The bright's disease, also known as nephritis or glomerulonephritis, is inflammation of the structures in the kidney, which produce urine: the nephrons and the glomeruli. The Bowman's capsule, a double-walled capsule, surrounds the glomeruli, which are small circular clusters of capillaries (microscopic blood vessels). In turn, this Bowman's capsule connects with a long tubule. The attached tubule and the capsule are called a nephron. Glomerulonephritis affects the nephrons, the glomeruli, and the tissues between the nephrons.
Bright's Disease Symptoms and Signs
Let us understand the Bright's disease symptoms and Signs in detail.
Bright's disease was named after an English physician named Richard Bright's, who first described the signs and symptoms of the disease in 1827. He identified 25 cases of dropsy (or oedema) in his Reports of Medical Cases, which he attributed to kidney disease. The signs and symptoms included are inflammation of serous membranes, apoplexy, haemorrhages, blindness, coma, and convulsions. Several of these cases were found to have albumin in their urine (which is detected by the candle-heat and spoon coagulation) and showed the striking morbid changes of the kidneys at autopsy. Bright's disease is characterised by a triad of albumin, kidney dropsy, and urinary disease.
Subsequent work by Bright, including others, indicated an association with cardiac hypertrophy, which was attributed by Bright's to heart stimulation. Frederick Akbar Mahomed's subsequent research showed that a rise in blood pressure, as well as a rise in blood pressure and increased resistance to flow, could precede the presence of albumin in the urine, which was thought to explain cardiac hypertrophy.
Bright's disease is now understood to be caused by a complex and wide variety of kidney diseases; as a result, the term Bright's disease is only used for historical purposes. Patients with diabetes were often diagnosed with the condition, and at least a few of these cases would most likely lead to a current diagnosis of diabetic nephropathy.
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Every kidney has nearly one million nephrons that filter water and other substances out of the blood to produce urine.
Glomerulonephritis can be caused by the disease states, which disrupt the normal function of the immune system (for example, systemic lupus erythematosus), compromise either the function or damage the glomeruli (for example, high blood pressure [hypertension] or the structure of systemic vasculature (for example., inflammation of the arteries), or diabetic (nephropathy). Also, glomerulonephritis may arise from streptococcal infections such as strep throat. However, in some of the cases, a cause may not be identified. Glomerulonephritis can only occur once or may recur. The successive stages of the disease are called subacute, acute, and chronic.
Acute glomerulonephritis can be characterized by severe inflammation, renal (or kidney) swelling, insufficiency, severe back pain, and increased blood pressure. Usually, recovery is fairly complete after an episode of acute glomerulonephritis, but minor infections can do further damage to the kidneys and bring on the chronic and subacute stages. In the disease's acute form, the kidneys are swollen, the capsule covering every kidney is stretched and taut, the surface is grey and smooth, and usually, there are several small haemorrhages from the capillaries. The whole complex of nephrons and glomeruli swells.
Subacute glomerulonephritis does not always accompany acute attacks; however, if it does, it is normally followed by an acute episode that occurred months or years before. The kidney will become considerably enlarged, the surface is pale and smooth, and the internal tissue is darker compared to normal. The paleness is caused by a reduction of blood flow to the surface of the kidney, as well as a high concentration of fat (or lipid) droplets.
Bowman's capsules fill up with extra surface (or epithelial) cells, mineral crystals, and red blood cells, causing the nephron tubules to degenerate. Due to the breakdown of kidney tissue, a larger amount of blood protein is lost in the urine than should be released normally. Red blood cells forced via constricted glomeruli become distorted, crushed, and fragmented; their loss is leading to anaemia.
Usually, chronic glomerulonephritis follows another two stages, if the affected person survives very long enough, but it has been found in some individuals who apparently have not had kidney disease previously. In this particular stage, the kidney is reduced mostly to scar tissue. It is shrivelled and small, and the surface is granular. Due to the blood being unable to filter waste products, abnormal quantities of the nitrogenous substances present in the blood cause the condition called uremia.
Treatment of all the forms of glomerulonephritis is majorly directed towards the controlling of high blood pressure with diuretics and antihypertensive agents and through changes in the diet that includes decreased salt intake and fluid restriction. Whereas a few patients respond to the treatment with some anti-inflammatory drugs, dialysis can be necessary to manage uremia.