dense immune deposits.
Note: the locations are different in different diseases.
Image from IM Bajema et al.: Revision of lupus nephritis classification. Kidney International · February 2018 DOI: 10.1016/j.kint.2017.11.023
12. Pathogenesis of glomerular injury
Glomerulonephritis (GN) is frequently caused by immunologic mechanisms both antibody-mediated
(mainly) and cell-mediated types of immunity play roles in the production of glomerular inflammation.
1. Antibody-mediated immune GN: there are 3 major mechanisms of antibody-mediated inflammation.
They are:
a) In situ immune complex formation: certain circulating antibodies react with certain antigens that
are already present in glomeruli formation deposition of these immune complexes in the
glomeruli. These deposits attract leukocytes and activate complement glomerular injury.
13. Pathogenesis of glomerular injury contd..
b) Antigen-antibody reaction take place in circulation and these preformed circulating immune
complexes are deposited in the glomeruli deposits trigger glomerular injury (by attracting
inflammatory cells and activate complements). (the antigen can be a bacteria, virus etc.)
14. Pathogenesis of glomerular injury contd..
c) Antineutrophil cytoplasmic autoantibodies (ANCAs): they cause a severe type of GN in which the
patients have circulating autoantibodies against antigens present in neutrophil cytoplasm. This
interaction leads to activation and adhesion of the neutrophils to endothelial cells lining the
capillaries especially the glomerular capillaries. The neutrophils release injurious products that
promote endothelial injury, vascular inflammation (vasculitis) and GN.
All 3 initiate of glomerular inflammatory injury by attraction and activation of leukocytes.
2. Cell mediated immune GN: sensitized T cells also cause glomerular injury.
https://unckidneycenter.org/files/2017/10/anca-vasculitis-vessel-wall.png
16. In blood
Serum creatinine and BUN
In urine analysis
Proteinuria: presence of abnormal quantities of protein in the urine
Hematuria: presence of rbcs in urine (smoky brown urine). It is a result of glomerular injury and rupture of
the glomerular capillaries with resultant bleeding into the Bowman’s/ urinary space.
Casts: these rbcs mix with proteinaceous material in the tubules and forms rbc casts (which are found in
the urine).
Common markers of renal diseases
https://unckidneycenter.org/files
18. Clinical manifestation of kidney disease
Nephritic syndrome Results from glomerular injury acute onset of hematuria (rbcs in urine), mild to
moderate proteinuria, azotemia, edema & hypertension.
Nephrotic syndrome heavy proteinuria (excretion of more than 3.5 g of protein/day in urine),
hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria.
Asymptomatic hematuria &/or
non-nephrotic proteinuria
a sign of mild glomerular abnormalities e.g. IgA nephropathy.
Rapidly progressive
glomerulonephritis
Results from severe glomerular injury loss of renal function within days or weeks
hematuria, dysmorphic rbcs, rbc casts in urine, mild to moderate proteinuria.
Acute kidney injury oliguria or anuria with recent onset of azotemia; can result from glomerular injury
(e.g. crescentic glomerulonephritis), interstitial injury, vascular injury (e.g. TMA) or
acute tubular injury/necrosis.
Chronic kidney disease any chronic renal diseases that progresses to end stage kidney requiring dialysis and
transplantation.
Urinary tract infection affect the kidney (pyelonephritis) or the bladder (cystitis) bacteriuria and pyuria
(bacteria and leukocytes in urine).
Nephrolithiasis (renal stones) renal colic, hematuria (without rbc casts).
19. DIFFUSE: majority of the glomeruli are involved
FOCAL: some of the glomeruli are involved
SEGMENTAL: only part of a glomerular tuft is involved
GLOBAL: involving the total glomerular tuft
Terminology
21. Nephrotic syndrome is a group of clinical features that include the
following:
1. Massive proteinuria: is the loss in the urine of >3.5 g of
protein/day. This is due abnormal permeability of the glomerular
capillary wall.
2. Hypoproteinemia or hypoalbuminemia: plasma albumin levels
<3g/dL (this due to the loss of protein in the urine)
3. Odema: Hypoproteinemia causes reduced plasma colloid osmotic
pressure, salt and water retention and odema.
4. Hyperlipidemia and lipiduria: hypoalbuminemia causes
compensatory increase in lipoprotein secretion by the liver
leading to hyperlipidemia. At the same time there is increased
loss of lipid in the urine, lipiduria (due to abnormal permeability
of the GBM).
Note: in the beginning there is little or no azotemia, hematuria, or
hypertension (not part of definition of nephrotic syndrome).
Nephrotic syndrome
22. PRIMARY CAUSES
Minimal change disease
Membranous GN
Focal segmental glomerulosclerosis (FSGS)
Membranoproliferative GN (can also present as nephritic syndrome)
Others
SECONDARY CAUSES
Diabetes mellitus (most common systemic causes)
Amyloidosis
Systemic lupus erythematosus (it can also present as nephritic syndrome)
Drugs (gold, penicillamine, "street heroin")
Others
NOTE: In children the most common cause of nephrotic syndrome is minimal-change disease. In adults
the most common primary glomerular diseases that causes nephrotic syndrome are membranous
glomerulopathy in Caucasians and Asians, and FSGS is the most common etiology in American blacks.
Causes of nephrotic syndrome
24. Minimal change disease (MCD) is also known as
lipoid nephrosis.
It causes nephrotic syndrome.
Pathogenesis: unknown usually idiopathic.
It is characterized by effacement of the foot
processes of the visceral epithelial cells (podocytes).
Light microscopy:
• Glomeruli look normal.
• The proximal convoluted tubular cells are heavily
laden with protein droplets and lipids.
• There is no tubular atrophy or interstitial fibrosis.
Immunofluorescence microscopy:
• Is negative for immunoglobulins and complement.
Minimal change disease /glomerulopathy
25. MCD:
Electron microscopy:
• MCD is characterized by diffuse fusion
or effacement of the epithelial cell
(podocyte) foot processes.
• This effacement is due to the retraction
of the foot processes as a result of
extensive cell swelling.
NOTE: effacement occurs in virtually all
cases of nephrotic proteinuria; it is not
specific for minimal-change
glomerulopathy.
26. MCD: clinical features, treatment and prognosis
C/F include:
Nephrotic syndrome
Treatment and prognosis:
Over 90% of children and few adults have complete remission with corticosteroid therapy.
Prognosis: good, especially in children.
Some patients become steroid dependent i.e. they relapse each time corticosteroid treatment is stopped.
Less than 5% develop chronic renal failure
28. FOCAL AND SEGMENTAL GLOMERULOSCLEROSIS
(FSGS)
LM:
Occurs in older children and adults.
Glomeruli at the corticomedullary junction are
commonly affected.
Only some of the glomeruli are involved (i.e. focal).
There is focal and segmental sclerosis of the
glomeruli (i.e. some glomeruli show sclerosis in a
segment of the glomerular tuft).
Adhesions and hyalinosis +/-
IF: Usually negative. Sometimes IgM is positive.
EM: There is patchy/focal effacement of podocyte foot
processes.
30. A frequent cause of the nephrotic syndrome in adults (commonly 30-50 years).
The proteinuria does not usually respond to corticosteroid therapy
Is an immune complex disease. The antigen-antibody immune complexes are formed either in-situ in the
glomeruli or are pre-formed in circulation and then deposited in the glomeruli.
It is characterized by deposition of electron dense immune complexes in the subepithelial area in the
glomeruli (between the podocytes and the GBM).
It is a slowly progressive disease. If not treated some cases progress to fibrosis of the kidneys
(glomerular sclerosis, atrophy of tubules and interstitial fibrosis) and end stage disease/ renal failure.
10% to 30% have a more benign course with good prognosis.
Membranous glomerulopathy/ nephropathy/ GN
31. Membranous glomerulopathy can be:
Primary/idiopathic membranous GN (80% of cases): in primary MN
there are autoantibodies against phospholipase A2 receptor 1
(PLA2R1) antigen.
Secondary membranous GN: causes include autoimmune disease
(SLE), infectious disease (hepatitis B virus infection), therapeutic
agents (penicillamine), neoplasms (lung cancer). Patient should be
investigated for secondary causes.
Membranous glomerulopathy/ nephropathy/ GN
32. Membranous glomerulopathy/ nephropathy/ GN
Light microscopy:
The capillary walls of the glomeruli are diffusely thickened (due
to the subepithelial deposits seen on EM).
The deposits are separated from each other by protrusions of
GBM matrix called spikes (bottom picture).
As the disease progresses there is glomerular sclerosis and
interstitial fibrosis.
33. Membranous GN
IF: granular positivity for immunoglobulin IgG and complement C3 along the GBM.
EM: the immune complex appear in capillary walls as electron-dense deposits in the
subepithelial space. There is diffuse effacement of epithelial cell foot processes also.
35. DIABETIC NEPHROPATHY (DM)
Long standing poorly controlled DM leads to kidney disease. Is a
common cause of secondary nephrotic syndrome.
LM: shows 2 types of lesions:
1. Diffuse glomerulosclerosis: all the glomeruli show increase in
mesangial matrix ending in sclerosis (top photo).
2. Nodular glomerulosclerosis (Kimmelstiel Wilson nodules): there
are nodules in the mesangium. These nodules are spherical and
eosinophilic, with a central acellular area. It is pathogonomic of
diabetic nephropathy (bottom photo).
Both show diffuse thickening of the glomerular basement membrane
If not treated can progress to end staged kidney/ renal failure.
IF: negative.
EM: there is diffuse increase in the thickness of the glomerular
basement membrane.
37. Nephritic syndrome is a clinical complex characterized by acute onset of:
Hematuria (smoky brown urine). The hematuria is a result of glomerular injury and inflammatory
rupture of the glomerular capillaries with resultant bleeding into the Bowman’s space. The rbcs pass
into the tubules and mix with proteinaceous material in the tubules and forms rbc casts (which are
passed in the urine). The hemodynamic changes caused by the rupture lead to a reduction in the
glomerular filteration rate (GFR).
Oliguria: is a result of the reduced GFR.
Azotemia: increased blood urea nitrogen and creatinine. It is also a result of reduced GRF.
Hypertension: it is a result of the fluid retention and renin release from the ischemic kidneys.
NOTE: There may be mild proteinuria and edema.
The example of nephritic syndrome include:
Post-infectious glomerulonephritis: it is the most classical example.
Lupus nephritis: can also present as nephrotic syndrome
Nephritic syndrome
39. Post-infectious glomerulonephritis (PIGN)
It is a type of acute diffuse proliferative GN.
It is caused by deposition of immune complexes in glomeruli.
The most common cause of post-infectious glomerulonephritis is infection with
group A, beta-hemolytic streptococci and is therefore also called post-
streptococcal glomerulonephritis . Other infections include pneumococcal and
staphylococcal infections and viral diseases (mumps, measles, chickenpox etc.).
Usually there is a latent period between the exposure and the occurrence of
glomerulonephritis
Classically PIGN develops in children 1 to 4 weeks after streptococcal infection of
the pharynx (pharyngitis) or tonsils (tonsillitis) or the skin (impetigo or infected
insect bite).
This disease was more common in the past (because now we have antibiotics), but
it is still one of the common childhood renal diseases.
40. Post-infectious GN: pathogenesis
The immune complexes are deposited in the glomeruli in the subepithelial area and are composed of IgG
and C3. The deposits initiate inflammation by
activating complements: this way the complements get used up leading to development of
hypocomplementemia (serum C3 levels are low during the acute phase of disease).
And activating various other inflammatory mediators
All these inflammatory mediators:
attracts and activate neutrophils and monocytes
stimulates proliferation of mesangial and endothelial cell proliferation.
These effects result in marked glomerular hypercellularity resulting in diffuse proliferative
glomerulonephritis.
41. Post-infectious GN: Light microscopy
There is diffuse enlargement and hypercellularity of glomeruli due to proliferation of
endothelial cells and mesangial cells and infiltration of neutrophils and monocytes.
Crescents maybe present.
Glomerular necrosis maybe present.
All histologic changes resolve completely in most patients after several months
42. https://www.stepwards.com/wp-
content/uploads/2016/01/j6npaxvA2gcDQTLLEm7mdQ_m.png
IF: coarse granular (lumpy bumpy) IgG and C3 are positive along the capillary walls.
EM: characteristic subepithelial electron dense immune deposits. They look like dome
shaped humps (called subepithelial humps). The deposits clear up and disappear in a few
months.
Post-infectious GN
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43. Post-infectious GN: clinical features
The onset of kidney disease is sudden.
Present as nephritic syndrome (oliguria, hematuria, hypertension and azotemia).
Serum C3 levels are low during the acute phase.
Diagnosis depends on serologic evidence of a rise in antibody titers to
streptococcal products e.g. ASO titre is positive.
This disease resolves in over 90% of patients. Rarely patients (usually adults)
develop progressive renal failure.
Grossly there is multiple punctate hemorrhagic spots on the kidney surface.
45. LUPUS NEPHROPATHY/ NEPHRITIS (LN)
Patients with the autoimmune disease called systemic lupus erythematosus (SLE) tend
to have renal involvement and it is known as lupus nephritis (LN).
It can present as nephrotic or nephritic syndrome.
LN is an immune complex mediated disease in which there is the deposition of antigen
antibody complexes in the glomeruli. The deposits trigger an inflammatory response
which in turn triggers the proliferation of the epithelial, endothelial and mesangial
cells of the glomeruli. It can even lead to glomerular necrosis.
LN can be active or chronic or a combination of both.
The LN lesions have been classified into 6 classes by the International Society of
Nephrology/Renal Pathology Society (ISN/RPS). This classification helps give
information regarding the activity, chronicity and the prognosis of the disease.
47. IgA nephropathy (IgAN) is one of the most common type of primary glomerulonephritis that
presents as hematuria
IgAN is characterized by the deposition of IgA immunoglobulin in the mesangium/ paramesangium
of glomeruli.
It usually present as hematuria only and sometimes as nephritic syndrome.
When it occurs in combination with vasculitis (leukocytoclastic vasculitis) and multiorgan
involvement then is referred to as Henoch-Schonlein purpura.
Hematuria
48. IgA Nephropathy/Bergers disease
LM: is very variable (may or may not show mesangial hypercellularity,
endocapillary hypercellularity, glomerular sclerosis, tubulo-interstitial scarring).
IF: dominant IgA stain positivity in the mesangium.
EM: immune complex deposits positive in the mesangium and paramesangial area.
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