Hypoalbuminemia (or hypoalbuminaemia) is a medical sign in which the level of albumin in the blood is abnormally low. It is a type of hypoproteinemia.

Albumin is a major protein in the human body, making up about 55-60% of total human plasma protein by mass. Many hormones, drugs, and other molecules are mostly bound to albumin in the bloodstream and must be released before becoming biologically active. For example, calcium binds to albumin and hypoalbuminemia leads to an increase in free ionized calcium.

Albumin is synthesized in the liver, and low serum albumin may be indicative of liver failure or diseases such as cirrhosis or chronic hepatitis. Hypoalbuminemia can also present as part of the nephrotic syndrome, in which protein is lost in the urine due to kidney damage. Low albumin levels can be an indicator of chronic malnutrition or protein losing enteropathy.

Hypoalbuminemia may cause generalized edema (swelling) via a decrease in oncotic pressure.

The serum albumin level is part of a standard panel of liver function tests. Levels below 3.5 grams per deciliter are generally considered low.

A low serum anion gap is frequently caused by hypoalbuminemia.

Along with obtaining a complete medical history, a series of biochemical tests are required in order to arrive at an accurate diagnosis that verifies the presence of the illness. In addition, imaging of the kidneys (for structure and presence of two kidneys) is sometimes carried out, and/or a biopsy of the kidneys. The first test will be a urinalysis to test for high levels of proteins, as a healthy subject excretes an insignificant amount of protein in their urine. The test will involve a 24-hour bedside urinary total protein estimation. The urine sample is tested for proteinuria (>3.5 g per 1.73 m per 24 hours). It is also examined for urinary casts, which are more a feature of active nephritis. Next a blood screen, comprehensive metabolic panel (CMP) will look for hypoalbuminemia: albumin levels of ≤2.5 g/dL (normal=3.5-5 g/dL). Then a Creatinine Clearance C test will evaluate renal function particularly the glomerular filtration capacity. Creatinine formation is a result of the breakdown of muscular tissue, it is transported in the blood and eliminated in urine. Measuring the concentration of organic compounds in both liquids evaluates the capacity of the glomeruli to filter blood. Electrolytes and urea levels may also be analysed at the same time as creatinine (EUC test) in order to evaluate renal function.

A lipid profile will also be carried out as high levels of cholesterol (hypercholesterolemia), specifically elevated LDL, usually with concomitantly elevated VLDL, is indicative of nephrotic syndrome.

A kidney biopsy may also be used as a more specific and invasive test method. A study of a sample’s anatomical pathology may then allow the identification of the type of glomerulonephritis involved. However, this procedure is usually reserved for adults as the majority of children suffer from minimum change disease that has a remission rate of 95% with corticosteroids. A biopsy is usually only indicated for children that are "corticosteroid resistant" as the majority suffer from focal and segmental glomeruloesclerosis.

Further investigations are indicated if the cause is not clear including analysis of auto-immune markers (ANA, ASOT, C3, cryoglobulins, serum electrophoresis), or ultrasound of the whole abdomen.

A broad classification of nephrotic syndrome based on underlying cause:

Nephrotic syndrome is often classified histologically:

There are no laboratory tests used to diagnose RVT.

Observing the patient's symptoms, medical history and imaging remain the fundamental source for diagnosing RVT. Imaging is used to detect the presence of a blood clot. In an abnormal kidney with RVT, a blood clot is present in the renal vein. In cases where the renal vein is suddenly and/or fully blocked, the kidneys will enlarge, reaching its maximum size within a week. An ultrasound imaging can be used to observe and track the size of the kidneys in RVT patients. Ultrasound is not efficient for use in detecting blood flow in the renal veins and artery. Instead a color doppler ultrasound may be used to detect renal blood flow. It is most commonly used to detect RVT in patients who have undergone renal transplantation. CT angiography is currently the top choice in diagnosing RVT. It is non-invasive, relatively cheap and fast with high accuracy. CT scanning can be used to detect renal enlargement, renal tumors, blood flow and other renal pathologies. An alternative is magnetic resonance angiography or MRA. It is non-invasive, fast and avoids radiation (unlike a CT scan) but it is relatively expensive. MRA produces detailed images of the renal blood flow, vesicle walls, the kidneys and any surrounding tissue. An inferior venocavography with selective venography can be used to rule out the diagnoses of RVT.

It is known that diabetes causes changes to factors associated with coagulation and clotting, however not much is known of the risk of thromboembolism, or clots, in diabetic patients. There are some studies that show that diabetes increases the risk of thromboembolism; other studies show that diabetes does not increase the risk of thromboembolism. A study conducted in the Umea University Hospital, in Sweden, observed patients that were hospitalized due to an thromboembolism from 1997 to 1999. The researchers had access to patient information including age, sex, vein thromboembolism diagnosis, diagnostic methods, diabetes type and medical history. This study concluded that there is, in fact, an increased risk of thromboembolism development in diabetic patients, possibly due to factors associated with diabetes or diabetes itself. Diabetic patients are twice as likely to develop a thromboembolism than are non-diabetic patient. The exact mechanism of how diabetes increases the risk of clot formation remains unclear and could possibly be a future direction for study.

From previous studies, it is known that long distance air travel is associated with high risk of venous thrombosis. Long periods of inactivity in a limited amount of space may be a reason for the increased risk of blood clot formation. In addition, bent knees compresses the vein behind the knee (the popliteal vein) and the low humidity, low oxygen, high cabin pressure and consumption of alcohol concentrate the blood. A recent study, published in the British Journal of Haematology in 2014, determined which groups of people, are most at risk for developing a clot during or after a long flight. The study focused on 8755 frequent flying employees from international companies and organizations. It found that travelers who have recently undergone a surgical procedure or who have a malignant disease such as cancer or who are pregnant are most at risk. Preventative measures before flying may be taken in these at-risk groups as a solution.

Patients who have undergone kidney transplant have a high risk of developing RVT (about 0.4% to 6%). RVT is known to account for a large proportion of transplanted kidney failures due to technical problems (damage to the renal vein), clotting disorders, diabetes, consumption of ciclosporin or an unknown problem. Patients who have undergone a kidney transplant are commonly prescribed ciclosporin, an immunosuppressant drug which is known to reduce renal blood flow, increase platelet aggregation in the blood and cause damage to the endothelial tissue of the veins. In a clinical study conducted by the Nuffield Department of Surgery at the Oxford Transplant Centre, UK, transplant patients were given low doses of aspirin, which has a some anti-platelet activity. There is risk of bleeding in transplant patients when using anticoagulants like warfarin and herapin. Low dosage of aspirin was used as an alternative. The study concluded that a routine low-dose of aspirin in kidney transplant patients who are also taking ciclosporin significantly reduces the risk of RVT development.

SCLS is often difficult to recognize and diagnose on initial presentation, and thus misdiagnoses are frequent. The characteristic triad of profound arterial hypotension, hemoconcentration (elevated hematocrit, leukocytosis, and thrombocytosis), and hypoalbuminemia in the absence of secondary causes of shock and infection, requires diagnosis in a monitored, hospital setting during or after an acute episode. The fact that the condition is exceedingly rare – an estimated one per million inhabitants – and that several other diseases exhibit features akin to SCLS, including secondary capillary-leak syndrome or hypoproteinemia, militate against early identification. Preserved consciousness, despite severe shock and hypotension, is an additional and most intriguing clinical manifestation often reported during episodes at hospital admission.

The natural history of SCLS episodes indicates they resolve spontaneously within 2-to-4 days, and that they consist of two distinct phases:

Physical examination to examine muscle wasting, laboratory investigations.

Disorders usually resolve after early treatment. If the treatment is delayed, the overall health of the child is improved but physical (reduced) and intellectual (mental disabilities) sequelae are feared. Without treatment or if treatment occurs too late, death is inevitable.

A high risk of death is identified by a brachial perimeter < 11 cm or by a weight-to-height threshold < -3 SD. In practice, malnourished children with edema are suffering from potentially life-threatening severe malnutrition.

Transfusion associated circulatory overload is prevented by avoiding unnecessary transfusions, closely monitoring patients receiving transfusions, transfusing smaller volumes of blood at a slower rate, and considering the use of diuretics. A pre-transfusion TACO checklist can be used to assess patients' risk of developing TACO.

TACO and TRALI are both respiratory complications following a transfusion. TACO and transfusion related acute lung injury (TRALI) are often difficult to distinguish in the acute situation. TACO is usually associated with hypertension and responds well to diuretics, TRALI is often associated with hypotension and diuretics have a minimal effect.

In children and some adults, FSGS presents as a nephrotic syndrome, which is characterized by edema (associated with weight gain), hypoalbuminemia (low serum albumin, a protein in the blood), hyperlipidemia and hypertension (high blood pressure). In adults, it may also present as kidney failure and proteinuria, without a full-blown nephrotic syndrome.

Ultrasound is routinely used in the evaluation of cirrhosis. It may show a small and nodular liver in advanced cirrhosis along with increased echogenicity with irregular appearing areas. Other liver findings suggestive of cirrhosis in imaging are an enlarged caudate lobe, widening of the fissures and enlargement of the spleen. An enlarged spleen (splenomegaly), which normally measures less than 11–12 cm in adults, is suggestive of cirrhosis with portal hypertension, in the right clinical context. Ultrasound may also screen for hepatocellular carcinoma, portal hypertension, and Budd-Chiari syndrome (by assessing flow in the hepatic vein).

Cirrhosis is diagnosed with a variety of elastography techniques. Because a cirrhotic liver is generally stiffer than a healthy one, imaging the liver's stiffness can give diagnostic information about the location and severity of cirrhosis. Techniques used include transient elastography, acoustic radiation force impulse imaging, supersonic shear imaging and magnetic resonance elastography. Compared to a biopsy, elastography can sample a much larger area and is painless. It shows a reasonable correlation with the severity of cirrhosis.

Other tests performed in particular circumstances include abdominal CT and liver/bile duct MRI (MRCP).

The severity of cirrhosis is commonly classified with the Child-Pugh score. This scoring system uses bilirubin, albumin, INR, the presence and severity of ascites, and encephalopathy to classify patients into class A, B, or C. Class A has a favourable prognosis, while class C is at high risk of death. This system was devised in 1964 by Child and Turcotte, and modified in 1973 by Pugh and others.

More modern scores, used in the allocation of liver transplants but also in other contexts, are the Model for End-Stage Liver Disease (MELD) score and its pediatric counterpart, the Pediatric End-Stage Liver Disease (PELD) score.

The hepatic venous pressure gradient, (difference in venous pressure between afferent and efferent blood to the liver) also determines the severity of cirrhosis, although it is hard to measure. A value of 16 mm or more means a greatly increased risk of death.

Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome in children and adolescents, as well as a leading cause of kidney failure in adults. It is also known as "focal glomerular sclerosis" or "focal nodular glomerulosclerosis". It accounts for about a sixth of the cases of nephrotic syndrome. (Minimal change disease (MCD) is by far the most common cause of nephrotic syndrome in children: MCD and primary FSGS may have a similar cause.)

The disease can be treated only to slow down the development, by use of cyclosporine A and ACE inhibitors, but not stopped or cured.

Affected male and carrier female dogs generally begin to show signs of the disease at two to three months of age, with proteinuria. By three to four months of age, symptoms include for affected male dogs: bodily wasting and loss of weight, proteinuria & hypoalbuminemia. Past nine months of age, hypercholesterolemia may be seen. In the final stages of the disease, at around 15 months of age for affected males, symptoms are reported as being renal failure, hearing loss and death. Since the condition is genetically dominant, diagnosis would also include analysis of the health of the sire and dam of the suspected affected progeny if available.

Once a pleural effusion is diagnosed, its cause must be determined. Pleural fluid is drawn out of the pleural space in a process called thoracentesis, and it should be done in almost all patients who have pleural fluid that is at least 10 mm in thickness on CT, ultrasonography, or lateral decubitus X-ray and that is new or of uncertain etiology. In general, the only patients who do not require thoracentesis are those who have heart failure with symmetric pleural effusions and no chest pain or fever; in these patients, diuresis can be tried, and thoracentesis is avoided unless effusions persist for more than 3 days. In a thoracentesis, a needle is inserted through the back of the chest wall in the sixth, seventh, or eighth intercostal space on the midaxillary line, into the pleural space. The use of ultrasound to guide the procedure is now standard of care as it increases accuracy and decreases complications. After removal, the fluid may then be evaluated for:

1. Chemical composition including protein, lactate dehydrogenase (LDH), albumin, amylase, pH, and glucose

2. Gram stain and culture to identify possible bacterial infections

3. White and red blood cell counts and differential white blood cell counts

4. Cytopathology to identify cancer cells, but may also identify some infective organisms

5. Other tests as suggested by the clinical situation – lipids, fungal culture, viral culture, tuberculosis cultures, lupus cell prep, specific immunoglobulins

The most reliable test for EPI in dogs and cats is serum trypsin-like immunoreactivity (TLI). A low value indicates EPI. Fecal elastase levels may also be used for diagnosis in dogs.

In dogs, the best treatment is to supplement its food with dried pancreatic extracts. There are commercial preparations available, but chopped bovine pancreas from the butcher can also be used (pork pancreas should not be used because of the rare transmission of pseudorabies). Symptoms usually improve within a few days, but lifelong treatment is required to manage the condition. A rare side-effect of use of dried pancreatic extracts is oral ulceration and bleeding.

Because of malabsorption, serum levels of cyanocobalamin (vitamin B12) and tocopherol (vitamin E) may be low. These may be supplemented, although since cyanocobalamin contains the toxic chemical cyanide, dogs that have serious cobalamin issues should instead be treated with hydroxocobalamin or methylcobalamin. Cyanocobalamin deficiency is very common in cats with EPI because about 99 percent of intrinsic factor (which is required for cyanocobalamin absorption from the intestine) is secreted by the pancreas. In dogs, this figure is about 90 percent, and only about 50 percent of dogs have this deficiency. Cats may suffer from Vitamin K deficiencies. If there is bacterial overgrowth in the intestine, antibiotics should be used, especially if treatment is not working. In dogs failing to gain weight or continuing to show symptoms, modifying the diet to make it low-fiber and highly digestible may help. Despite previous belief that low-fat diets are beneficial in dogs with EPI, more recent studies have shown that a high-fat diet may increase absorption of nutrients and better manage the disease. However, it has been shown that different dogs respond to different dietary modifications, so the best diet must be determined on a case-by-case basis.

One possible sequela, volvulus (mesenteric torsion) is a rare consequence of EPI in dogs.

Ultrasonography and magnetic resonance imaging of the hands and/or feet have been proposed as useful diagnostic investigations in RS3PE.

Some studies linked RS3PE to HLA-B27 whereas others have not.

A pleural effusion appears as an area of whiteness on a standard posteroanterior chest X-ray. Normally, the space between the visceral pleura and the parietal pleura cannot be seen. A pleural effusion infiltrates the space between these layers. Because the pleural effusion has a density similar to water, it can be seen on radiographs. Since the effusion has greater density than the rest of the lung, it gravitates towards the lower portions of the pleural cavity. The pleural effusion behaves according to basic fluid dynamics, conforming to the shape of pleural space, which is determined by the lung and chest wall. If the pleural space contains both air and fluid, then an air-fluid level that is horizontal will be present, instead of conforming to the lung space. Chest radiographs in the lateral decubitus position (with the patient lying on the side of the pleural effusion) are more sensitive and can detect as little as 50 mL of fluid. At least 300 mL of fluid must be present before upright chest X-rays can detect a pleural effusion (e.g., blunted costophrenic angles).

Chest computed tomography is more accurate for diagnosis and may be obtained to better characterize the presence, size, and characteristics of a pleural effusion. Lung ultrasound, nearly as accurate as CT and more accurate than chest X-ray, is increasingly being used at the point of care to diagnose pleural effusions, with the advantage that it is a safe, dynamic, and repeatable imaging modality. To increase diagnostic accuracy of detection of pleural effusion sonographically, markers such as boomerang and VIP signs can be utilized.

The three main tests used in considering a diagnosis of EPI are Fecal elastase test, fecal fat test, and a direct pancreatic function test. The latter being a limitedly used test that assesses exocrine function in the pancreas by inserting a tube into the small intestine to collect pancreatic secretions.

A doctor will take a thorough medical history, and may take blood tests as well as examining liver and kidney function. Improvements have also been reported from treating malnutrition associated with zinc deficiency and other minerals. Intracellular (red blood cell) assays are more sensitive than tests for plasma levels.

Other possible causes (eg differential diagnosis) of large folds within the stomach include: Zollinger-Ellison syndrome, cancer, infection (cytomegalovirus/CMV, histoplasmosis, syphilis), and infiltrative disorders such as sarcoidosis.

The large folds of the stomach, as seen in Ménétrier disease, are easily detected by x-ray imaging following a barium meal or by endoscopic methods. Endoscopy with deep mucosal biopsy (and cytology) is required to establish the diagnosis and exclude other entities that may present similarly. A non-diagnostic biopsy may lead to a surgically obtained full-thickness biopsy to exclude malignancy. CMV and helicobacter pylori serology should be a part of the evaluation.

Twenty-four-hour pH monitoring reveals hypochlorhydria or achlorhydria, and a chromium-labelled albumin test reveals increased GI protein loss. Serum gastrin levels will be within normal limits.

According the Fifth WHO Expert Committee on Filariasis , the most common method of classification of lymphedema is as follows: (The same classification method can be used for both primary and secondary lymphedema)

The International Society of Lymphology (ISL) Staging System is based solely on subjective symptoms, making it prone to substantial observer bias. Imaging modalities have been suggested as useful adjuncts to the ISL staging to clarify the diagnosis. The lymphedema expert Dr. Ming-Huei Cheng developed a Cheng’s Lymphedema Grading tool to assess the severity of extremity lymphedema based on objective limb measurements and providing appropriate options for management.