Nephrotic syndrome is a renal disorder characterized by proteinuria, hypoalbuminaemia, hyperlipidemia and hypogammaglobulineamia.Patient suffering from nephotic syndrome has increased plasma protein in urine due to increased permeability of the glomerular capillary membrane.Infection is one of the serious complications of nephrotic syndrome due to decreased Immunoglobulin G. The study aims to discuss if dietary protein intake affects IgG synthesis. In the study conducted, the researcher able to used material in comparing IgG synthesis rate and that is by utilizing both Fractional Synthesis rate (ASR) and absolute synthesis rate (ASR) of protein in the body. Though according to the study, that FSR are more feasible to measure but the researcher still utilized the ASR. ASR requires the knowledge of pool sized (muscle). The result of the study explained that during the normal protein intake of nephrotic patient with marked decreased of the IgG intravascular pool have a remarkable increased in IgG FSR and ASR, which is not decreased by Low protein diet. The manifestation in these patients of Increased in IgG FSR and ASR ruled out that there is possibility of abnormality in IgG synthesis that leads to worsening condititon of hypogammaglobulinaemia produce albumin which is useful in maintaining the oncotic pressure that will prevent. Therefore the manifestation of increase in IgG FSR and ASR is a compensatory mechanism that will prevent severe hypogammaglobulinaemia. Stated in Lippincott's manual of nursing practice that they are encouraging the patient to take high protein diet to decreased worsening edema patient is experiencing. On the other hand there is also beneficial effect on low protein diet because it will decrease protenuiria or protein excretion in urine. Potentially, low protein diet might impair the observed increased in IgG synthesis of nephrotic syndrome since IgG production is dependent on amino acid level.


1) what are the factors that will change IgG intravascular pool?

Sources: http://books.google.com.ph/books
http://en.wikipedia.org/wiki/IgG
Lippincott,J.B.,(2001). Lippincott's Manual of Nursing Practice, 21,720-721 (7th ed.).

Major immunoglobulin in normal human serum, distributed evenly between the intravascular and extra vascular pools; it is the major antibody of secondary immune responses and the exclusive antitoxin class.

An immunoglobulin isotype (subclass) that characterizes secondary immune responses. This isotype is further broken down into several smaller subclasses (IgG1, IgG2a, IgG2b, IgG3 in the mouse; IgG1-4 in the human), and each subclass is differentially synthesized and secreted into the serum upon differential immune stimuli.

The constant level of various proteins including albumin and cellular components in intravascular pool in vivo is strictly controlled by an unknown homeostatic mechanism, although there are fluctuations seen in pathologic conditions. Because the majority of the IgG in the serum is regarded as self-reactive natural autoantibodies, IgG may have a role to react with all proteins in vivo. It is hypothesized that like an immune system, a homeostatic mechanism for the protein pool also has a sensitive role to identify and memorize the extent and repertoire of both normal and pathogenic proteins on an individual basis, and IgG may be one of the major players in performing these functions.

*the marked increased IgG levels observed in self-limiting diseases presumed to come from immunological insults such as acute poststreptococcal glomerulonephritis and Kikuchi-Fujimoto disease

*an immediate reduction of all protein levels except immunoglobulins after intravenous immunoglobulin (IVIG) treatment in Kawasaki disease

*a unified explanation for the variety of immunomodulating effects exerted by IVIG

*the IgG-enzyme complexes observed in benign conditions such as macroamylasemia and hyperphosphatasemia

* the marked decreased IgG level, which is correlated with the albumin level in minimal change nephrotic syndrome. IgG may be a ‘watch-dog’ for the disturbances of protein homeostasis in vivo.

IgG may control the pathogenic proteins that appeared in disordered states, and it may help prevent the loss of proteins in case of nephrotic syndrome.

REFERENCES:

1.ndt.oxfordjournals.org/cgi/content/short/19/10/2494

2.www.fpnotebook.com/ID/Lab/ImnglblnG.htm

Nephrotic syndrome results from damage to the kidneys' glomeruli—tiny blood vessels that filter wastes and excess water from the blood and send them to the bladder as urine.

When the glomeruli are working properly, they keep protein in the blood from leaking into the urine. Healthy kidneys allow less than 1 gram of protein to escape through the urine in a day. In nephrotic syndrome, the damaged glomeruli allow 3 grams or more of protein to leak into the urine during a 24-hour period.

As a result of this protein loss, the blood is deficient. Normal amounts of blood protein are needed to help regulate fluid throughout the body. Protein acts like a sponge to soak up fluid into the bloodstream. When blood is low in protein, fluid accumulates in the body’s tissues rather than circulating. The fluid causes swelling and puffiness.

Nephrotic syndrome can occur with many diseases. In adults, the most common causes are diabetic nephropathy and membranous nephropathy. In older adults, the most common cause is amyloidosis. Prevention of nephrotic syndrome relies on controlling these diseases. Frequently, however, the cause of nephrotic syndrome is unknown.

Source: National Institute of Diabetes and Digestive and Kidney Diseases (Feb 2007), http://kidney.niddk.nih.gov

nephrotic syndrome a set of clinical manifestations arising from protein wasting caused by by diffuse glomerular damage,

assessment

proteinuria
hematuria
hypoalbuminemia
edema

the most common interventions are monitoring intake and output because fluid excess may arise, monitor daily weights and provide a low to moderate protein and sodium in diet(not restrict) that is adequate in carbohydrates and calories to prevent worstening azotemia and fluid retention.

References

L. silvesteri(2005) saunders 4th edition p 948,Canada, elvesier Inc.

Nephrotic syndrome is a nonspecific disorder in which the kidneys are damaged, causing them to excrete large amounts of protein from the blood into the urine. It is a group of symptoms including low blood protein levels, high cholesterol levels and inflammation.

Low plasma IgG levels are said to be an important complication of the nephrotic syndrome. Patients who are diagnosed with nephrotic syndrome are those with low plasma IgG levels and increased IgG FSR and ASR.

IgG may control the pathogenic proteins that are observed in the urine and it may help prevent protein loss from nephrotic syndrome.

Since protein loss is an effect of nephrotic syndrome, it is necessary to replace them. The protein loss may be corrected with proper nutrition. Patients who are diagnosed with the said disease can combat the loss by having an adequate in take of protein in their diet. However, the amount of protein intake must be sufficient to prevent further damage to the kidneys which may progress to renal insufficiency because the kidneys will have a hard time filtering more proteins.

Other dietary recommendations are as follows:
- Decrease sodium intake to 1000-2000 milligrams daily.
- Moderate amount of high protein animal food preferably lean cuts of meat, fish, and poultry
- Avoid saturated fats and increase unsaturated fat intake.
- Eat low-fat desserts.
- Increase intake of fruits and vegetables. Potassium and Phosphorus are not restricted.
- Monitor fluid intake.

http://en.wikipedia.org/wiki/Nephrotic_syndrome#Dietary_recommendations

Nephrotic syndrome is a condition often characterized by the following:
• very high levels of protein in the urine
• low levels of protein in the blood
• swelling, especially around the eyes, feet, and hands
• high cholesterol

Generally, nephrotic syndrome results from damage to the kidneys' glomeruli - the tiny blood vessels that filter waste and excess water from the blood and send them to the bladder as urine. However, in some cases, the cause remains unknown.

Nephrotic syndrome may occur with many diseases, including the kidney diseases caused by type 2 diabetes. Prevention of nephrotic syndrome relies on controlling these diseases.

Nephrotic syndrome is actually a set of symptoms and not a disease in and of itself. The following are the most common symptoms of nephrotic syndrome. However, each individual may experience symptoms differently. Symptoms may include:
• High blood pressure
• Swelling in the feet and hands, and around the eyes
• Edema over the legs which is pitting (i.e., leaves a little pit when the fluid is pressed out, which resolves over a few seconds).
• Fluid in the pleural cavity causing pleural effusion. More commonly associated with excess fluid is pulmonary edema.
• Fluid in the peritoneal cavity causing ascites.

Specific treatment for nephrotic syndrome will be determined by your physician based on:
• your age, overall health, and medical history
• extent of the disease
• your tolerance for specific medications, procedures, or therapies
• expectations for the course of the disease
• your opinion or preference

Treatment generally focuses on identifying the underlying cause, if possible, and reducing the following (often through diet, medications, or both):
• high cholesterol
• blood pressure
• protein in urine

References

1. http://en.wikipedia.org/wiki/Nephrotic_syndrome
2. http://www.healthsystem.virginia.edu/uvahealth/adult_urology/nephsyn.cfm

Alterations of serum immunoglobulins, especially hypogammaglobulinemia (HG), are a frequent finding in steroid sensitive nephrotic syndrome (SSNS). The exact mechanisms are unclear, especially the persistence of HG into remission. Therefore we studied serum immunoglobulins M, A and G including IgG subclasses 1–4 in 44 children with SSNS; 14 were studied during relapse (RL) and 30 in remission (RM). Data were compared with those of 23 healthy controls. In a subgroup of 23 patients (12 in RM and 11 in RL) we also studied IgG-1 specific antibodies to tetanus toxoid and IgG-2 specific antibodies to pneumococcus antigen. Increased serum concentrations of IgM in RL and reduction of serum IgG in RL and RM were confirmed. During relapse, HG was characterized to result from deficiency of IgG-1–3, whereas in early phases of relapse the reduction was due to low IgG-1 only. In RM the deficiency of IgG-2 persisted for 12 months and correlated strongly with the duration of remission (R=0.60, P<0.0001). IgG-4 levels were not altered in SSNS. In addition, IgG-2 specific antibodies to pneumococcus antigen were significantly reduced only in RL compared to RM (P<0.05). In conclusion, hypogammaglobulinemia of SSNS is characterized by a different constitution of IgG subclasses. In RL a reduction of serum levels of IgG-1–3 occurs, while low concentrations of IgG-2 might be the explanation for HG in remission of SSNS.


In the nephrotic syndrome, the plasma level of some proteins of hepatic origin is partially defended by an increase in their synthetic rate. The plasma levels of several liver-derived proteins, as well as immunoglobulin G (IgG) are increased in one condition where plasma albumin concentration and oncotic pressure (II) are reduced, i.e., hereditary analbuminemia. To determine whether the urinary loss of IgG, a protein derived from the immune system, is compensated for by an increased synthetic rate, we measured IgG synthesis in normal Sprague-Dawley rats (SD); two models of the nephrotic syndrome: Heymann nephritis (HN) and Adriamycin treatment; and in Nagase analbuminemic rats (NAR), a model of decreased II without urinary protein loss. Plasma IgG and total IgG mass were significantly reduced in both HN and Adriamycin, yet IgG synthesis was nearly identical in HN, Adriamycin, and SD. In contrast, plasma and total IgG and IgG synthesis were all markedly increased in NAR. We derived a pathogen-free colony of NAR by Caesarean section and found that plasma IgG was not increased in pathogen-free NAR, despite reduced II. Thus, unlike proteins of hepatic origin (e.g., albumin) where synthesis increases following urinary loss, no compensatory increase in IgG synthesis occurs. Increased plasma IgG as well as IgG synthesis in the NAR is not a compensatory response to the absence of albumin or reduction in II, but rather is due to subclinical infection. Profound hypogammaglobulinemia of nephrotic syndrome occurs in part because no compensatory synthetic mechanisms balance urinary loss, and alteration in plasma II does not modulate IgG synthesis.


References:
1. http://www.springerlink.com/content/16tp99k7y5ny9gdb/
2. http://ajprenal.physiology.org/cgi/content/abstract/262/3/F333

Having personally known someone who have nephrotic syndrome made me very used to with this disease, nephotic syndrome does not only deals with extremely high protein but as well as fluid problems and sometimes high blood pressure. This disorder is common among children. In a sudy i just read concluded that there is also an increase in pulmonary arterial pressure among those who have this disorder. And further work should be done to evaluate the aetiology and clinical implications of this abnormality.
Tranplantation is also seen to be one option for eople who are suffering this abnormality, though studies also show that even after kidney transplantation, some of the symptoms still arise.

References:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1763209&tool=pmcentrez
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1450337