This document provides an overview of kidney diseases focusing on glomerular diseases and nephrotic syndrome. It discusses the structure of the kidney and glomerulus. Glomerular diseases are often immunologically mediated involving circulating immune complexes or antibodies reacting within the glomerulus. Nephrotic syndrome is characterized by massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Primary causes include minimal change disease, membranous glomerulonephritis, and focal segmental glomerulosclerosis. Minimal change disease appears normal by light microscopy but shows diffuse foot process effacement by electron microscopy. Membranous glomerulonephritis involves subepithelial immune deposits along the glo
causes of macrocytic anemia pathopysiology, sign and symptoms and the difference between macrocytic anemia megaloblastIc anemia. causes of hypersegmented neutrophils and its association between them. investigation and medical management plus pictures illustration.
most of the glomerular diseases , either primary or secondary..touching all the aspects including light microscopy, electron microscopy and immunoflourescence.
IT INCLUDES ANATOMY, PHYSIOLOGY AND PATHOLOGY OF LIVER .
THE SOURCES ARE:-
THE MEDICAL TEXT BOOK OF ROBBIN'S PATHOLOGY
AND OTHERS
IMAGES SOURCE :- ATLAS BOOKS AND INTERNET
causes of macrocytic anemia pathopysiology, sign and symptoms and the difference between macrocytic anemia megaloblastIc anemia. causes of hypersegmented neutrophils and its association between them. investigation and medical management plus pictures illustration.
most of the glomerular diseases , either primary or secondary..touching all the aspects including light microscopy, electron microscopy and immunoflourescence.
IT INCLUDES ANATOMY, PHYSIOLOGY AND PATHOLOGY OF LIVER .
THE SOURCES ARE:-
THE MEDICAL TEXT BOOK OF ROBBIN'S PATHOLOGY
AND OTHERS
IMAGES SOURCE :- ATLAS BOOKS AND INTERNET
Aplastic anemia is one of the stem cell disorder which leads to pancytopenia in the peripheral blood and decrease production of all cell line in bone marrow. it require bone marrow transplantation to cure the patient.
Aplastic anemia is one of the stem cell disorder which leads to pancytopenia in the peripheral blood and decrease production of all cell line in bone marrow. it require bone marrow transplantation to cure the patient.
A comparison between Nephritic and Nephrotic syndrome from Professor Hossam Mowafy Internal Medicine textbook nephrology section, Please inform me if there is any error or wrong information include.
This presentation is made to teach aboudt approach to glomerulonephritis in children. Final diagnosis of this case was membranoproliferative glomerulonephritis.
Rapidly progressive glomerulonephritisajith joseph
Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of renal function,[4][5] (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months)[5] with glomerular crescent formation seen in at least 50%[5] or 75%[4] of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute renal failure[6] and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents (crescent-shaped scars)
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
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.
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. Presented By
Prof. Dr.
Nabil Tadros Mikhail
MBBS, MS Pathol., PhD Pathol.
Prof. of Pathology
Alexandria University - Egypt
Consultant & Chief Pathologist
King Fahad Central Hospital
Gizan - KSA
18.
Glomerular diseases are often
immunologically mediated
Whereas tubular and interstitium
are more likely caused by
toxic or infectious agents
19.
Damage to one component almost
always secondarily affect others.
1. Severe damage to glomeruli affect
peritubular blood flow,
2. Tubular destruction, by increasing
intraglomerular pressure may induce
glomerular atrophy.
3. All forms of chronic renal disease will
ultimately destroy all kidney components
and lead to CRF.
21. Glomerular diseases
Glomerular diseases are a major problem in
nephrology,
Chronic glomerulonephritis (GN) is one of
the most common cause of CRF in human .
25. Structure of glomerular wall
The glomerular capillary wall is the filtering
area
Consists of four basic structure:
1.
2.
3.
4.
Thin layer of fenestrated endothelial cells.
Glomerular basement membrane (GBM):
Visceral epithelium: (podocytes)
Mesangial cells and mesangial matrix:
26.
27.
28. Structure of glomerular wall
1- Thin layer of fenestrated endothelial cells.
2- Glomerular basement membrane (GBM):
It consists of
1. Collagen
2. Laminin
3. Fibronectin
4. Other proteins.
29. Structure of glomerular wall
3- Visceral epithelium: (podocytes)
It shows a characteristic foot processes
(pedicles) embedded and adherent to GBM.
These foot processes are
separated by 20-30 nm filtration slit
which are bridged by a thin diaphragm
composed of nephrin molecules.
30.
31. Structure of glomerular wall
3- Visceral epithelium: (podocytes)
Visceral epithelium is critical to maintain
glomerular barrier function.
It is the cell type that is largely responsible
for synthesis of GBM.
32. Structure of glomerular wall
4- Mesangial cells and mesangial matrix :
It serve as a support of glomerular tuft.
These cells is capable for proliferation.
The whole glomerulus is surrounded by
parietal epithelium, which lines the
bowman’s space (urinary space), the cavity
in which plasma filtrate first collect.
33.
34. 15% of glomerular filtration
through the mesangium,
85% of glomerular filtration
through the fenestrated epithelium.
35. PAS to highlight basement membranes.
The capillary loops of the glomerulus are well-defined and thin.
36. Glomerular barrier function
The major characteristic of glomerular
filtration are
1. High permeability to water and small
molecules
2. Almost impermeable to molecules of the
size of albumin (70KD).
37. Glomerular barrier function
The latter characteristic is called
glomerular barrier function,
Discriminates among protein depending on their size
(the larger, the less permeable).
Also the charge affect the permeability
(The more cationic the more permeable).
39. Glomerular diseases
Glomerular diseases may be
Primary ,where the kidney is the main or
the only organ affected.
Secondary to other disease as
1. SLE,
2. DM,
3. Amyloidosis. ,
4. Polyarteritis nodosa
5. others.
41. Amyloidosis may be
"AL" type in patients with plasma cell
dyscrasias (multiple myeloma) in which the
amyloid is associated with excess
immunoglobulin light chain production,
"AA" type or "amyloid associated" in which
the cause is often chronic inflammatory
diseases.
42. Pathogenesis of glomerular diseases
Immune mechanisms underlie most cases
of primary glomerular diseases .
It may be
1. Antibody mediated
2. Cell mediated.
44. Pathogenesis of glomerular diseases
1- Antibody mediated glomerular injury:
Two forms are recognized:
A- Injury resulting from
deposition of circulating immune complexes. (IC)
B- Injury by
antibody reacting in situ within the glomerulus
(antiglomerular basement membrane antibodies) & (the Heymann’s model)
48. A- Circulating immune complexes
The antigen may be
1. Endogenous as in SLE or
2. Exogenous as acute glomerulonephritis
follow certain
bacteria (Streptococci) or
viral (HBV).
49. A- Circulating immune complexes
Antigen antibody complexes
are formed in the circulation
and then trapped in the glomeruli,
where they produce injury
through binding of complement .
50. A- Circulating immune complexes
These IC are seen either by
Electron microscopy as
dense deposits
Immunofluorescence microscopy, as
granular deposits
52. Post-streptococcal glomerulonephritis is
immunologically mediated,
The immune deposits are distributed in the
capillary loops in
A granular, bumpy pattern because of the
focal nature of the deposition process
(granular immune deposits)
53. B- nephritis in situ
The best example is anti glomerular
basement membrane disease.
In this type antibody are directed against
fixed antigen in the GBM.
Also can react to planted non-glomerular
antigens interacting with intrinsic
component (Heymann’s model)
54. B- nephritis in situ
Some times the anti GBM antibodies cross
react with basement membrane of alveoli
resulting in simultaneous lung and kidney
disease (Good Pasture syndrome).
The antibody can be visualized along GBM
by indirect immunofluorescence microscopy,
giving a characteristic linear pattern.
55. Antibody to IgG, has a smooth, diffuse,
linear pattern that is characteristic for
glomerular basement membrane antibody
with Goodpasture's syndrome.
56. Clinical findings of good pasture
syndrome
There is picture of RPGN with haematuria
and may end in renal failure.
Haemorraghic interstitial pneumonitis with
haemoptysis, dyspnea,..
Iron ↓ anemia from recurrent hemorrahge.
57. Good Pasture Syndrome
It is an example of type II hypersensitivity
with cytotoxic antibodies
Circulating anti GBM antibodies can be
detected in serum (by EIA).
Renal biopsy:
shows a characteristic
linear immunofluorescence deposits
of IgG and C3.
58. Good Pasture Syndrome
Renal biopsy:
shows a characteristic
linear immunofluorescence deposits
of IgG and C3.
61. 2- Cell mediated immunity
There is increasing evidence that sensitized
T cells can cause glomerular injury .
These may be the case in some forms of
rapidly progressive glomerulonephritis.
62. Mediators of immune injury
Glomerular damage is reflected
physiologically by
loss of barrier function
manifested by proteinuria and
reduction of glomerular filtration rate
(GFR).
63. Mediators of immune injury
Many mechanisms are described:
Complement-leukocyte mechanism
C5-9 complement components
Cytotoxic antibodies
Monocytes and macrophage.
Platelets
64. Mediators of immune injury
1- Complement-leukocyte mechanism :
Activation of complement
Generation of chemotactic factors (C5a)
Attract neutrophils
1. Produce Proteases which degrade GBM,
2. O2 free radicals which cause tissue damage
3. Arachidonic acid metabolites (as TXA2) and
which lead to reduction of GFR.
65. Mediators of immune injury
Endothelin & other vasoconstrictors also
contribute to reduction of GFR.
In addition GFR is also ↓ as a result of
obstruction of glomerular lumen by
1. infiltrating inflammatory cells and
2. proliferating mesangial cells.
66. Mediators of immune injury
2- C5-9 complement component:
This component causes epithelial damage.
It also up regulates the transforming growth
factor receptors on epithelial cells , and
lead to excessive synthesis of extra cellular
matrix and GBM thickening.
67. Mediators of immune injury
3- Cytotoxic antibodies:
antibodies directed against glomerular
structure and produce cytotoxicity
(even if IC is absent)
68. Mediators of immune injury
4- Monocytes and macrophage:
They secrete a number of biologically active
mediators which contribute to glomerular
damage.
5- Platelet:
It aggregates in the glomerulus and release
PG and growth factors.
69. Mediators of immune injury
Epithelial injury:
is the most important factor in glomerular
damage.
This can be induced by
1. Antibody to visceral epithelium or by
2. Toxins or others.
Such injury is reflected
1. Morphologically by loss of foot processes
2. Functionally by proteinuria.
74. Nephrotic syndrome
Nephrotic syndrome refers to clinical
condition that include five main features;
1.
2.
3.
4.
5.
Massive proteinuria (more than 3.5 gm/day)
Hypo-albuminaemia (less than 3 gm/dl)
Generalized edema
Hyper-lipidaemia (increase cholesterol & triglycerides)
Lipiduria (Lipid casts in urine ).
At the onset renal function is normal (BUN,
creatinine) but later on it is impaired.
75. Pathogenesis of Nephrotic syndrome
The initial event is damage to capillary wall
resulting in increase permeability to plasma
protein.
With long standing heavy proteinuria serum
albumin tend to become depleted and
decreased.
The drop of osmotic pressure will lead to
generalized edema .
76. Pathogenesis of Nephrotic syndrome
1.
2.
3.
4.
As fluid escape from vessels to tissues,
there is decrease of plasma volume with
compensatory secretion of aldosterone
resulting in salt and water retention and
further aggravate the edema.
Hypo-albuminaemia trigger increased
synthesis of lipids in the liver.
77. Causes of Nephrotic syndrome
Nephrotic syndrome may be
1.Primary or
2.Secondary.
78. Causes of Nephrotic syndrome
Secondary nephrotic syndrome:
Many disease can lead to Nephrotic
changes in the kidney as
1. DM,
2. SLE,
3. Amyloidosis,
4. Drugs (gold, penicillamine),
5. Infection
(malaria, syphilis, HBV, HIV, ..)
79. Causes of nephrotic syndrome
Primary nephrotic syndrome:
It is encountered in primary glomerular
diseases as :
1.
2.
3.
4.
Lipoid nephrosis (minimal change disease)
Membranous glomerulonephritis
Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis
82. Minimal change disease
This disease is also called lipoid nephrosis.
It is the most frequent cause of nephrotic
syndrome in children.
It is characterized by normal appearance of
glomeruli under light microscope,
but it show loss of visceral foot processes
when viewed under electron microscope.
83. Lipoid nephrosis
Pathogenesis:
The current evidence suggest that minimal
change disease results from disorder in T
cells.
It is postulated that T cells elaborate a factor
that affect nephrin synthesis.
84. Morphology of minimal change disease
Light microscopy
With light microscopy the glomeruli appear
nearly normal.
The cells of proximal convoluted tubules
are heavily laden with lipids and this is the
basis of the name lipoid nephrosis.
85. The cells of proximal convoluted tubules are
heavily laden with lipids (lipoid nephrosis).
Slide 21.30
86. Diffuse loss of the foot processes of podocytes
The cells of proximal convoluted tubules are
heavily laden with lipids (lipoid nephrosis).
87. Morphology of minimal change disease
Electron microscopy
With electron microscopy,
The only obvious abnormality is the
uniform & diffuse loss of the foot
processes of podocytes
88. This is minimal change disease (MCD)
loss of the epithelial cell (podocyte) foot
processes .
89. Clinical course
Gradual onset of nephrotic syndrome .
It affect only children.
Renal function is preserved in most cases.
Hypertension is absent.
Protein loss is usually confined to small
molecular proteins (selective proteinuria).
90. Prognosis:
More than 90% of cases respond to
corticosteroids.
Recurrence may occur and CRF may
develop in less than 5% of cases after
about 25 years
93. Membranous glomerulonephritis
(MGN)
It is a slowly progressive disease
Affect adults between 30-50 years.
It is characterized by the presence of
subepithelial immunoglobulin containing
deposits along the GBM.
Diffuse thickening of GBM is shown under
light microscopy in well developed cases.
94. Causes of MGN
Primary
As a primary kidney involvement in
85 % of cases (idiopathic) .
It results from antibodies that react in situ
to endogenous glomerular antigen.
The glomerular damage is due to the action
of C5-9 lytic components of complement.
95. Causes of MGN
Secondary:
MGN may occur secondary to
Many known disorders as
1.
2.
3.
4.
HBV,
Syphilis
Malaria
SLE
Exposure to inorganic salts as
1. Gold
2. Mercury
Exposure to drugs as
1. Penicillamin captopril
2. Non-steroidal anti-inflammatory drugs.
96. Morphology of MGN
The basic change seen by light microscope
is diffuse thickening of GBM.
By electron microscopy ,there is
subepithelial deposits along GBM as well as
loss of foot processes.
98. Morphology of MGN
With further progression glomeruli become
sclerosed and hyalinized.
Immunoflurescence staining of patient
glomerulus show typical granular deposition
of immunoglobulin and complement along
GBM.
99. Membranous glomerulonephritis in which the capillary loops
are thickened & prominent, but the cellularity is not increased.
100. silver stain of the glomerulus highlights the proteinaceous basement membranes in
black. There are characteristic "spikes" seen with membranous glomerulonephritis
in which the black basement membrane material appears as projections around
the capillary loops.
101. By electron microscopy in membranous glomerulonephritis,
the darker electron dense immune subepithelial deposits
are seen scattered within the thickened basement membrane.
103. Clinical picture of MGN
Gradual onset of nephrotic syndrome.
It affect only adults,
In contrast to lipoid nephrosis,
proteinuria is not selective
(i.e. ↑permeability also to large size proteins as globulins)
Does not respond to corticosteroids.
104. Clinical picture of MGN
40% of patients suffer from
progressive disease terminating in
renal failure after 2 - 20 years.
It is necessary to rule out secondary
causes.
108. Focal segmental glomerulosclerosis
(FSG)
FSG is characterized
histologically by sclerosis affecting
1. Some but not all glomeruli
(focal)
2. Involving only segments of
each glomerulus (segmental).
109. Causes of FSG
Primary or idiopathic:
FSG account for about 10% of all cases of
nephrotic syndrome.
It affect both children and adult.
In children it is important to be differentiated
from minimal change disease.
110. Causes of FSG
The following aspects are found in FSG only
not found in minimal change disease;
Hypertension,
Non-selective proteinuria,
Haematuria,
Poor response to corticosteroid.
Poor prognosis ,
50% develop CRF within 10 years
111. Causes of FSG
Secondary FSG: occur in
HIV nephropathy,
IgA nephropathy ,….
112. Morphology of FSG
The disease affect only some of glomeruli
(focal) initially the juxtamedullary
glomeruli.
It affect only some tufts within the
glomerulus and sparing the others
(segmental).
The lesion exhibit
1. Increased mesangial matrix and
2. Deposition of hyaline masses and lipid droplets.
113. FSG morphology
On electron microscopy ,
1. Visceral epithelium show loss of foot processes as in
lipoid nephrosis and also
2. Greater degree of epithelial detachment
On progression
1. Glomeruli are completely sclerosed (global sclerosis)
2. With tubular atrophy.
114. This is focal segmental glomerulosclerosis (FSGS).
An area of collagenous sclerosis runs across the middle of this glomerulus.
117. Membranoproliferative glomerulonephritis (MPGN)
MPGN is manifested histologically by
1. Alterations of basement membrane & mesangium
2. Proliferation of glomerular cells.
It affect both children and adult.
It account for 10-15 % of cases of
nephrotic syndrome
118. Pathogenesis of MPGN
Two types are recognized.
Most cases of type I MPGN appear to be caused
by circulating IC.
It could be also secondary to SLE, HBV, and other
conditions .
The pathogenesis of type II MPGN is not clear .
It could result from activation of alternative
complement pathway through C3 nephritic factor.
119. Morphology of MPGN
By light microscope both types of MPGN are
similar.
The glomeruli are
1. large
2. Proliferation of mesangium,
3. Infiltrating leucocytes
4. lobular appearance.
120. Morphology of MPGN
The GBM is thickened and show double
contour appearance.
This splitting of GBM is caused by
mesangial cells inclusion between GBM
laminae.
It is not easily seen by ordinary
microscope.
EM or special stain is required.
124. Morphology of MPGN
Immunofluorescence and electron
microscopy differentiate between the two
types of MPGN;
type I MPGN is characterized by
subendothelial deposits(C3 and IgG).
Type II MPGN is characterized by
intramembranous dense deposits of C3
mainly (dense deposit disease)
126.
A mesangial cell at the lower left that is interposing its cytoplasm at the arrow into the
basement membrane, leading to splitting and reduplication of basement membrane.
This is MPGN type I. These are characteristic subendothelial immune deposits.
127. This EM demonstrates the dense deposits in the basement membrane of MPGN type II.
There are dark electron dense deposits within the basement membrane
that often coalesce to form a ribbon-like mass of deposits
128. Clinical picture of MPGN
Nephrotic syndrome
is present in 50% of cases.
40% progress to CRF.
Type II has a worse prognosis.
129. Clinical picture of MPGN
However MPGN may begin with
Acute nephritic syndrome
With haematuria & mild proteinuria
Others has a combined
nephritic- nephrotic picture.
132. Nephritic Syndrome
It is a clinical complex usually of acute onset
characterized by five criteria:
1.
2.
3.
4.
5.
Haematuria with diagnostic red cell casts.
Oliguria and impairment of kidney function.
Hypertension.
Mild proteinuria.
Mild edema (localized to face)
133. Pathogenesis
GFR is decreased due to obstruction of
glomerular lumen by
The proliferating glomerular cells
Infiltrating inflammatory cells
Due to haemodynamic changes
(vasoconstriction).
The inflammatory reactions injure the
capillary wall and produce hematuria.
134. pathogenesis
Reduced GFR is manifested clinically by oliguria.
Hypertension is the result of both
1. Fluid retention and
2. Renin release from ischemic kidney.
Acute nephritic syndrome may be produced
Secondary to other disorders as SLE or
may as a result of Primary glomerular disease.
135. Kidney Diseases Associated With
Nephritic Syndrome
1. Acute diffuse proliferative post streptococcal
glomerulonephritis The commonest type
2. Rapidly progressive glomerulonephritis
(Crescentic)
3. IgA nephropathy (Berger Disease)
4. Hereditary nephritis
5. Chronic glomerulonephritis
138. Acute diffuse proliferative post streptococcal glomerulonephritis (PGN)
It is one of the more common glomerular disease
typically caused by Immune complex.
The commonest organism is streptococci,
however it can be caused by
1. Pneumococci.
2. Staphylococci,
3. Viruses as
Measles
Mumps.
139. Acute diffuse proliferative post streptococcal glomerulonephritis (PGN)
PGN is an IC disease .
IC are deposited as granular pattern on GBM
there is also blood decrease of complement
(due to increase consumption).
140. Morphology of PGN
Light microscopy
Increased cellularity of glomerular tuft
Affect all glomeruli and hence it is termed diffuse.
This is caused mainly by three cells:
1.
2.
3.
Proliferation and swelling of endothelial cells
Proliferation of mesangial cells
Infiltration by neutrophils and macrophages
141. Morphology of PGN
In few cases there may be also crescent
inside bowman capsule.
Electron Microscopy:
Show immune complex deposits
Arranged subepithelial along GBM
(called humps)
142. Morphology of PGN
Immuno fluorescence microscopy
Characteristic granular deposits
of IgG & complement.
143. This glomerulus is hypercellular and capillary loops are poorly defined.
144.
The hypercellularity of post-streptococcal glomerulonephritis is due to
increased numbers of epithelial, endothelial, and mesangial cells as well as
neutrophils in and around the capillary loops.. (high power)
145. By electron microscopy, the electron dense immune deposits of poststreptococcal glomerulonephritis are predominantly subepithelial, as
seen here with a large subepithelial "hump" at the right of the
basement membrane (BM).
146. Clinical picture of PGN
History of previous streptococcal infection
2-3 weeks before.
Onset is sudden with fever ,and malaise.
There is picture of nephritic syndrome
1. Oliguria ,
2. Haematuria,
3. Hypertension
147. Laboratory finding of PGN
1- urine :
Smoky in color,
Many RBCs are found,
Diagnostic red cell casts
148. Laboratory finding of PGN
2- Evidence of recent streptococcal
infection:
1. Increased ASOT
2. Anti DNAse
3- Mild elevation of urea and creatinine.
4- Decreased serum complement.
149. Prognosis of PGN
Recovery occur in most children.
Few cases develop RPGN.
(Rapidly progressive glomerulonephritis)
In adult 15-50% develop ESRD
(End stage renal disease) over few years
152. 2-Rapidly progressive ,(Crescentic), glomerulonephritis (RPGN)
RPGN is characterized by
1. Rapid and progressive loss of renal function
2. Associated with severe oliguria and
3. Death from renal failure within weeks if not treated.
RPGN may be caused by many diseases,
1. Some are Restricted to the kidney
2. Others are systemic.
153. Types of RPGN
Three types are recognized:
Type I
It is due to anti GBM antibody. The typical
example is good pasture syndrome.
Diagnosis of this type is important because
the patient improve from treatment by
plasmapheresis which remove pathological
antibodies
154. Types OF RPGN
Type II
It is an immune complex mediated disorder.
It can be a complication of any IC nephritis as
post streptococcal GN,
IgA nephropathy,
henoch-schonlien purpura, and SLE.
In some cases the underlying cause is unknown.
Immunofluorescence studies reveal granular
deposition of IC
155. Types of RPGN
Type III:
It is also called pauci-immune type .
There is no anti GBM or IC by
immunofluorescence or even by EM.
Most of these patients have
Anti Neutrophil Cytoplasmic Antibodies
in serum. (ANCA)
These antibodies play a role in some vasculitis .
156. Types of RPGN
Type III:
This type may be associated with
disorders of systemic vasculitis as
1. PAN
2. wegener granulomatosis.
However in many cases this type is
1. Limited to the kidney &
2. Idiopathic.
157. Morphology of RPGN
Histological picture is characterized by the
presence of crescents in most of the
glomeruli. (Crescentic GN).
Crescents are formed by
1. Proliferation of parietal cells of the bowman capsule
2. Infiltration of mononuclear cells and
3. Deposition of fibrin within bowman space.
158. Morphology of RPGN
The crescents eventually obliterate
bowman space and compress the glomeruli.
EM may reveal subepithelial deposits in
some cases
159. Seen here within the glomeruli are crescents composed of proliferating epithelial cells.
Note in the lower left glomerulus that
the capillary loops are markedly thickened
(the so-called "wire loop" lesion of lupus nephritis.
161.
RPGN may be idiopathic or
may result from
1. SLE,
2. Post-infectious GN
(some cases of post-streptococcal GN),
3. Various types of vasculitis, and
4. Goodpasture's syndrome.
162. This immunofluorescence micrograph of a glomerulus demonstrates
positivity with antibody to fibrinogen.
With a rapidly progressive GN, the glomerular damage is so severe that fibrinogen
leaks into Bowman's space, leading to proliferation of the epithelial cells
and formation of a crescent
163. Clinical picture of RPGN
Onset is rapid with marked oliguria and
azotemia (Increase urea and creatinine).
Anuria may occur in some cases (require
dialysis).
Prognosis is not good, renal failure occur
within weeks if proper treatment in not done
rapidly.
166. IgA nephropathy (Berger disease)
It is one of the most common causes of
recurrent gross or microscopic hematuria.
Pathogenesis:
Increase IgA concentration is found in more than
50% of cases.
Patients with IgA nephropathy have increased
production of IgA in bone marrow.
Also there is abnormalities in IgA clearance.
167. Pathogenesis of IgA nephropathy
It may be genetic and associated with HLA
types
It could also be acquired due to increase
IgA synthesis in response to respiratory or
GIT infection.
168. Pathogenesis of IgA nephropathy
IgA nephropathy occur also in increased
frequency in patients with celiac disease
(intestinal mucosal defect).
IgA and IgA complexes are then entrapped
in mesangium where they activate
alternative complement pathway and initiate
glomerular injury.
169. Morphology of Berger disease
The lesions vary considerably.
The glomeruli may show focal and segmental
mesangial proliferation or diffuse proliferation.
Immunofluorescence staining show a
characteristic mesangial deposition of IgA often
with C3 and properdin.
EM demonstrate electron dense deposits in the
mesangium.
171. This is Berger's disease, or IgA nephropathy.
The IgA is deposited mainly in mesangium, which then
increases mesangial cellularity as shown at the arrow.
172. This immunofluorescence micrograph demonstrates positivity with antibody to IgA.
Note that the pattern is that of mesangial staining.
This is IgA nephropathy. (Berger Disease)
173. Clinical picture of Berger disease
The disease often present with gross
hematuria after infection of respiratory tract
or GIT.
It affects children or young adults
30-40% has only microscopic hematuria.
174. Clinical picture of Berger disease
Diagnosis depend on renal biopsy with
immunofluorescence mesangial IgA
deposition.
It is usually recurrent.
Many patients maintain normal renal function,
CRF occur in 25% of cases after many years.
177. Hereditary nephritis
The most important disease is Alport’s syndrome .
It is hereditary nephritis associated with nerve
deafness and eye disorders (cataract,…).
It is due to gene abnormalities which encode
collagen production and so interfere with GBM
structure
It affect male more frequently between 5-20 years.
178. Hereditary nephritis
Morphology
A characteristic foam cells is present due to
accumulation of fat.
There is glomerular proliferation.
180. Alport's syndrome
The renal tubular cells appear foamy
because of the accumulation of neutral fats and mucopolysaccharides.
The glomeruli show irregular thickening and splitting of basement membranes
183. Chronic glomerulonephritis (CGN)
CGN is a most important cause of ESRD
(end stage renal disease) presenting as
CRF.
It probably represents the end stage of
many disease as RPGN, FSG,MGN and
MPGN.
However 20% of cases arise with no
history of symptomatic renal disease
185. Morphology of CGN
Gross: the kidneys are symmetrically
contracted with diffuse granular surface.
Microscopically: There is wide spread
replacement of glomerular tuft by avascular
acellular hyaline materials (hyalinization)
with complete glomerular obliteration.
There is also marked interstitial fibrosis and
tubular atrophy (due to impact on its blood
flow)
187. Clinical picture of CGN
Gradual onset ,usually discovered late in its
course after the onset of renal insufficiency.
First manifestations include hypertension
,proteinuria ,haematuria, azotemia
Progression to CRF and death unless renal
dialysis or transplantation is done.