paper english 3 - done
Post on 07-Apr-2018
222 Views
Preview:
TRANSCRIPT
-
8/6/2019 Paper English 3 - DONE
1/21
THE PATHOPHYSIOLOGY OF NEPHROTIC SYNDROME IN
CHILDREN
Written by:Written by:
Sarita AmeliaSarita Amelia
030.07.235030.07.235
The Faculty of Medicine Trisakti UniversityThe Faculty of Medicine Trisakti University
1
-
8/6/2019 Paper English 3 - DONE
2/21
CHAPTER I
INTRODUCTION
Nephrotic syndrome (NS) is defined by the presence of nephrotic-range proteinuria,
edema, hyperlipidemia, and hypoalbuminemia. Nephrotic-range proteinuria in adults is
characterized by protein excretion of 3.5 g or more per day. Nephrotic-range proteinuria in
children is protein excretion of more than 40 mg/m2/h. Because 24-hour urine collections are
potentially unreliable and burdensome, especially in young children, many pediatric
nephrologists instead rely on a single, first-morning urine sample to quantify protein
excretion by the ratio of protein to creatinine.
The glomerular disorders that cause nephrotic syndrome generally can be divided into
congenital, primary and secondary etiologies. Causes of nephrotic syndrome include the
following:
INS (Idiopathic Nephrotic Syndrome)
Primary nephrotic syndrome (PNS), also known as idiopathic nephrotic syndrome
(INS), is associated with glomerular diseases intrinsic to the kidney and not related to
systemic causes. This includes 80-90 % cases of nephrotic syndrome in children.
The subcategories of INS are based on histological descriptions, but clinical-
pathological correlations have been made. A wide variety of glomerular lesions can be
seen in INS. Primary causes of nephrotic syndrome include:
o MCNS (Minimal Change Nephrotic Syndrome): 85 % of childhood cases
o FSGS (Focal Segmental Glomerulosclerosis): 9 % of childhood cases
2
-
8/6/2019 Paper English 3 - DONE
3/21
o MPGN (Mesangial Proliferative Glomerulonephritis) : about 2 % of childhood
cases
o Membranoproliverative glomerulonephritis (MPGN)
o IgA nephropathy
Secondary nephrotic syndrome
By definition, secondary nephritic syndrome refers to an etiology extrinsic to the
kidney. Secondary causes of nephrotic syndrome include:
o Infections, include: congenital syphilis, TORCH, Malaria, HIV, etc.
o Drugs, include: penicillamine, gold, nonsteroidal anti-inflammatory drugs
(NSAIDs) , interferon, mercury, heroin, pamidronate and lithium
o Systemic disease, include: Systemic lupus erythematosus, Malignancy -
Lymphoma, leukemia, Vasculitis-Wegener granulomatosis, Henoch-Schnlein
purpura (HSP), etc.
Genetic nephrotic syndrome/congenital nephrotic syndrome
In some rare cases, nephrotic syndrome may also be caused by genetic abnormalities.
Infantile NS (presenting before age 3 mo) and congenital NS (presenting at age 4-12
mo) have been associated with the following genetic defects:
o Finnish-type congenital nephrotic syndrome (NPHS1, nephrin), Denys-Drash
syndrome (WT1), Frasier syndrome (WT1), Autosomal recessive, familial FSGS
(NPHS2, podocin), Autosomal dominant, familial FSGS (ACTN4, -actinin-
4; TRPC6), etc.
The features of the nephrotic syndrome include:
Glomerular dysfunction leading to excessive urinary protein excretion
(formerly defined as >3.5 g/day but there appears to be individual variation)
3
http://emedicine.medscape.com/article/981516-overviewhttp://emedicine.medscape.com/article/969023-overviewhttp://emedicine.medscape.com/article/1004557-overviewhttp://emedicine.medscape.com/article/969023-overviewhttp://emedicine.medscape.com/article/1004557-overviewhttp://emedicine.medscape.com/article/981516-overview -
8/6/2019 Paper English 3 - DONE
4/21
Hypoalbuminaemia as a result of urinary protein loss (albumin levels usually
in range
-
8/6/2019 Paper English 3 - DONE
5/21
CHAPTER II
PATHOPHYSIOLOGY OF NEPHROTIC SYNDROME IN CHILDREN
2.1. Physiology
In normal people, all your blood flows through your kidneys, which are the
key organs in the complex system that removes excess fluid and waste material from
the blood. Blood that flows into your kidneys is diffused through filtering structures
called nephrons. Each nephron contains a tuft of capillary blood vessels (glomerulus)
and tiny tubules that lead to larger collecting tubes. The glomeruli filter fluid from
your blood, extracting both waste products and substances your body needs
sodium, phosphorus and potassium. The substances your body needs are reabsorbed
into your bloodstream. The rest is excreted in your urine through tubules that lead into
the ureters the tubes that lead to the bladder.
5
-
8/6/2019 Paper English 3 - DONE
6/21
Nephrotic syndrome is a kidney disorder that causes your body to excrete too
much protein in your urine. Nephrotic syndrome is usually caused by damage to the
clusters of small blood vessels, called glomeruli, in your kidneys that filter waste and
excess water from your blood. When healthy, these vessels keep blood protein from
seeping into your urine and out of your body. When damaged, they don't perform this
function effectively, where millions of tiny kidney filters leaking protein into the
urine which can be detected by urine dip stick. So less protein left in blood then fluid
can leak out of your blood and lead to swelling all over your body (edema).
Since the major cause of nephrotic Syndrome in children is the primary
etiology that leads to the primary Nephrotic Syndrome, which is about 80-90% cases
of all, this paper focuses on the pathophysiology of the primary Nephrotic Syndrome
or also known as the Idiopathic Nephrotic Syndrome (INS). Here are the explanations
of each element in the pathophysiology of Nephrotic Syndrome in children or the
Idiopatic Nephrotic Syndrome based on the recent studies and research.
2.2. Proteinuria and Hypoalbuminemia
2.2.1. The Immune System and Proteinuria
6
-
8/6/2019 Paper English 3 - DONE
7/21
The hallmark of Idiopathic Nephrotic Syndrome (INS) is massive proteinuria,
leading to decreased circulating albumin levels. The initiating event that produces
proteinuria remains unknown. INS is believed to have an immune pathogenesis.
Studies have shown abnormal regulation of T-cell subsets and expression of a
circulating glomerular permeability factor. Evidence of the immune-mediated nature
of INS is demonstrated by the fact that immunosuppressive agents, such as
corticosteroids and alkylating agents, can result in remission of nephrotic syndrome.
However, the precise nature of the immune pathogenic process has yet to be defined.
A circulating factor may play a role in the development of proteinuria in INS.
This can be demonstrated by the rapid development of proteinuria in recurrence of
nephrotic syndrome after kidney transplantation, the improvement in nephrotic
syndrome in such patients after treatment with plasmapheresis, and the experimental
induction of proteinuria in animals by plasma from patients with INS. However, the
nature of this circulating factor is not known. Various cytokines and molecules have
been implicated, including interleukin (IL)-2, IL-2 receptor, IL-4, IL-12, IL-13, IL-15,
IL-18, interferon-, tumor growth factor (TGF)-, vascular permeability factor,
nuclear factor (NF)-B, and tumor necrosis factor (TNF)-.
The association of allergic responses with nephrotic syndrome also illustrates
the role of the immune system in INS. Nephrotic syndrome has been reported to occur
after allergic reactions to bee stings, fungi, poison ivy, ragweed, house dust, jellyfish
stings and cat fur. Food allergy might play a role in relapses of INS; a reduced-
antigenic diet was associated with improved proteinuria and complete remission in
one study.5 Additionally, INS is 3-4 times more likely in children with human
leukocyte antigen (HLA)-DR7. Steroid sensitive INS has also been associated with
7
-
8/6/2019 Paper English 3 - DONE
8/21
HLA-B8 and the DQB1 gene of HAL-DQW2. A greater incidence of INS is also
observed in children with atopy and HLA-B12.
We can apply this pathophysiology of this immune system-related proteinuria
in nephrotic syndrome to MCNS (minimal change nephrotic syndrome). MCNS is the
most common cause of the nephrotic syndrome in children, accounting for 90% of
cases under the age of 10 years and more than 50% in older children. It has been
proposed that MCNS reflects a disorder of T-lymphocytes. These T cells are thought
to release a cytokine so-called permeability factor that injures the glomerular
epithelial cells. The identity of this permeability factor is still uncertain. Epithelial cell
damage may lead to albuminuria in MCNS by altering the metabolism of polyanions,
such as heparan sulphates, that constitute most of the normal charge barrier to the
glomerular filtration of macromolecules such as albumin. This can lead to the
increased glomerular permeability that allows the increased passage of large amounts
of low-molecular weight anionic proteins during ultrafiltration.
Therefore, eventhough the exact nature of the immune pathogenic process in
nephrotic syndrome has yet to be defined, we can explain how the immune reaction in
the body can cause the glomerular injury that leads to increased glomerular
permeability then patients will show proteinuria in their laboratory test results.
2.2.2. Genetics, the Podocyte, and Proteinuria
8
-
8/6/2019 Paper English 3 - DONE
9/21
Perhaps the most exciting development in recent years in understanding the
pathophysiology of nephrotic syndrome has occurred in the area of podocyte biology
(see the image below).
Schematic drawing of the glomerular barrier. Podo = podocytes; GBM = glomerular
basement membrane; Endo = fenestrated endothelial cells; ESL = endothelial cell
surface layer (often referred to as the glycocalyx). Primary urine is formed through
the filtration of plasma fluid across the glomerular barrier (arrows); in humans, the
glomerular filtration rate (GFR) is 125 mL/min. The plasma flow rate (Qp) is close to
700 mL/min, with the filtration fraction being 20%. The concentration of albumin in
serum is 40 g/L, while the estimated concentration of albumin in primary urine is 4
mg/L, or 0.1% of its concentration in plasma.
The glomerular filtration barrier consists of the fenestrated capillary
endothelium, the extracellular basement membrane, and the intercalated podocyte foot
processes, connected by 35-45 nm slit diaphragms. Nephrotic syndrome is associated
with the biopsy finding of fusion (effacement) of podocyte foot processes. This
effacement of the podocytes long was thought to be a secondary phenomenon of
nephrotic syndrome.
However, theories have shifted towards the podocyte as playing a primary role
in the development of proteinuria. The understanding of the pathophysiology of
proteinuria in renal diseases has greatly expanded with insights into the molecular
9
-
8/6/2019 Paper English 3 - DONE
10/21
-
8/6/2019 Paper English 3 - DONE
11/21
The classical explanation for edema formation is a decrease in plasma oncotic
pressure, as a consequence of low serum albumin levels, causing the increased
transudation or extravasation of plasma water into the interstitial space. This
transudation can lead to the accumulation of fluid in the extracellular space (eg,
tissue), or edema. A decrease in intravascular volume is thought to cause renal
hypoperfusion further enhancing salt and water retention by leading to stimulation of
the renin-angiotensin-aldosterone system and anti diuretic hormone due to the
resulting contraction in plasma volume.
While the classical model of edema (also known as the "underfill hypothesis")
seems logical, certain clinical and experimental observations do not completely
support this traditional concept. First, the plasma volume (PV) has not always been
found to be decreased and, in fact, in most adults, measurements of PV have shown it
to be increased. Only in young children with MCNS have most (but not all) studies
demonstrated a reduced PV. Additionally, most studies have failed to document
elevated levels of renin, angiotensin, or aldosterone, even during times of avid sodium
retention. Active sodium reabsorption also continues despite actions that should
suppress renin effects (such as albumin infusion or ACE inhibitor administration).
Another model of edema formation is known as the "overfill hypothesis." In
this model, a primary defect in renal sodium handling is postulated. A primary
increase in renal sodium reabsorption leads to net salt and water retention and
subsequent hypertension. ANP might play a role is this mechanism; studies have
shown an impaired response to ANP in nephrotic syndrome. This ANP resistance, in
part, might be caused by overactive efferent sympathetic nervous activity, as well as
enhanced tubular breakdown of cyclic guanosine monophosphate. Other mechanisms
11
http://www.patient.co.uk/DisplayConcepts.asp?WordId=FLUID%20RETENTION&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=FLUID%20RETENTION&MaxResults=50 -
8/6/2019 Paper English 3 - DONE
12/21
that contribute to a primary increase in renal sodium retention include overactivity of
the Na+ -K+ -ATPase and renal epithelial sodium channel (RENaC) in the cortical
collecting duct and shift of the Na+/H+ exchangerNHE3 from the inactive to active
pools in the proximal tubule.
A more recent theory of edema formation states that massive proteinuria leads
to tubulointerstitial inflammation and release of local vasoconstrictors and inhibition
of vasodilation. This leads to a reduction in single-nephron glomerular filtration rate
and sodium and water retention.
Thus, the precise cause of the edema and its persistence is uncertain. A
complex interplay of various physiologic factors (such as decreased oncotic pressure,
increased activity of aldosterone and vasopressin, diminished atrial natriuretic
hormone, activities of various cytokines and physical factors within the vasa recti)
probably contribute to the accumulation and maintenance of edema. And since the
exact pathophysiology of this condition remains unknown, many people still stick to
the classical theory to explain the process of forming edema in nephrotic syndrome.
2.4. Hyperlipidemia
INS is accompanied by disordered lipid metabolism. Apolipoprotein (apo)-B
containing lipoproteins are elevated, including very-low-density lipoprotein (VLDL),
intermediate-density lipoprotein (IDL), and low-density lipoproteins (LDL) and
lipoprotein(a), with resultant increases in total cholesterol and LDL-cholesterol. High-
density lipoprotein (HDL)-cholesterol is normal or low. Elevations in triglycerides
occur with severe hypoalbuminemia. The traditional explanation for hyperlipidemia in
12
-
8/6/2019 Paper English 3 - DONE
13/21
INS was the increased synthesis of lipoproteins that accompany increased hepatic
albumin synthesis due to hypoalbuminemia. However, serum cholesterol levels have
been shown to be independent of albumin synthesis rates.
Decreased plasma oncotic pressure may play a role in increased hepatic
lipoprotein synthesis, as demonstrated by the reduction of hyperlipidemia in patients
with INS receiving either albumin or dextran infusions. Also contributing to the
dyslipidemia of INS are abnormalities in regulatory enzymes, such as lecithin-
cholesterol acyltransferase, lipoprotein lipase and cholesterol ester transfer protein.
Therefore, to be concluded, we can say that hyperlipidemia in patients with
nephrotic syndrome is thought to be caused by these following aspects: the
stimulation of the liver to increase synthesis of all plasma proteins (including the
lipoproteins), due to their low level in the blood; and reduction of lipoprotein
catabolism due to reduced levels of lipoprotein lipase in blood.
2.5. Thrombosis
Patients with nephrotic syndrome are at increased risk for thrombosis. Various
factors play a role in the increased incidence of thrombosis. Abnormalities described
in INS include increased platelet activation and aggregation; elevation in factors V,
VII, VIII, and XIII and fibrinogen; decreased antithrombin III, proteins C and S, and
factors XI and XII; and increased activities of tissue plasminogen activator and
plasminogen activator inhibitor-1. These abnormalities in hemostatic factors,
combined with potential hypovolemia, immobility, and increased incidence of
infection, lead to a hypercoagulable state in INS.
13
http://www.patient.co.uk/DisplayConcepts.asp?WordId=SERUM%20PROTEIN%20ELECTROPHORESIS&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=SERUM%20PROTEIN%20ELECTROPHORESIS&MaxResults=50 -
8/6/2019 Paper English 3 - DONE
14/21
Thus, we can say that in nephrotic syndrome, there are increased risks of
arterial andvenous thrombosis due to loss of anti-thrombin III and plasminogen in the
urine, combined with an increase in hepatic synthesis of clotting factors.
2.6. Infection
Patients with INS are at increased risk of infection, especially with
Streptococcus pneumoniae, but other infections are common as well. INS is
associated with low immunoglobulin (Ig)G levels, which appear to be the result of
urinary losses at first. But according to the recent studies, they do not appear to be that
way. Instead, low IgG levels seem to be the result of impaired synthesis, again
pointing to a primary disorder in lymphocyte regulation in INS. Additionally,
increased urinary losses of factor B are noted, a cofactor protein of C3b in the
alternative pathway of complement, which plays an important role in the opsonization
of encapsulated organisms such as S pneumoniae.
Impaired T-cell function may also be present in INS, which contributes to the
susceptibility to infection. Finally, the medications used to treat INS, such as
corticosteroids and alkylating agents, further suppress the immune system and
increase the risk of infection.
2.7. Overview
14
http://www.patient.co.uk/DisplayConcepts.asp?WordId=PHLEBITIS%20AND%20THROMBOPHLEBITIS&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=PHLEBITIS%20AND%20THROMBOPHLEBITIS&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=PHLEBITIS%20AND%20THROMBOPHLEBITIS&MaxResults=50 -
8/6/2019 Paper English 3 - DONE
15/21
According to the explanation of each aspect of pathophysiology of nephrotic
syndrome, the pathophysiology of nephrotic syndrome in children can be summarized
to the following overview.
The commonest cause of nephrotic syndrome in children, which includes 80-
90 % cases of all, is the primary etiology leading to the idiopathic nephrotic syndrome
(INS). INS is believed to have immune pathogenesis in which occurs some idiopathic
immune reaction where some abnormality of T-lymphocytes occurs in patients with
nephrotic syndrome. These impaired T-lymphocytes are thought to release various
cytokines so called the permeability factor that causing the glomerular injury. This
immune reaction is considered idiopathic because according to the recent studies, the
initiating event of the immune reaction and the identity of this permeability factor is
still uncertain.
This glomerular injury may lead to proteinuria in nephrotic syndrome by
altering the metabolism of polyanions, such as heparan sulphates, that constitute most
of the normal charge barrier to the glomerular filtration of macromolecules such as
albumin. This can cause the increased glomerular permeability that allows the
increased passage of large amounts of low-molecular weight anionic proteins during
the filtration process in glomeruli leading to excessive protein urinary excretion.
Thus, proteinuria will be found in the results of laboratory test of patients with
nephrotic syndrome. This proteinuria will lead to the other characteristics that we can
find in patients with nephrotic syndrome.
Massive proteinuria can cause low levels in serum albumin. So thats why you
can find hypoalbuminemia in patients with nephrotic syndrome. Then as result,
plasma oncotic pressure is decreased that leads to the increased transudation, or
15
-
8/6/2019 Paper English 3 - DONE
16/21
extravasation of plasma water into interstitial spaces. This can cause an accumulation
of fluid in extracellular space or tissue that is called edema.
If the process of forming edema keeps continuing in the body where the
plasma water is leaking out the blood vessel, intravascular volume will be decreasing
then the renal hypoperfusion will occur in advance and activate the Renin-
Angiotensin-Aldosteron system.
Renin-angiotensin-aldosteron system is stimulated by the decreased plasma
volume that triggers the production of renin by kidneys as a first step. Renin is an
enzyme which activates angiotensinogen produced by liver to angiotensin I. Then
angiotensin I is converted to angiotensin II by ACE (Angiotensin Converting
Enzyme) produced by lungs. Angiotensin II can trigger the production of aldosteron
and anti diuretic hormone which enhanced the salt and water retention. The resultant
retention of sodium and water by the renal tubules contributes to the extension and
maintenance of edema.
As mentioned above, proteinuria in nephrotic syndrome can lead to
hypoalbuminemia or low levels of serum albumin. This hypoalbuminemia also
induces the stimulation of the liver to increase synthesis of all plasma proteins. This
stimulation includes the synthesis of lipoproteins. Besides that, in idiopathic nephrotic
syndrome, we can also find abnormalities in regulating enzymes of lipid metabolism
such as lipoprotein lipase and cholesterol ester transfer protein. Thus, the increased
synthesis of lipoproteins in liver, combined with the reduction of lipoprotein
catabolism due to reduced levels of lipoprotein lipase in blood, both contribute to the
increased serum lipoprotein levels which leads to hyperlipidemia in patients with
nephrotic syndrome.
16
-
8/6/2019 Paper English 3 - DONE
17/21
Patients with nephrotic syndrome are also have an increased risk for
thrombosis due to various abnormalities such as decreased antithrombin III, proteins
C and S; and increased activities of tissue plasminogen activator and plasminogen
activator inhibitor-1. This abnormality is thought to be related with massive
proteinuria in idiopathic nephrotic syndrome when there is loss of anti thrombin,
protein C and S in the urine along with the other plasma proteins. This condition,
combined with an increase in hepatic synthesis of clotting factors, both contribute to
the increased risk for thrombosis in nephrotic syndrome.
Aside from thrombus, patients with nephrotic syndrome have also an
increased risk for infection which is thought to be related with the massive proteinuria
as well. According to the old theory, this increased risk for infection is due to the loss
of immunoglobulin in urine along with other plasma proteins. But according to the
new theory, it states that what occurs during proteinuria contributing to the risk of
infection in nephrotic syndrome is actually the increased urinary losses of factor B, a
cofactor protein of C3b in the alternative pathway of complement, which plays an
important role in the opsonization of encapsulated organisms such as S pneumoniae.
The recent studies also suggest that low levels of IgG that does occur in nephrotic
syndrome is probably due to the primary disorder of lymphocyte regulation in
idiopathic nephrotic syndrome. Thus, the urinary losses of factor B, combined with
the idiopathic low levels of IgG, both contribute to the increased risk for infection in
nephrotic syndrome.
CHAPTER III
CONCLUSION
17
-
8/6/2019 Paper English 3 - DONE
18/21
Nephrotic syndrome (NS) is defined by the presence of nephrotic-range proteinuria,
edema, hyperlipidemia, and hypoalbuminemia. Nephrotic-range proteinuria in adults is
characterized by protein excretion of 3.5 g or more per day. The reported annual incidence
rate for nephrotic syndrome is 2-7 cases per 100,000 children younger than 16 years. The
glomerular diseases that cause nephrotic syndrome generally can be divided into congenital,
primary and secondary etiologies. 80-90 % cases of nephrotic syndrome in children is the
primary or idiopathic one leading to idiopathic nephrotic syndrome.
The pathophysiology of nephrotic syndrome in children comprises following element:
Proteinuria and hypoalbuminemia
o Proteinuria and immune system
The hallmark of Idiopathic Nephrotic Syndrome (INS) is massive proteinuria,
leading to decreased circulating albumin levels. The initiating event that produces
proteinuria remains unknown. INS is believed to have an immune pathogenesis.
Studies have shown abnormal regulation of T-cell subsets and expression of a
circulating glomerular permeability factor.
o Genetics, the podocyte and proteinuria
The glomerular filtration barrier consists of the fenestrated capillary endothelium,
the extracellular basement membrane, and the intercalated podocyte foot
processes, connected by slit diaphragms. The effacement of the podocytes long
was thought to be a secondary phenomenon of nephrotic syndrome. Various
forms of INS have been described with mutations in podocyte genes.
18
-
8/6/2019 Paper English 3 - DONE
19/21
Edema
The classical explanation for edema formation is a decrease in plasma oncotic
pressure, as a consequence of low serum albumin levels, causing an extravasation of
plasma water into the interstitial space. The resulting contraction in plasma volume
leads to stimulation of the renin-angiotensin-aldosterone axis and antidiuretic
hormone. The resultant retention of sodium and water by the renal tubules contributes
to the extension and maintenance of edema.
Hyperlipidemia
Hyperlipidemia in patients with nephrotic syndrome is thought to be caused by these
following aspects: the stimulation of the liver to increase synthesis of all plasma
proteins (including the lipoproteins), due to their low level in the blood; and reduction
of lipoprotein catabolism due to reduced levels of lipoprotein lipase in blood.
Thrombus
In nephrotic syndrome, there are increased risks of arterial and venous thrombosis due
to loss of anti-thrombin III and plasminogen in the urine, combined with an increase
in hepatic synthesis of clotting factors.
Infection
Idiopathic nephrotic syndrome is associated with low IgG levels, which appear to be
the result of urinary losses at first. But according to the recent studies, low IgG levels
seem to be the result of impaired synthesis due to a primary disorder in lymphocyte
regulation in INS. Additionally, increased urinary losses of factor B are noted, a
cofactor protein of C3b in the alternative pathway of complement, which plays an
19
http://www.patient.co.uk/DisplayConcepts.asp?WordId=SERUM%20PROTEIN%20ELECTROPHORESIS&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=SERUM%20PROTEIN%20ELECTROPHORESIS&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=PHLEBITIS%20AND%20THROMBOPHLEBITIS&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=SERUM%20PROTEIN%20ELECTROPHORESIS&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=SERUM%20PROTEIN%20ELECTROPHORESIS&MaxResults=50http://www.patient.co.uk/DisplayConcepts.asp?WordId=PHLEBITIS%20AND%20THROMBOPHLEBITIS&MaxResults=50 -
8/6/2019 Paper English 3 - DONE
20/21
important role in the opsonization of encapsulated organisms such as S pneumoniae.
Thus, the urinary losses of factor B, combined with the idiopathic low levels of IgG,
both contribute to the increased risk for infection in nephrotic syndrome.
REFERENCES
1. Lane JC. Pediatric Nephrology: Nephrotic Syndrome. Available at:
http://emedicine.medscape.com/article/982920-overview. Accessed: May 30th, 2010.
2. Lee TH, Cho MH. Pathophysiology of Minimal Change Nephrotic Syndrome.
Available at: http://www.interscience.wiley.com. Accessed: May 30th, 2010.
3. McMillan JI. Nephrotic Syndrome: Glomerular Disorders: Merck Manual
Professional. Available at: http://www.merck.com/mmpe/sec17/ch235/ch235c.html.
Accessed: May 30th, 2010.
4. Draper RS. Features of Nephrotic Syndrome. Available at:
http://www.patient.co.uk/doctor/Nephrotic-Syndrome.htm. Accessed at: May 31st, 2010.
5. Eakin JD. Care Based Pediatrics: Nephrotic Syndrome. Available at:
http://www.hawaii.edu/medicine/pediatrics/pedtext/s13c02.html.
6. Fivush B, Jabs KM. Childhood Nephrotic Syndrome. Available at:
http://kidney.niddk.nih.gov/kudiseases/pubs/childkidneydiseases/nephrotic_syndrom/ind
ex.htm. Accessed: May 30th, 2010.
20
http://emedicine.medscape.com/article/982920-overviewhttp://www.interscience.wiley.com/http://www.interscience.wiley.com/http://www.merck.com/mmpe/sec17/ch235/ch235c.htmlhttp://www.merck.com/mmpe/sec17/ch235/ch235c.htmlhttp://www.merck.com/mmpe/sec17/ch235/ch235c.htmlhttp://www.patient.co.uk/doctor/Nephrotic-Syndrome.htmhttp://www.patient.co.uk/doctor/Nephrotic-Syndrome.htmhttp://www.hawaii.edu/medicine/pediatrics/pedtext/s13c02.htmlhttp://kidney.niddk.nih.gov/kudiseases/pubs/childkidneydiseases/nephrotic_syndrom/index.htmhttp://kidney.niddk.nih.gov/kudiseases/pubs/childkidneydiseases/nephrotic_syndrom/index.htmhttp://kidney.niddk.nih.gov/kudiseases/pubs/childkidneydiseases/nephrotic_syndrom/index.htmhttp://emedicine.medscape.com/article/982920-overviewhttp://www.interscience.wiley.com/http://www.merck.com/mmpe/sec17/ch235/ch235c.htmlhttp://www.patient.co.uk/doctor/Nephrotic-Syndrome.htmhttp://www.hawaii.edu/medicine/pediatrics/pedtext/s13c02.htmlhttp://kidney.niddk.nih.gov/kudiseases/pubs/childkidneydiseases/nephrotic_syndrom/index.htmhttp://kidney.niddk.nih.gov/kudiseases/pubs/childkidneydiseases/nephrotic_syndrom/index.htm -
8/6/2019 Paper English 3 - DONE
21/21
7. Terri FF. Nephrotic Syndrome. Available at: http://www.mayoclinic.com/nephrotic-
syndrome. Accessed: May 31st, 2010.
8. McPhee SJ, Ganong WF. Pathophysiology of Disease: An introduction to Clinical
Medicine. New York: The McGraw-Hill Companies. 2006; 16:476.
9. Symons JM. Nephrotic syndrome in childhood. Lancet. 2003; 362:629-39.
10. Van den Berg JG, Weening JJ. Role of the immune system in the pathogenesis
of idiopathic nephrotic syndrome. London: Clin Sci. 2004; 107(2):125-36.
21
http://www.mayoclinic.com/nephrotic-syndromehttp://www.mayoclinic.com/nephrotic-syndromehttp://www.mayoclinic.com/nephrotic-syndromehttp://www.mayoclinic.com/nephrotic-syndrome
top related