Bright's disease

Bright's disease is a historical classification of kidney diseases that would be described in modern medicine as acute or chronic nephritis. The term is no longer used, as diseases are now classified according to their more fully understood causes^.

It is typically denoted by the presence of serum albumin (blood plasma protein) in the urine, and frequently accompanied by edema and hypertension.

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 (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, 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 happens readily 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 Alkali and Acid balance through consuming various foods and drink, 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.

Nephritis

Nephritis is inflammation of the nephrons in the kidneys. The word "nephritis" was imported from Latin, which took it from Greek: νεφρίτιδα. The word comes from the Greek νεφρός - nephro- meaning "of the kidney" and -itis meaning "inflammation". Nephritis is often caused by infections, toxins, and auto-immune diseases.

• Glomerulonephritis is inflammation of the glomeruli. (When the term "nephritis" is used without qualification, this is often the condition meant.)
• Interstitial nephritis or tubulo-interstitial nephritis is inflammation of the spaces between renal tubules.
• Pyelonephritis is inflammation that results from a urinary tract infection that reaches the pyelum (pelvis) of the kidney.
• Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system.

Nephritis is the most common producer of glomerular injury. It is a disturbance of the glomerular structure with inflammatory cell proliferation. This can lead to reduced glomerular blood flow, leading to reduced urine output (oliguria) and retention of waste products (uremia). As a result, red blood cells may leak out of damaged glomeruli, causing blood to appear in the urine (hematuria). Low renal blood flow activates the renin-angiotensin-aldosterone system (RAAS), causing fluid retention and mild hypertension.

Nephritis refers to inflammation of one or both kidneys. It can be caused by infection, but is most commonly caused by autoimmune disorders that affect the major organs. For example, those with lupus are at a much higher risk for developing nephritis. In rare cases nephritis can be genetically inherited, though it may not present in childhood.

Nephritis is a serious medical condition which is the ninth highest cause of human death. As the kidneys inflame, they begin to excrete needed protein from the body into the urine stream. This condition is called proteinuria. Loss of necessary protein due to nephritis can result in several life-threatening symptoms. Most dangerous in cases of nephritis is the loss of protein that keeps blood from clotting. This can result in blood clots causing sudden stroke.

Hyperglycemia

Hyperglycemia, or high blood sugar, is a condition in which an excessive amount of glucose circulates in the blood plasma. This is generally a glucose level higher than 10 mmol/l (180 mg/dl), but symptoms may not start to become noticeable until even higher values such as 15-20 mmol/l (270-360 mg/dl). However, chronic levels exceeding 7 mmol/l (125 mg/dl) can produce organ damage.

The origin of the term is Greek: hyper-, meaning excessive; -glyc-, meaning sweet; and -emia, meaning "of the blood".

Signs and symptoms

Temporary hyperglycemia is often benign and asymptomatic. Blood glucose levels can rise well above normal for significant periods without producing any permanent effects or symptoms. However, chronic hyperglycemia at levels more than slightly above normal can produce a very wide variety of serious complications over a period of years, including kidney damage, neurological damage, cardiovascular damage, damage to the retina etc.

In diabetes mellitus (by far the most common cause of chronic hyperglycemia), treatment aims at maintaining blood glucose at a level as close to normal as possible, in order to avoid these serious long-term complications.

Acute hyperglycemia involving glucose levels that are extremely high is a medical emergency and can rapidly produce serious complications (such as fluid loss through osmotic diuresis). It is most often seen in persons who have uncontrolled insulin-dependent diabetes.

The following symptoms may be associated with acute or chronic hyperglycemia, with the first three composing the classic hyperglycemic triad:

• Polyphagia - frequent hunger, especially pronounced hunger
• Polydipsia - frequent thirst, especially excessive thirst
• Polyuria - frequent urination
• Blurred vision
• Fatigue (sleepiness).
• Weight loss
• Poor wound healing (cuts, scrapes, etc.)
• Dry mouth
• Dry or itchy skin
• Tingling in feet or heels
• Erectile dysfunction
• Recurrent infections, external ear infections (swimmer's ear)
• Cardiac arrhythmia
• Stupor
• Coma

Frequent hunger without other symptoms can also indicate that blood sugar levels are too low. This may occur when people who have diabetes take too much oral hypoglycemic medication or insulin for the amount of food they eat. The resulting drop in blood sugar level to below the normal range prompts a hunger response. This hunger is not usually as pronounced as in Type I diabetes, especially the juvenile onset form, but it makes the prescription of oral hypoglycemic medication difficult to manage.

Polydipsia and polyuria occur when blood glucose levels rise high enough to result in excretion of excess glucose via the kidneys (glycosuria), producing osmotic diuresis.

Symptoms of Diabetic Ketoacidosis may include:

• Ketoacidosis
• Kussmaul hyperventilation: deep, rapid breathing
• Confusion or a decreased level of consciousness
• Dehydration due to glycosuria and osmotic diuresis
• Acute hunger and/or thirst
• 'Fruity' smelling breath odor
• Impairment of cognitive function, along with increased sadness and anxiety

Causes

Diabetes mellitus

Chronic hyperglycemia that persists even in fasting states is most commonly caused by diabetes mellitus, and in fact chronic hyperglycemia is the defining characteristic of the disease. Intermittent hyperglycemia may be present in prediabetic states. Acute episodes of hyperglycemia without an obvious cause may indicate developing diabetes or a predisposition to the disorder.

In diabetes mellitus, hyperglycemia is usually caused by low insulin levels (Diabetes mellitus type 1) and/or by resistance to insulin at the cellular level (Diabetes mellitus type 2), depending on the type and state of the disease. Low insulin levels and/or insulin resistance prevent the body from converting glucose into glycogen (a starch-like source of energy stored mostly in the liver), which in turn makes it difficult or impossible to remove excess glucose from the blood. With normal glucose levels, the total amount of glucose in the blood at any given moment is only enough to provide energy to the body for 20-30 minutes, and so glucose levels must be precisely maintained by the body's internal control mechanisms. When the mechanisms fail in a way that allows glucose to rise to abnormal levels, hyperglycemia is the result.

Drugs

Certain medications increase the risk of hyperglycemia, including corticosteroids, octreotide, beta blockers, epinephrine, thiazide diuretics, corticosteroids, niacin, pentamidine, protease inhibitors, L-asparaginase, and some antipsychotic agents. The acute administration of stimulants such as amphetamine typically produces hyperglycemia; chronic use, however, produces hypoglycemia. Some of the newer, double action anti-depressants such as Zyprexa (Olanzapine), and Cymbalta (Duloxetine), can also cause significant hyperglycemia.

Critical illness

A high proportion of patients suffering an acute stress such as stroke or myocardial infarction may develop hyperglycemia, even in the absence of a diagnosis of diabetes. Human and animal studies suggest that this is not benign, and that stress-induced hyperglycemia is associated with a high risk of mortality after both stroke and myocardial infarction.

Plasma glucose >120 mg/dl in the absence of diabetes is a clinical sign of sepsis.

Physical trauma, surgery and many forms of severe stress can temporarily increase glucose levels.

Physiological stress

Hyperglycemia occurs naturally during times of infection and inflammation. When the body is stressed, endogenous catecholamines are released that - amongst other things - serve to raise the blood glucose levels. The amount of increase varies from person to person and from inflammatory response to response. As such, no patient with first-time hyperglycemia should be diagnosed immediately with diabetes if that patient is concomitantly ill with something else. Further testing, such as a fasting plasma glucose, random plasma glucose, or two-hour postprandial plasma glucose level, must be performed.

Treatment

Treatment of hyperglycemia requires elimination of the underlying cause, e.g., treatment of diabetes when diabetes is the cause. Acute hyperglycemia can be treated by direct administration of insulin in most cases. Severe hyperglycemia can be treated with oral hypoglycemic therapy and lifestyle modification.