<unk>  can be caused through a number of different mechanisms, each with the end result of decreasing albumin levels. These include: 1) impaired synthesis within the liver, 2) increased utilization by tissue, 3) distributional issues, and 4) increased excretion or loss. Often, the cause is multifactorial as in liver cirrhosis, where reduced hepatic synthesis and increased capillary leakage combine to further decrease albumin levels. Inflammation and infection Albumin is considered a negative acute phase reactant, which means that as inflammation and other acute physiologic processes occur, its levels decrease. This is in contrast to acute phase reactants like C-reactive protein (CRP), whose levels increase with inflammatory processes. With respect to mechanism, inflammation leads to decreased production of albumin as a result of increased levels of cytokines, specifically IL-1, IL-6, and TNF-α. In patients with the overwhelming infections common in sepsis and septic shock,<unk>  occurs as a result of the combinatorial effects of decreased synthesis as above, increased utilization by tissues, and increased transcapillary leakage from blood vessels due to increased vascular permeability. Liver disease Healthy and cirrhotic liver. If present,<unk>  suggests advanced liver disease as seen in cirrhosis. Albumin is synthesized in the liver, and low serum albumin can be indicative of liver failure or diseases such as cirrhosis and chronic hepatitis. If present,<unk>  is generally considered to be a sign of advanced hepatic cirrhosis, or irreversible damage to the liver. Production of albumin can be one 60–80% lower in advanced cirrhosis than in healthy liver, an effect amplified by dilution (salt and water retention), fluid shifts (following the accumulation of albumin in extracellular space and ascitic fluid), and even post-transcriptional changes to albumin itself. Kidney disease Kidney biopsy showing focal segmental glomerulosclerosis, one of the causes of nephrotic syndrome commonly seen in children.Hypoalbuminemia can also present as part of the nephrotic syndrome, in which significant quantities of protein are lost in the urine due to kidney damage. Under normal conditions, less than 30 milligrams per day of albumin are lost via the glomerulus. In nephrotic syndrome, protein loss can be as great as 3.5 grams over 24 hours, much of which is albumin, itself leading to<unk> . In children, nephrotic syndrome is commonly a primary disease process that is largely idiopathic, although more genetic causes are being identified with the cost and accessibility of whole exome sequencing. After renal biopsy, these syndromes are commonly diagnosed as minimal change disease, membranoproliferative glomerulonephritis, or focal segmental glomerulosclerosis. In adults, on the other hand, nephrotic syndrome is commonly a secondary disease process due to a variety of inciting factors. These inciting factors can be diverse, including toxins, drugs, heavy metals, autoantibodies, post-infectious antibody complexes, or immune complexes formed after malignancies like multiple myeloma. Albuminuria and resultant<unk>  can also occur in chronic kidney disease without protein loss levels as high as seen in nephrotic syndrome. Here, albumin loss from the kidneys occur due to decreased glomerular filtration rate (GFR) and subsequent loss of 30 to 300 milligrams of albumin per day. Over the course of months, this can lead to<unk> , a common feature of end stage renal disease. Alterations in fluid distribution and the presence of ongoing inflammation in chronic kidney disease in combination with<unk>  make fluid status control especially difficult. Malnutrition or malabsorption A girl with the physical signs and symptoms of Kwashiorkor, which is an extreme form of malnutrition-associated<unk> . Kwashiorkor is a disease of malnutrition characterized by decreased protein intake and amino acid deficiency resulting in<unk>  and a characteristic physical presentation. This is an extreme example of how malnutrition can result in<unk> . More typical is malnutrition-associated<unk>  in the elderly, who appear thin and frail but not with the rounded abdomen and edema seen in Kwashiorkor. Albumin is an acute negative phase respondent and not a reliable indicator of nutrition status Low albumin levels can also indicate chronic malnutrition from protein losing enteropathy. This is often caused or exacerbated by ulcerative colitis, but can also be seen in cardiac disease and systemic lupus erythematosus. Broadly, protein-losing enteropathy can be caused by increased lymphatic pressure in the gastrointestinal tract as in lymphangiectasis, mucosal erosion-induced lack of absorption as in Crohn's disease and ulcerative colitis, and other diseases of malabsorption without mucosal erosions as in Celiac disease. Eosinophilic gastritis presents with epigastric pain, peripheral blood eosinophilia, anemia, and<unk> .
Hypoalbuminemia
Bisalbuminemia
Albuminuria
Proteinuria
Proteinopathy
Bilirubinuria
Renal glycosuria
Lipiduria