"trunk, and ends under the collarbone. (2)The Bladder, a Yang organ, stores and removes fluid from the body by receiving Kidney chi. Imbalance of the Bladder leads to frequent or uncontrolled urination. The Bladder Meridian begins in the corner of the eye, moves down the back, and ends on the back of the knee. The Bladder also has another line, which starts alongside the previous line, moves down to the outer edge of the foot and ends on the small toe. The body in traditional Chinese medicine The model of the body in traditional Chinese medicine (TCM) has the following"
"begins in the immune system cells). Lupus nephritis Lupus nephritis (also known as SLE nephritis) is an inflammation of the kidneys caused by systemic lupus erythematosus (SLE), an autoimmune disease. It is a type of glomerulonephritis in which the glomeruli become inflamed. As the result of SLE, the cause of glomerulonephritis is said to be ""secondary"" and has a different pattern and outcome from conditions with a ""primary"" cause originating in the kidney. Class I disease (minimal mesangial glomerulonephritis) in its histology has a normal appearance under a light microscope, but mesangial deposits are visible under an electron microscope. At"
"Lupus nephritis Lupus nephritis (also known as SLE nephritis) is an inflammation of the kidneys caused by systemic lupus erythematosus (SLE), an autoimmune disease. It is a type of glomerulonephritis in which the glomeruli become inflamed. As the result of SLE, the cause of glomerulonephritis is said to be ""secondary"" and has a different pattern and outcome from conditions with a ""primary"" cause originating in the kidney. Class I disease (minimal mesangial glomerulonephritis) in its histology has a normal appearance under a light microscope, but mesangial deposits are visible under an electron microscope. At this stage urinalysis is normal. Class"
"therefore it is sometimes called Berger’s disease. IgA nephropathy IgA nephropathy (IgAN), also known as IgA nephritis, Berger's disease () (and variations), or synpharyngitic glomerulonephritis, is a disease of the kidney (or nephropathy) and the immune system; specifically it is a form of glomerulonephritis or an inflammation of the glomeruli of the kidney. Aggressive Berger's disease (a rarer form of the disease) can attack other major organs, such as the liver, skin and heart. IgA nephropathy is the most common glomerulonephritis worldwide, however aggressive Berger's disease is on the NORD list of rare diseases. Primary IgA nephropathy is characterized by"
"glomerulosclerosis (8%) and mesangiocapillary glomerulonephritis (6%). In adults the most common disease is mesangiocapillary glomerulonephritis (30-40%), followed by focal and segmental glomeruloesclerosis (15-25%) and minimal change disease (20%). The latter usually presents as secondary and not primary as occurs in children. Its main cause is diabetic nephropathy. It usually presents in a patient's 40s or 50s. Of the glomerulonephritis cases approximately 60% to 80% are primary, while the remainder are secondary. There are also differences in epidemiology between the sexes, the disease is more common in men than in women by a ratio of 2 to 1. The epidemiological data"
"IgA nephropathy IgA nephropathy (IgAN), also known as IgA nephritis, Berger's disease () (and variations), or synpharyngitic glomerulonephritis, is a disease of the kidney (or nephropathy) and the immune system; specifically it is a form of glomerulonephritis or an inflammation of the glomeruli of the kidney. Aggressive Berger's disease (a rarer form of the disease) can attack other major organs, such as the liver, skin and heart. IgA nephropathy is the most common glomerulonephritis worldwide, however aggressive Berger's disease is on the NORD list of rare diseases. Primary IgA nephropathy is characterized by deposition of the IgA antibody in the"
"it usually affects the entire glomerulus, it can affect parts of the glomerulus in some cases. Treatment of secondary membranous nephropathy is guided by the treatment of the original disease. For treatment of idiopathic membranous nephropathy, the treatment options include immunosuppressive drugs and non-specific anti-proteinuric measures. Recommended first line therapy often includes: cyclophosphamide alternating with a corticosteroid. Perhaps the most difficult aspect of membranous glomerulonephritis is deciding which people to treat with immunosuppressive therapy as opposed to simple ""background"" or anti-proteinuric therapies. A large part of this difficulty is due to a lack of ability to predict which people will"
"the afferent arteriole. It contains three components: the macula densa, juxtaglomerular cells, and extraglomerular mesangial cells. Diseases of the nephron predominantly affect either the glomeruli or the tubules. Glomerular diseases include diabetic nephropathy, glomerulonephritis and IgA nephropathy; renal tubular diseases include acute tubular necrosis, renal tubular acidosis, and polycystic kidney disease. Nephron The nephron (from Greek νεφρός – nephros, meaning ""kidney"") is the microscopic structural and functional unit of the kidney. It is composed of a renal corpuscle and a renal tubule. The renal corpuscle consists of a tuft of capillaries called a glomerulus and an encompassing Bowman's capsule. The"
"lead to end stage renal disease. Factors associated with a poorer prognosis in these cases include level of proteinuria, blood pressure control and kidney function (GFR). Without treatment nephrotic syndrome has a very bad prognosis especially ""rapidly progressing glomerulonephritis"", which leads to acute kidney failure after a few months. Nephrotic syndrome can affect any age, although it is mainly found in adults with a ratio of adults to children of 26 to 1. The syndrome presents in different ways in the two groups: the most frequent glomerulopathy in children is minimal change disease (66% of cases), followed by focal segmental"
"water from within the nephron and returning it to the venous vasculature when appropriate. Some diseases of the nephron predominantly affect either the glomeruli or the tubules. Glomerular diseases include diabetic nephropathy, glomerulonephritis and IgA nephropathy; renal tubular diseases include acute tubular necrosis and polycystic kidney disease. The nephron is the functional unit of the kidney. Each nephron is composed of a renal corpuscle, the initial filtering component; and a renal tubule that processes and carries away the filtered fluid. The renal corpuscle is the site of the filtration of blood plasma. The renal corpuscle consists of the glomerulus, and"
"Glomerulus (kidney) The glomerulus (), plural glomeruli, is a network of capillaries known as a ""tuft"", located at the beginning of a nephron in the kidney. The tuft is structurally supported by intraglomerular mesangial cells. The blood is filtered across the capillary walls of this tuft through the glomerular filtration barrier, which yields its filtrate of water and soluble substances to a cup-like sac known as Bowman's capsule. The filtrate then enters the renal tubule, of the nephron. The glomerulus receives its blood supply from an afferent arteriole of the renal arterial circulation. Unlike most capillary beds, the glomerular capillaries"
"cholesterol, and sweets are more acid-producing, while fruits, vegetables, legumes, and whole grains are more base-producing. IgA nephropathy is the most common glomerulonephritis throughout the world Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus. The classic presentation (in 40-50% of the cases) is episodic frank hematuria which usually starts within a day or two of a non-specific upper respiratory tract infection (hence ""synpharyngitic"") as opposed to post-streptococcal glomerulonephritis which occurs some time (weeks) after initial infection. Less commonly gastrointestinal or urinary infection can be the inciting agent. All of these infections have in common"
"Nephritis Nephritis is inflammation of the kidneys and may involve the glomeruli, tubules, or interstitial tissue surrounding the glomeruli and tubules. Nephritis is often caused by infections, and toxins, but is most commonly caused by autoimmune disorders that affect the major organs like kidneys. Nephritis can produce glomerular injury, by disturbing 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"
"which helps regulate blood volume and pressure. Damage to the glomerulus by disease can allow passage through the glomerular filtration barrier of red blood cells, white blood cells, platelets, and blood proteins such as albumin and globulin. Underlying causes for glomerular injury can be inflammatory, toxic or metabolic. These can be seen in the urine (urinalysis) on microscopic and chemical (dipstick) examination. Examples are diabetic kidney disease, glomerulonephritis, and IgA nephropathy. In 1666, Italian biologist and anatomist Marcello Malpighi first described the glomeruli and demonstrated their continuity with the renal vasculature (281,282). About 175 years later, surgeon and anatomist William"
"membrane). Immune complexes can be visualized by staining with fluorescent antibodies directed against immunoglobulins or complement, resulting in a granular fluorescent staining pattern. In due course, glomerular injury gives rise to scarring (glomerulosclerosis). Most of these patients have hematuria with moderate to severe proteinuria, hypertension, and renal insufficiency. Diffuse proliferative nephritis Diffuse proliferative nephritis (DPN) or glomerulonephritis (DPGN) is a type of glomerulonephritis that is the most serious form of renal lesions in SLE and is also the most common, occurring in 35% to 60% of patients. Most of the glomeruli show endothelial and mesangial proliferation affecting the entire glomerulus,"
"an individual who has been so diagnosed with the condition Nephritis Nephritis is inflammation of the kidneys and may involve the glomeruli, tubules, or interstitial tissue surrounding the glomeruli and tubules. Nephritis is often caused by infections, and toxins, but is most commonly caused by autoimmune disorders that affect the major organs like kidneys. Nephritis can produce glomerular injury, by disturbing 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,"
"a slight fever, nausea and a mild nephritic syndrome of moderately increased blood pressure, gross haematuria, and smoky-brown urine. Circulating immune complexes that deposit in the glomerules may lead to an inflammatory reaction. Diagnosis may be made on clinical findings or through antistreptolysin O antibodies found in the blood. A biopsy is seldom done, and the disease is likely to self-resolve in children in 1–4 weeks, with a poorer prognosis if adults are affected. Membranoproliferative GN (MPGN), also known as ""mesangiocapillary glomerulonephritis,"" is characterised by an increase in the number of cells in the glomerulus, and alterations in the glomerular"
"Diffuse proliferative nephritis Diffuse proliferative nephritis (DPN) or glomerulonephritis (DPGN) is a type of glomerulonephritis that is the most serious form of renal lesions in SLE and is also the most common, occurring in 35% to 60% of patients. Most of the glomeruli show endothelial and mesangial proliferation affecting the entire glomerulus, leading to diffuse hypercellularity of the glomeruli, producing in some cases epithelial crescents that fill Bowman's space. When extensive, immune complexes create an overall thickening of the capillary wall, resembling rigid ""wire loops"" on routine light microscopy. Electron microscopy reveals electron-dense subendothelial immune complexes (between endothelium and basement"
"nephron that processes blood filtrate produced from glomeruli or glomera- large embryonic glomeruli. The filtrate is deposited into the coelom. It then passes through thin ciliated tubules into the pronephric nephron where it is processed for solute recovery. The organ is active in adult forms of some primitive fish, like lampreys or hagfish. It is present at the embryo of more advanced fish and at the larval stage of amphibians where it plays an essential role in osmoregulation. In human beings, it is rudimentary, appears at the end of the third week (day 20) and replaced by mesonephros after 3.5"
"or without nephrotic syndrome, hypertension, and elevated serum creatinine. Class IV disease (diffuse proliferative nephritis) is both the most severe, and the most common subtype. More than 50% of glomeruli are involved. Lesions can be segmental or global, and active or chronic, with endocapillary or extracapillary proliferative lesions. Under electron microscopy, subendothelial deposits are noted, and some mesangial changes may be present. Clinically, haematuria and proteinuria are present, frequently with nephrotic syndrome, hypertension, hypocomplementemia, elevated anti-dsDNA titres and elevated serum creatinine. Class V disease (membranous glomerulonephritis) is characterized by diffuse thickening of the glomerular capillary wall (segmentally or globally), with"
"commonly, glomerulonephritis can develop in chronic cases secondary to immune complex deposition. The great variability of clinical signs in individual cases of FCV is related to the relative virulence of different strains of the virus. VS-FCV can cause a rapid epidemic, with a mortality rate of up to 67%. Initial clinical signs include discharge from the eyes and nose, ulceration in the mouth, anorexia, and lethargy, and occur in the first one to five days. Later signs include fever, edema of the limbs and face, jaundice, and multiple organ dysfunction syndrome. Diagnosis of FCV is difficult without specific tests, because"
"glomerulus are filtered through the visceral layer of podocytes, resulting in the glomerular filtrate. The glomerular filtrate next moves to the renal tubule, where it is further processed to form urine. The different stages of this fluid are collectively known as the tubular fluid. The renal tubule is the portion of the nephron containing the tubular fluid filtered through the glomerulus. After passing through the renal tubule, the filtrate continues to the collecting duct system. The components of the renal tubule are: Blood from the efferent arteriole, containing everything that was not filtered out in the glomerulus, moves into the"
"II disease (mesangial proliferative glomerulonephritis) is noted by mesangial hypercellularity and matrix expansion. Microscopic haematuria with or without proteinuria may be seen. Hypertension, nephrotic syndrome, and acute kidney insufficiency are very rare at this stage. Class III disease (focal glomerulonephritis) is indicated by sclerotic lesions involving less than 50% of the glomeruli, which can be segmental or global, and active or chronic, with endocapillary or extracapillary proliferative lesions. Under the electron microscopy, subendothelial deposits are noted, and some mesangial changes may be present. Immunofluorescence reveals positively for IgG, IgA, IgM, C3, and C1q. Clinically, haematuria and proteinuria are present, with"
"a similar constellation but without the assumption of inflammation. Membranous nephritis (in which inflammation is implied, but the glomerulus not explicitly mentioned) is less common, but the phrase is occasionally encountered. These conditions are usually considered together. By contrast, membranoproliferative glomerulonephritis has a similar name, but is considered a separate condition with a distinctly different causality. Membranoproliferative glomerulonephritis involves the basement membrane and mesangium, while membranous glomerulonephritis involves the basement membrane but not the mesangium. (Membranoproliferative glomerulonephritis has the alternate name ""mesangiocapillary glomerulonephritis"", to emphasize its mesangial character.) Membranous glomerulonephritis Membranous glomerulonephritis (MGN) is a slowly progressive disease of the"
"of the medullary countercurrent exchange system. The filtrate that has passed through the three-layered filtration unit enters Bowman's space. From there, it flows into the renal tubule - the nephron - which follows a U-shaped path to the collecting ducts, finally exiting into a renal calyx as urine. The main function of the glomerulus is to filter plasma to produce glomerular filtrate, which passes down the length of the nephron tubule to form urine. The rate at which the glomerulus produces filtrate from plasma (the glomerular filtration rate) is much higher than in systemic capillaries because of the particular anatomical"
"can affect many other organ systems. Inflammation of the interior portion of the eye, known as uveitis, can cause blurred vision and eye pain, especially when exposed to light (photophobia). Inflammation may also involve the white part of the eye (sclera), a condition called episcleritis. Both episcleritis and uveitis can lead to loss of vision if untreated. Crohn's disease that affects the ileum may result in an increased risk of gallstones. This is due to a decrease in bile acid resorption in the ileum and the bile gets excreted in the stool. As a result, the cholesterol/bile ratio increases in"
"involved (as opposed to diffuse), ""segmental""—only part of each glomerulus is involved (as opposed to global), ""glomerulosclerosis""—refers to scarring of the glomerulus (a part of the nephron (the functional unit of the kidney)). The glomerulosclerosis is usually indicated by heavy PAS staining and findings of immunoglobulin M (IgM) and C3-convertase (C3) in the sclerotic segment. Depending on the cause it is broadly classified as: There are many other classification schemes also. Five mutually exclusive variants of focal segmental glomerulosclerosis may be distinguished by the pathologic findings seen on renal biopsy: Recognition of these variants may have prognostic value in individuals"
"platelets and large proteins do not. As a result, the filtrate leaving the Bowman's capsule is very similar to blood plasma (filtrate or glomerular filtrate is composed of blood plasma minus plasma protein i.e. it contains all the components of blood plasma except the proteins) in composition as it passes into the proximal convoluted tubule. Measuring the glomerular filtration rate (GFR) is a diagnostic test of kidney function. A decreased GFR may be a sign of renal failure. A number of diseases can result in various problems within the glomerulus. Examples include acute proliferative (endocapillary) glomerulonephritis, mesangioproliferative glomerulonephritis, mesangiocapillary (membranoproliferative)"
"change disease (MCD) Membranoproliferative Glomerulonephritis Over 50 mutations are known to be associated with this condition. The renal glomerulus filters the blood that arrives at the kidney. It is formed of capillaries with small pores that allow small molecules to pass through that have a molecular weight of less than 40,000 Daltons, but not larger macromolecules such as proteins. In nephrotic syndrome, the glomeruli are affected by an inflammation or a ""hyalinization"" (the formation of a homogenous crystalline material within cells) that allows proteins such as albumin, antithrombin or the immunoglobulins to pass through the cell membrane and appear in"
"Bowman elucidated in detail the capillary architecture of the glomerulus and the continuity between its surrounding capsule and the proximal tubule. Glomerulus (kidney) The glomerulus (), plural glomeruli, is a network of capillaries known as a ""tuft"", located at the beginning of a nephron in the kidney. The tuft is structurally supported by intraglomerular mesangial cells. The blood is filtered across the capillary walls of this tuft through the glomerular filtration barrier, which yields its filtrate of water and soluble substances to a cup-like sac known as Bowman's capsule. The filtrate then enters the renal tubule, of the nephron. The"
"DN begin with long-standing poorly controlled blood glucose levels. This is followed by multiple changes in the filtration units of the kidneys, the nephrons. (There are normally about 750,000–1.5 million nephrons in each adult kidney). Initially, there is constriction of the efferent arterioles and dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration; this gradually changes to hypofiltration over time. Concurrently, there are changes within the glomerulus itself: these include a thickening of the basement membrane, a widening of the slit membranes of the podocytes, an increase in the number of mesangial cells, and an increase in mesangial"
"include painful peripheral neuropathy (often manifesting as mononeuritis multiplex in 19-44% of cases), kidney disease (primarily membranoproliferative glomerulonephritis (30%), joint pain (28%), and, less commonly, dry eye syndrome, Raynaud phenomenon (i.e. episodic painful reductions in blood flow to the fingers and toes). While the glomerulonephritis occurring in mixed disease appears to be due to inflammatory vasculitis, the glomerulonephritis occurring in type I disease appears due to the interruption of blood flow. The hematological, infectious, and autoimmune diseases underlying type II cryoglobulinemic disease and the infectious and autoimmune diseases underlying type III cryoglobulinemic disease are also critical parts of the disease's"
"the urine (called albuminuria). As diabetic nephropathy progresses, a structure in the glomeruli known as the glomerular filtration barrier (GFB) is increasingly damaged. This barrier is composed of three layers including the fenestrated endothelium, the glomerular basement membrane, and the epithelial podocytes. The GFB is responsible for the highly selective filtration of blood entering the kidney's glomeruli and normally only allows the passage of water, small molecules, and very small proteins (albumin does not pass through the intact GFB). Damage to the glomerular basement membrane allows proteins in the blood to leak through, leading to proteinuria. Deposition of abnormally large"