Albumin infusion in hepatic resection (>40%), nephrotic syndrome (with diuretics and corticosteroids), spontaneous bacterial peritonitis (with antibiotics), and hepatorenal syndrome (with terlipressin)
Frequency
70% (elderly inpatients)
Hypoalbuminemia (or hypoalbuminaemia) is a
internal organs. Laboratory tests aimed at assessing liver function diagnose hypoalbuminemia. Once identified, it is a poor prognostic indicator for patients with a variety of different diseases. Yet, it is only treated in very specific indications in patients with cirrhosis and nephrotic syndrome
. Treatment instead focuses on the underlying cause of the hypoalbuminemia. Albumin is an acute negative phase respondent and not a reliable indicator of nutrition status.
Signs and symptoms
Pitting edema of the lower extremities commonly seen in conditions associated hypoalbuminemia.
Patients with hypoalbuminemia are more likely to present with it as a sign of an underlying disease process than as a primary disease process. By itself, hypoalbuminemia decreases the total
heterogeneity of presentation is not well understood.[3]
Hypoalbuminemia can be caused through a number of different mechanisms, each with the 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.[7] Often, the cause is multifactorial as in liver cirrhosis, where reduced hepatic synthesis and increased capillary leakage combine to further decrease albumin levels. [citation needed]
Inflammation and infection
Albumin is considered a negative
TNF-α.[7] In patients with the overwhelming infections common in sepsis and septic shock, hypoalbuminemia 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.[3]
Liver disease
Healthy and cirrhotic liver. If present, hypoalbuminemia suggests advanced liver disease as seen in cirrhosis.
Albumin is synthesized in the
ascitic fluid), and even post-transcriptional changes to albumin itself.[8]
end-stage renal disease.[3] Alterations in fluid distribution and the presence of ongoing inflammation in chronic kidney disease in combination with hypoalbuminemia make fluid status control especially difficult.[5]
Malnutrition or malabsorption
A girl with the physical signs and symptoms of Kwashiorkor, which is an extreme form of malnutrition-associated hypoalbuminemia.
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.[10]
Low albumin levels can also indicate chronic
systemic lupus erythematosus.[3] 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.[3]
extravascular spaces (60%) within the body's different tissues. In the blood plasma, albumin makes up 55 to 60% of total plasma protein by mass, with globulins making up a large part of the rest. In hypoalbuminemia, the amount of albumin in the intravascular space or blood plasma is what is being measured, meaning that abnormal distribution within the two compartments may contribute to a relative hypoalbuminemia in the bloodstream with a normal level in the whole body.[3]
Once released into the body, albumin performs a number of functions that can be negatively affected by the reduced levels seen in hypoalbuminemia. These functions include regulation of
complement 5a (C5a) to reduce the overall inflammatory response.[7]
A number of
thyroxine, cortisol, testosterone), drugs, and other molecules are bound to albumin in the bloodstream and must be released from albumin before becoming biologically active. For example, calcium binds to albumin; in hypoalbuminemia, there is an increased amount of free ionized calcium, its biologically active form. In the presence of hypoalbuminemia, these functions are differentially affected, and the mechanisms by which they affect disease outcomes remains an area of active debate.[3]
Diagnosis
The serum albumin level is part of a standard panel of
brain natriuretic peptide to assess for cardiac failure.[3] If protein-losing enteropathy is suspected based on clinical suspicion, an alpha-1 antitrypsin test can be performed. If stool alpha-1 antitrypsin is elevated, this suggests excessive gastrointestinal protein loss.[3]
Management
Treatment of hypoalbuminemia is largely focused on the underlying cause and not on the hypoalbuminemia itself.
bacterial infections other than spontaneous bacterial peritonitis, hepatic encephalopathy, and chronic ascites. Its use in these indications remains controversial.[8] In kidney disease and nephrotic syndrome, albumin infusions as replacement for albumin loss to proteinuria is used in some cases of congenital nephrotic syndrome.[9]
Prognosis
By itself, low albumin levels are associated with increased mortality rate in the general population.[8] In disease states specifically, hypoalbuminemia has been used a predictive factor for poor outcomes in a number of conditions,[3] including periprosthetic joint infection treatment failure,[13] and cirrhosis.[8] Amongst patients admitted to intensive care units (ICUs), hypoalbuminemia is specifically associated with ICU-acquired muscle weakness.[14] In chronic kidney disease, hypoalbuminemia is an indicator of frailty, which is itself associated with complications, mental distress, quality of life impairment, resource utilization, and mortality.[15]
Epidemiology
Hypoalbuminemia is commonly found in hospitalized patients, patients in the ICU, and the elderly within the hospital and the community.[3] Amongst elderly patients, prevalence can be as high as 70%, as shown in a study from Southern Brasil.[3]
