Bright’s disease. From Wikipedia, the free encyclopedia
Bright’s disease. From Wikipedia, the free encyclopedia
Bright’s disease is a historical classification of kidney diseases that would be described in modern medicine as acute or chronic nephritis. It is typically denoted by the presence of serum albumin (blood plasma protein) in the urine, and frequently accompanied by edema and hypertension.
Contents
1 Symptoms
2 Treatment
3 Notable people with Bright’s disease
4 References
Symptoms
These common symptoms of kidney disease were first described in 1827 by the English physician Richard Bright. It is now known that the symptoms accompany various morbid kidney conditions. Thus, the term Bright’s disease is retained strictly for historical application.
The formation of bilateral kidney stones often indicates underlying chronic kidney disease. These stones involve salt crystal formations such as calcium oxalate. Excess serum calcium can result from hypovitaminosis D, or vitamin D deficiency, that causes the body initially to lose serum calcium to the point where parathyroid hormone is produced to leach sufficient amounts of calcium from the bones, (resulting in bone loss) to more than make up the difference (shutting down parathyroid hormone production). Oxalic acid is found in chocolate, peanuts, certain types of berries, and other foods,[4] and when combined with calcium will form calcium oxalate crystal kidney stones that can drive up blood pressure like any other serum salt, block urinary flow within the kidneys, and cause physical kidney damage and pain. Researchers at Rockefeller University Hospital are studying arteriosclerosis in connection with this vitamin D deficiency, calcium plaque build-up, and kidney problems.
The symptoms are usually severe. Back pain, phantom testicular pain in males, elevated blood pressure, vomiting and fever commonly signal an attack. Edema, varying in degree from slight puffiness of the face to an accumulation of fluid sufficient to distend the whole body, and sometimes severely restricted breathing, is very common. Urine is reduced in quantity, is of dark, smoky or bloody color, and has higher levels of albumin (albuminuria). Under the microscope, blood corpuscles and urinary casts are found in abundance.
This state of acute inflammation may severely limit normal daily activities, and if left unchecked, may lead to one of the chronic forms of Bright’s disease. In many cases though, the inflammation is reduced, marked by increased urine output and the gradual disappearance of its albumen and other abnormal by-products. A reduction in edema and a rapid recovery of strength usually follows.
Treatment
Acute Bright’s disease was treated with local depletion (bleeding or blood-letting to reduce blood pressure), warm baths, diuretics, and laxatives. The disease was diagnosed often in diabetic patients. There was no successful treatment for chronic Bright’s disease, though dietary modifications were sometimes suggested. See Hay diet, named after William Howard Hay MD, who suffered from the illness and supposedly cured himself after accepted medical methods of the early 1900s failed to do so. The diet involves promoting alkali and acid balance through consuming various foods and beverages, thereby lowering the kidney’s involvement with blood pH balancing. Successful treatment for type II diabetes would reverse elevated glucose and insulin insensitivity problems throughout the body, especially in nerves and kidneys.
http://en.wikipedia.org/wiki/Bright%27s_disease
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