How many plasma proteins

Abnormal proteinuria can also result from various medical conditions. The reasons why a GP may request measurement of plasma protein include investigations of symptoms, allergies, and immunity see Box 1. Liver panel tests , for example, those requested as part of drug monitoring, may reveal protein abnormalities that require further investigation. Testing urine for protein may assist in the diagnosis of urinary infection, primary renal disease including nephrotic syndrome, secondary renal disease for example in diabetes, multiple myeloma, and pre-eclampsia in pregnancy.

The conditions associated with abnormal globulin and albumin levels are detailed below and summarised in Table 1. Decreased globulin levels as a fraction of total protein are seen in individuals with malnutrition and patients with nephrotic syndrome when there is renal protein loss.

High total protein levels associated with increased globulin may be seen in dehydration, in response to acute infections such as pneumonia and hepatitis, and in chronic inflammatory conditions such as rheumatoid arthritis and systemic lupus erythematosus SLE. Other causes of a low serum albumin level include severe malnutrition which may accompany alcohol-related liver disease.

Severe inflammatory conditions or shock may also be associated with low serum albumin levels, when a catabolic state develops and the synthetic function of the liver switches to the production of other proteins.

An important symptom of low serum albumin is the development of peripheral oedema. High serum albumin levels generally reflect dehydration. Causes of transient elevated proteinuria include: 1 3.

Urine may test falsely positive for protein when the sample has been contaminated by vaginal mucous. Causes of persistent proteinuria include: 1 3. If serum albumin is low and nephrotic syndrome is suspected, testing the urine for protein will help inform the diagnosis. C-reactive protein is an acute-phase reactant; a protein synthesised by the liver and released into the blood in response to tissue injury, infection, or other inflammatory processes.

Its physiological role is thought to involve binding to the surface of dead or dying cells and some types of bacteria to activate the complement system. In chronic inflammatory conditions, CRP level can be valuable in monitoring disease activity, with high levels suggestive of an acute exacerbation or ineffective treatment and falling or low levels indicative of remission. Raised CRP is a feature of infection or inflammation, but it is a non-specific marker of an acute response.

C-reactive protein typically returns to normal when the acute infective or inflammatory process is resolved. Although standard liver panel tests and on-site urine protein testing give a general indication of protein levels, protein electrophoresis can be used to separate the mixture of proteins present in either plasma or urine into subdivisions to provide additional diagnostic information. The distance travelled by each protein depends on a range of variables, including its molecular size and electrical charge.

The separated proteins are then visualised using a stain, which reveals a characteristic pattern of bands. Serum proteins are separated into six major groups by protein electrophoresis: albumin and alpha 1 , alpha 2 , beta 1 , beta 2 , and gamma globulins. The size of each band gives a qualitative indication of the amount of that protein fraction. This pattern of bands is often converted into a graph, with vertical spikes or peaks where there are large amounts of protein and smaller peaks or valleys where there are small amounts of protein.

Abnormal electrophoresis patterns are associated with a variety of different pathological conditions. The most common elevation in gamma globulin levels is polyclonal and typically due to increased immune system activity caused by acute or chronic infection, tissue damage or autoimmune connective tissue diseases such as rheumatoid arthritis, SLE, scleroderma, chronic active autoimmune hepatitis, and primary biliary cholangitis. Isolated alpha 1 abnormalities are usually due to changes in alpha 1 antitrypsin, with decreased levels occurring in congenital alpha 1 antitrypsin deficiency.

Cell Structure 3. Membrane Structure 4. Membrane Transport 5. Origin of Cells 6. Cell Division 2: Molecular Biology 1. Metabolic Molecules 2. Water 3. Protein 5. Enzymes 6. Cell Respiration 9. Photosynthesis 3: Genetics 1.

Genes 2. Chromosomes 3. Meiosis 4. Inheritance 5. Genetic Modification 4: Ecology 1. Energy Flow 3. Table 2. Figure 3. All quantified proteins and percent changes. The Mascot quantification results from all patients and MS repeat runs were averaged and the percent change values were calculated. The proteins are represented as UniProtKB protein and gene names and accessions. Supplementary Material Supplementary Material. References C. Gabay and I.

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