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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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Despite expensive treatments, lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis.
The long-term use of lithium, a medication commonly used to treat bipolar disorder and schizoaffective disorders, is known to cause nephropathy.
Minimal change disease has been called by many other names in the medical literature, including minimal change nephropathy, minimal change nephrosis, minimal change nephrotic syndrome, minimal change glomerulopathy, foot process disease (referring to the foot processes of the podocytes), nil disease (referring to the lack of pathologic findings on light microscopy), nil lesions, lipid nephrosis, and lipoid nephrosis.
There are three main mechanisms to cause proteinuria:
- Due to disease in the glomerulus
- Because of increased quantity of proteins in serum (overflow proteinuria)
- Due to low reabsorption at proximal tubule (Fanconi syndrome)
Proteinuria can also be caused by certain biological agents, such as bevacizumab (Avastin) used in cancer treatment. Excessive fluid intake (drinking in excess of 4 litres of water per day) is another cause.
Also leptin administration to normotensive Sprague Dawley rats during pregnancy significantly increases urinary protein excretion.
Proteinuria may be a sign of renal (kidney) damage. Since serum proteins are readily reabsorbed from urine, the presence of excess protein indicates either an insufficiency of absorption or impaired filtration. People with diabetes may have damaged nephrons and develop proteinuria. The most common cause of proteinuria is diabetes, and in any person with proteinuria and diabetes, the cause of the underlying proteinuria should be separated into two categories: diabetic proteinuria versus the field.
With severe proteinuria, general hypoproteinemia can develop which results in
diminished oncotic pressure. Symptoms of diminished oncotic pressure may include ascites, edema and hydrothorax.
Proteinuria may be a feature of the following conditions:
- Nephrotic syndromes (i.e. intrinsic renal failure)
- Pre-eclampsia
- Eclampsia
- Toxic lesions of kidneys
- Amyloidosis
- Collagen vascular diseases (e.g. systemic lupus erythematosus)
- Dehydration
- Glomerular diseases, such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease (lipoid nephrosis)
- Strenuous exercise
- Stress
- Benign orthostatic (postural) proteinuria
- Focal segmental glomerulosclerosis (FSGS)
- IgA nephropathy (i.e. Berger's disease)
- IgM nephropathy
- Membranoproliferative glomerulonephritis
- Membranous nephropathy
- Minimal change disease
- Sarcoidosis
- Alport's syndrome
- Diabetes mellitus (diabetic nephropathy)
- Drugs (e.g. NSAIDs, nicotine, penicillamine, lithium carbonate, gold and other heavy metals, ACE inhibitors, antibiotics, or opiates (especially heroin)
- Fabry's disease
- Infections (e.g. HIV, syphilis, hepatitis, poststreptococcal infection, urinary schistosomiasis)
- Aminoaciduria
- Fanconi syndrome in association with Wilson disease
- Hypertensive nephrosclerosis
- Interstitial nephritis
- Sickle cell disease
- Hemoglobinuria
- Multiple myeloma
- Myoglobinuria
- Organ rejection:
- Ebola virus disease
- Nail patella syndrome
- Familial Mediterranean fever
- HELLP Syndrome
- Systemic lupus erythematosus
- Granulomatosis with polyangiitis
- Rheumatoid arthritis
- Glycogen storage disease type 1
- Goodpasture's syndrome
- Henoch–Schönlein purpura
- A urinary tract infection which has spread to the kidney(s)
- Sjögren's syndrome
- Post-infectious glomerulonephritis
Osmotic nephrosis refers to structural changes that occur at the cellular level in the human kidney. Cells, primarily of the straight proximal tubule, swell due to the formation of large vacuoles in the cytoplasm. These vacuoles occur in the presence of large amounts of certain solutes circulating in the tubules. However, despite the condition's name, the solutes do not cause change through osmotic forces but through pinocytosis. Once inside the cytoplasm, pinocytic vacuoles combine with each other and with lysosomes to form large vacuoles that appear transparent under microscopic examination.
There may be no symptomatic presentation with this condition, or it may confused with other nephrotic conditions such as Tubular calcineurin-inhibitor toxicity. Affected cells of the proximal tubule may be passed in the urine, but a kidney biopsy is the only sure way to make a diagnosis.
Responsible exogenous solutes include sucrose-containing IVIg, mannitol, dextran, contrast dye, and hydroxyethyl starch. Prevention includes standard preventions for iatrogenic kidney damage. Osmotic nephrosis is usually reversible but can lead to chronic renal failure.
Minimal change disease is most common in very young children but can occur in older children and adults. It is by far the most common cause of nephrotic syndrome in children between the ages of 1 and 7, accounting for the majority (about 90%) of these diagnoses. Among teenagers who develop nephrotic syndrome, it is caused by minimal change disease about half the time. It can also occur in adults but accounts for less than 20% of adults diagnosed with nephrotic syndrome. Among children less than 10 years of age, boys seem to be more likely to develop minimal change disease than girls. Minimal change disease is being seen with increasing frequency in adults over the age of 80.
People with one or more autoimmune disorders are at increased risk of developing minimal change disease. Having minimal change disease also increases the chances of developing other autoimmune disorders.
Nephrosis is any of various forms of kidney disease (nephropathy). In an old and broad sense of the term, it is any nephropathy, but in current usage the term is usually restricted to a narrower sense of nephropathy without inflammation or neoplasia, in which sense it is distinguished from nephritis, which involves inflammation. It is also defined as any purely degenerative disease of the renal tubules. Nephrosis is characterized by a set of signs called the nephrotic syndrome. Nephrosis can be a primary disorder or can be secondary to another disorder. Nephrotic complications of another disorder can coexist with nephritic complications. In other words, nephrosis and nephritis can be pathophysiologically contradistinguished, but that does not mean that they cannot occur simultaneously.
Types of nephrosis include amyloid nephrosis and osmotic nephrosis.
Glomerulonephrosis is a non-inflammatory disease of the kidney (nephrosis) presenting primarily in the glomerulus (a glomerulopathy).
It can be contrasted to glomerulonephritis, which implies inflammation.
It can be caused by diethylnitrosamine.
The hypovolemia (extracellular volume loss) is due to total body sodium loss. The hyponatremia is caused by a relatively smaller loss in total body water.
- any cause of hypovolemia such as prolonged vomiting, decreased oral intake, severe diarrhea
- diuretic use (due to the diuretic causing a volume depleted state and thence ADH release, and not a direct result of diuretic-induced urine sodium loss)
- Addison's disease and congenital adrenal hyperplasia in which the adrenal glands do not produce enough steroid hormones (combined glucocorticoid and mineralocorticoid deficiency)
- pancreatitis
Prolonged periods of exercise may be a cause, known as exercise-associated hyponatremia (EAH). It is common in marathon runners and participants of other endurance events. The use of MDMA can result in hyponatremia. This likely occurs as a result of fluid loss via sweating and replacement with water without electrolytes.
There is volume expansion in the body, no edema, but hyponatremia occurs
- SIADH (and its many causes)
- Hypothyroidism
- Not enough ACTH
Daentl Townsend Siegel syndrome is a very rare disorder characterized by blue sclerae, kidney malfunction, thin skin, and hydrocephalus. It was first identified by D.L. Daentl et al. in 1978. Daentl Townsend Siegel syndrome is also known as "Hydrocephalus blue sclera nephropathy" and "Familial nephrosis, hydrocephalus, thin skin, blue sclerae syndrome".