This is why the concentration of albumin in the urine is one of the single sensitive indicators of kidney disease, particularly for those with diabetes or hypertension, compared to routine proteinuria examination.As the loss of proteins from the body progresses, the suffering will gradually become symptomatic.The exception applies to the scenario when theres an overproduction of proteins in the body, in which the kidney is not to blame. Diagnosis
Conventionally, proteinuria is diagnosed by a simple dipstick test, although it is possible for the test to give a false negative reading, even with nephrotic range proteinuria if the urine is dilute. False negatives may also occur if the protein in the urine is composed mainly of globulins or Bence Jones proteins because the reagent on the test strips, bromophenol blue, is highly specific for albumin. Traditionally, dipstick protein tests would be quantified by measuring the total quantity of protein in a 24-hour urine collection test, and abnormal globulins by specific requests for protein electrophoresis. Trace results may be produced in response to excretion of Tamm–Horsfall mucoprotein. More recently developed technology detects human serum albumin (HSA) through the use of liquid crystals (LCs). The presence of HSA molecules disrupts the LCs supported on the AHSA-decorated slides thereby producing bright optical signals which are easily distinguishable. Using this assay, concentrations of HSA as low as 15 µg/mL can be detected.Alternatively, the concentration of protein in the urine may be compared to the creatinine level in a spot urine sample. This is termed the protein/creatinine ratio.
Adults
In 2001 the American Thoracic Society, drawing on the work of the British and Canadian Thoracic Societies, established guidelines for the management of adult CAP by dividing patients into four categories based on common organisms:
Healthy outpatients without risk factors: This group (the largest) is composed of otherwise-healthy patients without risk factors for DRSP, enteric gram-negative bacteria, pseudomonas or other, less common, causes of CAP. Primary microorganisms are viruses, atypical bacteria, penicillin-sensitive streptococcus pneumoniae and haemophilus influenzae. Recommended drugs are macrolide antibiotics, such as azithromycin or clarithromycin, for seven to ten days. A shorter course of these antibiotics has been investigated, however, there is not sufficient evidence to make recommendations. Outpatients with underlying illness or risk factors: Although this group does not require hospitalization, they have underlying health problems such as emphysema or heart failure or are at risk for DRSP or enteric gram-negative bacteria. They may be treated with a quinolone active against streptococcus pneumoniae (such as levofloxacin) or a β-lactam antibiotic (such as cefpodoxime, cefuroxime, amoxicillin or amoxicillin/clavulanic acid) and a macrolide antibiotic, such as azithromycin or clarithromycin, for seven to ten days. Hospitalized patients without risk for pseudomonas: This group requires intravenous antibiotics, with a quinolone active against streptococcus pneumoniae (such as levofloxacin), a β-lactam antibiotic (such as cefotaxime, ceftriaxone, ampicillin/sulbactam or high-dose ampicillin plus a macrolide antibiotic (such as azithromycin or clarithromycin) for seven to ten days. Intensive-care patients at risk for pseudomonas aeruginosa: These patients require antibiotics targeting this difficult-to-eradicate bacterium.