query: which section of the kidney does the glomerulus belong to

pos: Glomerulus (kidney) 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

pos: Glomerulus (kidney) 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

neg: Glomerulus (kidney) exit into efferent arterioles rather than venules. The resistance of the efferent arterioles causes sufficient hydrostatic pressure within the glomerulus to provide the force for ultrafiltration. The glomerulus and its surrounding Bowman's capsule constitute a renal corpuscle, the basic filtration unit of the kidney. The rate at which blood is filtered through all of the glomeruli, and thus the measure of the overall renal function, is the glomerular filtration rate (GFR). The glomerulus is a tuft of small blood vessels called capillaries located within Bowman's capsule within the kidney. Glomerular mesangial cells structurally support the tufts. Blood enters the capillaries

neg: Mesonephros part of the mature kidney or nephrons. In humans, the mesonephros consists of units which are similar in structure and function to nephrons of the adult kidney. Each of these consists of a glomerulus, a tuft of capillaries which arises from lateral branches of dorsal aorta and drains into the inferior cardinal vein; a Bowman's capsule, a funnel like structure which surrounds the glomerulus; and a "mesonephric tubule", a tube which connects the Bowman's capsule to the mesonephric duct. A unit consisting of a single glomerulus and the Bowman's capsule surrounding it is called "renal corpuscle", and a unit consisting

neg: Glomerulus (kidney) 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

neg: Glomerulus (kidney) 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

neg: Juxtaglomerular apparatus Juxtaglomerular apparatus The juxtaglomerular apparatus (also known as the juxtaglomerular complex) is a structure in the kidney that regulates the function of each nephron, the functional units of the kidney. The juxtaglomerular apparatus is named because it is next to (juxta-) the glomerulus. The juxtaglomerular apparatus consists of three types of cells: The juxtaglomerular apparatus is part of the kidney nephron, next to the glomerulus. It is found between afferent arteriole and the distal convoluted tubule of the same nephron. This location is critical to its function in regulating renal blood flow and glomerular filtration rate.The swollen smooth muscle cells

neg: Extraglomerular mesangial cell been associated with the secretion of erythropoietin and secretion of renin. They are distinguished from intraglomerular mesangial cells, which are situated between the basement membrane and the epithelial cells within the glomerulus. Extraglomerular mesangial cell Extraglomerular mesangial cells (also known as Lacis cells, Polkissen cells, or Goormaghtigh cells) are light-staining pericytes in the kidney found outside the glomerulus, near the vascular pole. They resemble smooth muscle cells and play a role in renal autoregulation of blood flow to the kidney and regulation of systemic blood pressure through the renin–angiotensin system. Extraglomerular mesangial cells are part of the juxtaglomerular apparatus, along

neg: Glomerulus (kidney) characteristics of the glomerulus. Unlike systemic capillaries, which receive blood from high-resistance arterioles and drain to low-resistance venules, glomerular capillaries are connected in both ends to high-resistance arterioles: the afferent arteriole, and the efferent arteriole. This arrangement of two arterioles in series determines the high hydrostatic pressure on glomerular capillaries, which is one of the forces that favour filtration to the Bowman's capsule. If a substance has passed through the glomerular capillary endothelial cells, glomerular basement membrane, and podocytes, then it enters the lumen of the tubule and is known as glomerular filtrate. Otherwise, it exits the glomerulus through the

neg: Macula densa part of the body's blood pressure regulation, the macula densa monitors filtrate osmolarity; if it falls too far, the macula densa causes the afferent arterioles of the kidney to dilate, thus increasing the pressure at the glomerulus and increasing the glomerular filtration rate. The macula densa does not regulate the dilation of the efferent arterioles and afferent arterioles do not dilate in response to increases in filtrate osmolarity. Macula densa In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the distal tubule, at the point where the thick ascending limb meets

neg: Renal corpuscle Renal corpuscle A renal corpuscle is the blood-filtering component of the nephron of the kidney. It consists of a glomerulus - a tuft of capillaries composed of endothelial cells, and a glomerular capsule known as Bowman's capsule. The renal corpuscle is composed of two structures, the glomerulus and the Bowman's capsule. The glomerulus is a small tuft of capillaries containing two cell types. Endothelial cells, which have large fenestrae, are not covered by diaphragms. Mesangial cells are modified smooth muscle cells that lie between the capillaries. They regulate blood flow by their contractile activity and secrete extracellular matrix, prostaglandins, and

neg: Efferent arteriole Efferent arteriole The efferent arterioles are blood vessels that are part of the urinary tract of organisms. Efferent (from Latin ex + ferre) means "outgoing", in this case meaning carrying blood out away from the glomerulus. The efferent arterioles form from a convergence of the capillaries of the glomerulus, and carry blood away from the glomerulus that has already been filtered. They play an important role in maintaining the glomerular filtration rate despite fluctuations in blood pressure. In the mammalian kidney they follow two markedly different courses, depending on the location of the glomeruli from which they arise. In the

neg: Mesangial cell Mesangial cell Mesangial cells are specialised cells in the kidney that make up the mesangium of the glomerulus. Together with the mesangial matrix, they form the vascular pole of the renal corpuscle. The mesangial cell population accounts for approximately 30-40% of the total cells in the glomerulus. Mesangial cells can be categorised as either extraglomerular mesangial cells or intraglomerular mesangial cells, based on their relative location to the glomerulus. The extraglomerular mesangial cells are found between the afferent and efferent arterioles towards the vascular pole of the glomerulus. The extraglomerular mesangial cells are adjacent to the intraglomerular mesangial cells that

neg: Loin pain hematuria syndrome crystals in the kidney tubules may also play a part in bleeding and pain. Other speculations on cause include It has also been reported to be caused by microscopic granules of calcium oxylate into the glomerulus itself, causing blood vessels to rupture and increase the distention of the renal capsule. This condition may persist for some years, and can be lifelong. Damage to the kidneys leading to kidney failure does not occur. However, because LPHS is unusual in patients older than 60 years, some clinicians believe that LPHS eventually resolves. At this time no cure has been found for this

neg: Hepatorenal syndrome can also lead to inflammation of the glomerulus of the kidney. Other causes of kidney failure in individuals with liver disease include drug toxicity (notably, the antibiotic gentamicin) or contrast nephropathy, caused by intravenous administration of contrast agents used for medical imaging tests. The kidney failure in hepatorenal syndrome is believed to arise from abnormalities in blood vessel tone in the kidneys. The predominant theory (termed the "underfill" theory) is that blood vessels in the kidney circulation are constricted because of the dilation of blood vessels in the splanchnic circulation (which supplies the intestines), which is mediated by factors released

neg: Regeneration in humans glomerulus, tubules, the collecting duct and peritubular capillaries. The regenerative capacity of the mammalian kidney is limited compared to that of lower vertebrates. In the mammalian kidney, the regeneration of the tubular component following an acute injury is well known. Recently regeneration of the glomerulus has also been documented. Following an acute injury, the proximal tubule is damaged more, and the injured epithelial cells slough off the basement membrane of the nephron. The surviving epithelial cells, however, undergo migration, dedifferentiation, proliferation, and redifferentiation to replenish the epithelial lining of the proximal tubule after injury. Recently, the presence and participation of

neg: Hyperchloremia flow as well at glomerulus filtration, all of which are prompting researchers to investigate if these changes or others may exist in patients. Some studies have reported a possible relationship between increased chloride levels and death or acute kidney injury in severely ill patients that may frequent the hospital or have prolonged visits. There are other studies that have found no relationship. As studies continue, it is important to include a large patient sample size, diverse patient population, and a diverse range of hospitals involved in these studies. Hyperchloremia does not have many noticeable symptoms and can only be confirmed

neg: Glomerulus (kidney) are not spanned by diaphragms. They allow for the filtration of fluid, blood plasma solutes and protein, at the same time preventing the filtration of red blood cells, white blood cells, and platelets. The glomerulus has a glomerular basement membrane (GBM) consisting mainly of laminins, type IV collagen, agrin and nidogen, which are synthesized and secreted by both endothelial cells and podocytes: thus the GBM is sandwiched between the glomerular capillaries and the podocytes. The GBM is 250–400 nm in thickness, which is thicker than basement membranes of other tissue. It is a barrier to blood proteins such as albumin

neg: Glomerulus (kidney) of the glomerulus by a single arteriole called an afferent arteriole and leaves by an efferent arteriole. The capillaries consist of a tube lined by endothelial cells with a central lumen. The walls have a unique structure: there are pores between the cells that allow water and soluble substances to exit, and after passing through the glomerular basement membrane, and between podocyte foot processes, enter the capsule as ultrafiltrate. Capillaries of the glomerulus are lined by endothelial cells. These contain numerous pores - also called fenestrae - 50–100 nm in diameter. Unlike those of other capillaries with fenestrations, these fenestrations

neg: Kidney disease transplant is the only treatment option. Chronic kidney disease causes the gradual loss of kidney function over time. Acute kidney disease is now termed acute kidney injury and is marked by the sudden reduction in kidney function over seven days. About one in eight Americans (as of 2007) suffer from chronic kidney disease. Causes of kidney disease include deposition of the Immunoglobulin A antibodies in the glomerulus, administration of analgesics, xanthine oxidase deficiency, toxicity of chemotherapy agents, and long-term exposure to lead or its salts. Chronic conditions that can produce nephropathy include systemic lupus erythematosus, diabetes mellitus and high blood

neg: Nonsteroidal anti-inflammatory drug At these elevated levels, angiotensin II also constricts the afferent arteriole into the glomerulus in addition to the efferent arteriole it normally constricts. Since NSAIDs block this prostaglandin-mediated effect of afferent arteriole dilation, particularly in kidney failure, NSAIDs cause unopposed constriction of the afferent arteriole and decreased RPF (renal perfusion flow) and GFR. Common ADRs associated with altered kidney function include: These agents may also cause kidney impairment, especially in combination with other nephrotoxic agents. Kidney failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor (which removes angiotensin II's vasoconstriction of the efferent arteriole)

neg: Human serum albumin however at high concentrations of reactive species leads to the irreversible oxidation to sulfinic (HSA-SO2H) or sulfonic acid (HSA-SO3H) affecting its structure. Presence of reactive oxygen species (ROS), can induce irreversible structural damage and alter protein activities. In the healthy kidney, albumin's size and negative electric charge exclude it from excretion in the glomerulus. This is not always the case, as in some diseases including diabetic nephropathy, which can sometimes be a complication of uncontrolled or of longer term diabetes in which proteins can cross the glomerulus. The lost albumin can be detected by a simple urine test. Depending on

neg: Inulin inulin with those of para-aminohippuric acid (PAH). PAH is partially filtered from plasma at the glomerulus and not reabsorbed by the tubules, in a manner identical to inulin. PAH is different from inulin in that the fraction of PAH that bypasses the glomerulus and enters the nephron's tubular cells (via the peritubular capillaries) is completely secreted. Renal clearance of PAH is thus useful in calculation of renal plasma flow (RPF), which empirically is (1-hematocrit) times renal blood flow. Of note, the clearance of PAH is reflective only of RPF to portions of the kidney that deal with urine formation, and,

neg: Renal physiology word "excretion" with respect to the urinary system is urination itself, renal clearance is also conventionally called excretion (for example, in the set term "fractional excretion of sodium"). The blood is filtered by nephrons, the functional units of the kidney. Each nephron begins in a renal corpuscle, which is composed of a glomerulus enclosed in a Bowman's capsule. Cells, proteins, and other large molecules are filtered out of the glomerulus by a process of ultrafiltration, leaving an ultrafiltrate that resembles plasma (except that the ultrafiltrate has negligible plasma proteins) to enter Bowman's space. Filtration is driven by Starling forces. The

neg: Tubuloglomerular feedback Tubuloglomerular feedback In the physiology of the kidney, tubuloglomerular feedback (TGF) is a feedback system inside the kidneys. Within each nephron, information from the renal tubules (a downstream area of the tubular fluid) is signaled to the glomerulus (an upstream area). Tubuloglomerular feedback is one of several mechanisms the kidney uses to regulate glomerular filtration rate (GFR). It involves the concept of purinergic signaling, in which an increased distal tubular sodium chloride concentration causes a basolateral release of adenosine from the macula densa cells. This initiates a cascade of events that ultimately brings GFR to an appropriate level. The kidney

neg: Glomerulus (kidney) and globulin. The part of the podocyte in contact with the GBM is called a "podocyte foot process" or "pedicle" (Fig. 3): there are gaps between the foot processes through which the filtrate flows into Bowman's space of the capsule. . The space between adjacent podocyte foot processes is spanned by slit diaphragms consisting of a mat of proteins, including podocin and nephrin. In addition, foot processes have a negatively charged coat (glycocalyx) that repels negatively charged molecules such as serum albumin. The space between the capillaries of a glomerulus is occupied by intraglomerular mesangial cells. They are not part

neg: Renal medulla Renal medulla The renal medulla is the innermost part of the kidney. The renal medulla is split up into a number of sections, known as the renal pyramids. Blood enters into the kidney via the renal artery, which then splits up to form the interlobar arteries. The interlobar arteries each in turn branch into arcuate arteries, which in turn branch to form interlobular arteries, and these finally reach the glomeruli. At the glomerulus the blood reaches a highly disfavourable pressure gradient and a large exchange surface area, which forces the serum portion of the blood out of the vessel and

neg: Glomerulonephritis electron microscopy within the glomerules may show a fusion of the foot processes of the podocytes (cells lining the basement membrane of the capillaries of glomerulus). It is typically managed with corticosteroids and does not progress to chronic kidney disease. Focal segmental glomerulosclerosis is characterised by a sclerosis of segments of some glomerules. It is likely to present as a nephrotic syndrome. This form of glomerulonephritis may be associated with conditions such as HIV and heroin abuse, or inherited as Alport syndrome. The cause of about 20–30% of focal-segmental glomerulosclerosis is unknown. On microscopy, affected glomerules may show an increase

neg: Glucose uptake is generated through the active functioning of the NaKATPase. As the cotransport of glucose with sodium from the lumen does not directly require ATP hydrolysis but depends upon the action of the ATPase, this is described as secondary active transport. There are two types of secondary active transporter found within the kidney tubule; close to the glomerulus, where glucose levels are high, SGLT2 has a low affinity yet high capacity for glucose transport. Close to the loop of Henle and in the distal convoluted tubule of the nephron where much glucose has been reabsorbed into the bloodstream, SGLT1 transporters are

neg: Glomerulonephritis They are categorized into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differs in different types. Primary causes are intrinsic to the kidney. Secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic disorders (SLE, vasculitis), or diabetes. Glomerulonephritis refers to an inflammation of the glomerulus, which is the unit involved in filtration in the kidney. This inflammation typically results in one or both of the nephrotic or nephritic syndromes. The nephrotic syndrome is characterised by the finding of

neg: N-Acetylmannosamine therapy to treat GNE myopathy. There is a growing body of evidence that reduced activity of the GNE enzyme in the sialylation pathway in kidney tissue could contribute to several glomerular kidney diseases, due to the lack of the Neu5Ac terminal sugar on several kidney glycoproteins. Three kidney diseases that affect both children and adults are minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS) and membranous nephropathy (MN). These diseases are characterized by proteinuria (protein in the urine) and in the case of FSGS, a tendency to progressive scarring of the glomerulus (the filtering units of the kidneys) that leads

neg: Microalbuminuria Microalbuminuria Microalbuminuria is a term to describe a moderate increase in the level of urine albumin. It occurs when the kidney leaks small amounts of albumin into the urine, in other words, when an abnormally high permeability for albumin in the glomerulus of the kidney occurs. Normally, the kidneys filter albumin, so if albumin is found in the urine, then it is a marker of kidney disease. The term microalbuminuria is now discouraged by Kidney Disease Improving Global Outcomes and has been replaced by moderately increased albuminuria. Microalbuminuria is an important adverse predictor of glycemic outcomes in prediabetes. Prediabetes individuals

neg: Camillo Golgi which he understood to be due to renal cell proliferation. In 1884, he described tubular cell mitoses in the kidney of a person suffering from tubulointerstitial nephritis, and he noted that the process was an essential part of repairing the kidney tissue. He was the first to dissect out intact nephrons, and show that the distal tubulus (loop of Henle) of the nephron returns to its originating glomerulus, a finding that he published in 1889 ("Annotazioni intorno all'Istologia dei reni dell'uomo e di altri mammifieri e sull'istogenesi dei canalicoli oriniferi". "Rendiconti R. Acad. Lincei" 5: 545–557, 1889). A French Army

neg: Kidney venules that converge into interlobular veins. As with the arteriole distribution, the veins follow the same pattern: the interlobular provide blood to the arcuate veins then back to the interlobar veins, which come to form the renal vein exiting the kidney for transfusion for blood. The table below shows the path that blood takes when it travels through the glomerulus, traveling "down" the arteries and "up" the veins. However, this model is greatly simplified for clarity and symmetry. Some of the other paths and complications are described at the bottom of the table. The interlobar artery and vein (not to

neg: Glomerulus (kidney) glomerular capillaries is one of the forces that resist filtration. Because large and negatively charged proteins have a low permeability, they cannot filtrate easily to the Bowman's capsule. Therefore, the concentration of these proteins tends to increase as the glomerular capillaries filtrate plasma, increasing the oncotic pressure along the length of a glomerular capillary. The rate of filtration from the glomerulus to the Bowman's capsule is determined (as in systemic capillaries) by the Starling equation: The walls of the afferent arteriole contain specialized smooth muscle cells that synthesize renin. These juxtaglomerular cells play a major role in the renin–angiotensin system,

neg: Bowman's capsule is not used widely anymore, probably to avoid confusion with Malpighian bodies of the spleen. Bowman's capsule Bowman's capsule (or the Bowman capsule, capsula glomeruli, or glomerular capsule) is a cup-like sack at the beginning of the tubular component of a nephron in the mammalian kidney that performs the first step in the filtration of blood to form urine. A glomerulus is enclosed in the sac. Fluids from blood in the glomerulus are collected in the Bowman's capsule (i.e., glomerular filtrate) and further processed along the nephron to form urine. This process is known as ultrafiltration.The Bowman's capsule is named

neg: Bowman's capsule Bowman's capsule Bowman's capsule (or the Bowman capsule, capsula glomeruli, or glomerular capsule) is a cup-like sack at the beginning of the tubular component of a nephron in the mammalian kidney that performs the first step in the filtration of blood to form urine. A glomerulus is enclosed in the sac. Fluids from blood in the glomerulus are collected in the Bowman's capsule (i.e., glomerular filtrate) and further processed along the nephron to form urine. This process is known as ultrafiltration.The Bowman's capsule is named after Sir William Bowman, who identified it in 1842. Outside the capsule, there are two

neg: Kidney development position at the tips of the renal tubules. These cells differentiate into the cells of the definitive glomerulus. In humans, all of the branches of the ureteric bud and the nephronic units have been formed by 32 to 36 weeks of gestation. However, these structures are not yet mature, and will continue to mature after birth. Once matured, humans have an estimated two million nephrons (approximately 1,000,000 per kidney) but this number is highly variable ranging widely from approximately 300,000 to over 2 million per kidney. After inducing the metanephric mesenchyme the lower portions of the nephric duct will migrate

neg: Focal segmental glomerulosclerosis 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

neg: Nephron 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 renal tubule extends from the capsule. The capsule and tubule are connected and are composed of epithelial cells with a lumen. A healthy adult has 0.8 to 1.5 million nephrons in each kidney. Blood is filtered as it passes through three layers: the endothelial cells of the capillary wall, its basement

neg: Glomerular basement membrane Glomerular basement membrane The glomerular basement membrane (GBM) of the kidney is the basal lamina layer of the glomerulus. The glomerular endothelial cells, the GBM and the filtration slits between the podocytes perform the filtration function of the glomerulus, separating the blood in the capillaries from the filtrate that forms in Bowman's capsule. The GBM is a fusion of the endothelial cell and podocyte basal laminas. The GBM contains three layers: The glomerular membrane consists of mesangial cells, modified pericytes that in other parts of the body separate capillaries from each other. The podocytes adjoining them have filtration slits of

neg: Glomerular basement membrane diameter 25 nm that are formed by the pseudopodia arising from them. The filtration slits are covered by a diaphragm that includes the transmembrane protein nephrin. Glomerular basement membrane The glomerular basement membrane (GBM) of the kidney is the basal lamina layer of the glomerulus. The glomerular endothelial cells, the GBM and the filtration slits between the podocytes perform the filtration function of the glomerulus, separating the blood in the capillaries from the filtrate that forms in Bowman's capsule. The GBM is a fusion of the endothelial cell and podocyte basal laminas. The GBM contains three layers: The glomerular membrane

neg: Glomerulus (kidney) of the filtration barrier but are specialized pericytes that participate in the regulation of the filtration rate by contracting or expanding: they contain actin and myosin filaments to accomplish this. Some mesangial cels are in physical contact with capillaries, others are in physical contact with podocytes. There is two-way chemical cross talk among the mesangial cells, the capillaries, and the podocytes to fine-tune the GFR. Blood exits the glomerular capillaries by an efferent "arteriole" instead of a "venule", as is seen in the majority of capillary systems (Fig. 4). This provides tighter control over the blood flow through the glomerulus,

neg: Henoch–Schönlein purpura less than 20. The presence of three or more of these indicators has an 87% sensitivity for predicting HSP. Biopsy of the kidney may be performed both to establish the diagnosis or to assess the severity of already suspected kidney disease. The main findings on kidney biopsy are increased cells and Ig deposition in the mesangium (part of the glomerulus, where blood is filtered), white blood cells, and the development of crescents. The changes are indistinguishable from those observed in IgA nephropathy. HSP can develop after infections with streptococci (β-haemolytic, Lancefield group A), hepatitis B, herpes simplex virus, parvovirus B19,

neg: Hypertensive kidney disease the underlying mechanism remains unclear. The two proposed mechanisms of HN’s pathophysiology both centre around how the glomerulus, a network of dense capillaries that carries out the kidney filtration process, is affected; with one theory identifying glomerular ischemia as the main contributor to HN and the other identifying glomerular hypertension and glomerular hyperfiltration at the centre of HN’s pathogenesis. High blood pressure in the long term can damage the endothelium, commonly known as the blood vessel lining. This leads to a build-up of plaques and they can be deposited in the renal arteries causing stenosis and ischemic kidney disease. In

neg: Nephron 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

neg: Diabetic nephropathy and eventually kidney transplantation to replace the failed kidney function. Diabetic nephropathy is associated with an increased risk of death in general, particularly from cardiovascular disease. The onset of symptoms is 5 to 10 years after the disease begins. A usual first symptom is frequent urination at night: nocturia. Other symptoms include tiredness, headaches, a general feeling of illness, nausea, vomiting, frequent daytime urination, lack of appetite, itchy skin, and leg swelling. The incidence of diabetic nephropathy is higher in people with diabetes that have one or more of the following conditions: The pathophysiology of the glomerulus in DN can

neg: Juxtaglomerular cell is manifested as a lower renal perfusion pressure. Juxtaglomerular cell The juxtaglomerular cells (JG cells, or granular cells) are cells in the kidney that synthesize, store, and secrete the enzyme renin. They are specialized smooth muscle cells mainly in the walls of the afferent arterioles, and some in the efferent arterioles, that deliver blood to the glomerulus. In synthesizing renin, they play a critical role in the renin–angiotensin system and thus in autoregulation of the kidney. Juxtaglomerular cells secrete renin in response to a drop in pressure detected by stretch receptors in the vascular walls, or when stimulated by macula

neg: Juxtaglomerular cell Juxtaglomerular cell The juxtaglomerular cells (JG cells, or granular cells) are cells in the kidney that synthesize, store, and secrete the enzyme renin. They are specialized smooth muscle cells mainly in the walls of the afferent arterioles, and some in the efferent arterioles, that deliver blood to the glomerulus. In synthesizing renin, they play a critical role in the renin–angiotensin system and thus in autoregulation of the kidney. Juxtaglomerular cells secrete renin in response to a drop in pressure detected by stretch receptors in the vascular walls, or when stimulated by macula densa cells. Macula densa cells are located in

neg: Nephron 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

neg: Hematuria urinary system can cause microscopic hematuria. Causes can be separated into glomerular, arising from the filtering system of the kidney, and non-glomerular, arising from the kidney (outside the glomerulus), ureters, urinary bladder, prostate, or urethra. Inflammation of or injury to the glomeruli can cause leakage of red blood cells, resulting in misshapen cells and red blood cell casts in the urine. Glomerular bleeding is frequently accompanied by proteinuria, or leakage of protein into the urine. Common causes include In many cases of asymptomatic microscopic hematuria without proteinuria, no etiology is found. Common causes of microscopic hematuria in pediatric populations include:

neg: Pyelonephritis consisting in purulent exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, the glomerulus and vessels are normal. Gross pathology often reveals pathognomonic radiations of bleeding and suppuration through the renal pelvis to the renal cortex. Chronic pyelonephritis implies recurrent kidney infections and can result in scarring of the renal parenchyma and impaired function, especially in the setting of obstruction. A perinephric abscess (infection around the kidney) and/or pyonephrosis may develop in severe cases of pyelonephritis. Xanthogranulomatous pyelonephritis is an unusual form of chronic

neg: Organ-on-a-chip requires patients to go to a clinic up to three times per week. A more transportable and accessible form of treatment would not only increase the patient’s overall health (by increasing frequency of treatment), but the whole process would become more efficient and tolerable. Artificial kidney research is striving to bring transportability, wearability and perhaps implantation capability to the devices through innovative disciplines: microfluidics, miniaturization and nanotechnology. The nephron is the functional unit of the kidney and is composed of a glomerulus and a tubular component. Researchers at MIT claim to have designed a bioartificial device that replicates the function

neg: 1,5-Anhydroglucitol marker of short-term glycemic control. 1,5-AG is ingested from nearly all foods during the course of a regular diet and is nearly 100% non-metabolized. It is carried in the blood stream and filtered by the glomerulus, where it enters the kidney. Once in the kidney, 1,5-AG is re-absorbed back into the blood through the renal proximal tubule. A small amount, equal to the amount ingested, of 1,5-AG is released in the urine to maintain a constant amount in the blood and tissue. Glucose is a competitive inhibitor of the re-absorption. If blood glucose values rise over 180 mg/dL for any

neg: Alport syndrome do well on dialysis or with a kidney transplant. Transplantation can rarely be associated with the formation of antibodies to type IV collagen in the donor kidney resulting in progressive graft failure as a result of Goodpasture syndrome ('Alport post-transplant anti-GBM disease'). Gene therapy has been frequently discussed, but delivering it to the podocytes in the glomerulus that normally produce the type IV collagen in the glomerular basement membrane is challenging. It is not known whether ACE inhibitors or other treatments affect hearing loss. For those with classic Alport syndrome, hearing aids are often required in teenage or young adult

neg: Kidney kidney participates in the control of the volume of various body fluid compartments, fluid osmolality, acid-base balance, various electrolyte concentrations, and removal of toxins. Filtration occurs in the glomerulus: one-fifth of the blood volume that enters the kidneys is filtered. Examples of substances reabsorbed are solute-free water, sodium, bicarbonate, glucose, and amino acids. Examples of substances secreted are hydrogen, ammonium, potassium and uric acid. The kidneys also carry out functions independent of the nephron. For example, they convert a precursor of vitamin D to its active form, calcitriol; and synthesize the hormones erythropoietin and renin. Renal physiology is the study

neg: Extraglomerular mesangial cell Extraglomerular mesangial cell Extraglomerular mesangial cells (also known as Lacis cells, Polkissen cells, or Goormaghtigh cells) are light-staining pericytes in the kidney found outside the glomerulus, near the vascular pole. They resemble smooth muscle cells and play a role in renal autoregulation of blood flow to the kidney and regulation of systemic blood pressure through the renin–angiotensin system. Extraglomerular mesangial cells are part of the juxtaglomerular apparatus, along with the macula densa cells of the distal convoluted tubule and the juxtaglomerular cells of the afferent arteriole. The specific function of extraglomerular mesangial cells is not well understood, although it has

neg: Bowman's capsule glomerulonephritis, acute crescentic glomerulonephritis, focal segmental glomerulonephritis, and diabetic glomerulosclerosis. Bowman's capsule is named after Sir William Bowman (1816–1892), a British surgeon and anatomist. However, thorough microscopical anatomy of kidney including the nephronic capsule was described by the Russian surgeon and anatomist in Moscow from the Russian Empire, Prof. (1748–1795), in his 1788 doctoral thesis "De structura renum: Tractatus physiologico-anatomicus" ("About Kidney Structure: an Physiological-Anatomical Treatise", in Latin); thus, much prior to Bowman. Together with the glomerulus it is known as a renal corpuscle, or a Malpighian corpuscle, named after Marcello Malpighi (1628–1694), an Italian physician and biologist. This name

neg: Mesangial cell also develop during the early phase of diabetes. Glomerular hypertension causes mesangial cells to stretch which causes induced expression of GLUT1 leading to increased cellular glucose. The repetition of stretching and relaxation cycle of mesangial cells due to hypertension increases mesangial cell proliferation and the production of extracellular matrix which can then accumulate and lead to glomerular disease. Mesangial cell Mesangial cells are specialised cells in the kidney that make up the mesangium of the glomerulus. Together with the mesangial matrix, they form the vascular pole of the renal corpuscle. The mesangial cell population accounts for approximately 30-40% of the

neg: Nephritic syndrome Nephritic syndrome Nephritic syndrome (or acute nephritic syndrome) is a syndrome comprising signs of nephritis, which is kidney disease involving inflammation. It often occurs in glomerulonephritis, which is characterized by a thin glomerular basement membrane and small pores in the podocytes of the glomerulus, large enough to permit proteins and red blood cells to pass into the urine (yielding proteinuria and hematuria). By contrast, nephrotic syndrome is characterized by only proteins moving into the urine. Nephritic syndrome, like nephrotic syndrome, may involve hypoalbuminemia due to the protein albumin moving from the blood to the urine. Historically, nephritic syndrome has been

neg: Glomerulus (kidney) since arterioles dilate and constrict more readily than venules, owing to their thick circular smooth muscle layer (tunica media). The blood exiting the efferent arteriole enters a renal venule, which in turn enters a renal interlobular vein and then into the renal vein. Cortical nephrons near the corticomedullary junction (15% of all nephrons) are called juxtamedullary nephrons. The blood exiting the efferent arterioles of these nephrons enter the vasa recta, which are straight capillary branches that deliver blood to the renal medulla. These vasa recta run adjacent to the descending and ascending loop of Henle, and participate in the maintenance

neg: Nephritic syndrome Because nephritic syndrome is not a disease, the prognosis depends on the underlying cause. The prognosis of nephritic syndrome in children due to poststreptococcal glomerulonephritis is good. Nephritic syndrome Nephritic syndrome (or acute nephritic syndrome) is a syndrome comprising signs of nephritis, which is kidney disease involving inflammation. It often occurs in glomerulonephritis, which is characterized by a thin glomerular basement membrane and small pores in the podocytes of the glomerulus, large enough to permit proteins and red blood cells to pass into the urine (yielding proteinuria and hematuria). By contrast, nephrotic syndrome is characterized by only proteins moving into

neg: Alport syndrome is the major isoform in most human basement membranes. When mutations prevent the formation of 345 type IV collagen network in the glomerulus, the 112 network, which is formed in fetal development but usually replaced by 345, persists into adult life. Alport syndrome can have different inheritance patterns depending on which specific mutation is present. Clinical utility gene card for: Alport syndrome. The diagnosis can usually be made on a combination of clinical, family history and biopsy criteria. To be helpful, kidney biopsies need to be taken before the disease is too advanced. Changes on conventional (light) microscopy are not

neg: Diabetic nephropathy blood. Treatment with an angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB), which dilates the arteriole exiting the glomerulus, thus reducing the blood pressure within the glomerular capillaries, which may slow (but not stop) progression of the disease. Three classes of diabetes medications – GLP-1 agonists, DPP-4 inhibitors, and SGLT2 inhibitors – are also thought to slow the progression of diabetic nephropathy. Diabetic nephropathy is the most common cause of ESKD and is a serious complication that affects approximately one quarter of adults with diabetes in the United States. Affected individuals with end-stage kidney disease often require hemodialysis

neg: Renal physiology This filtrate then flows along the length of the nephron, which is a tubular structure lined by a single layer of specialized cells and surrounded by capillaries. The major functions of these lining cells are the reabsorption of water and small molecules from the filtrate into the blood, and the secretion of wastes from the blood into the urine. Proper function of the kidney requires that it receives and adequately filters blood. This is performed at the microscopic level by many hundreds of thousands of filtration units called renal corpuscles, each of which is composed of a glomerulus and a

neg: Glomerulus (cerebellum) granule cells themselves each have a single or multiple dendrites, and each participates in a different glomerulus. Glomeruli also contain the GABAergic (inhibitory) synapses of Golgi cells onto granule cells, and the glutamatergic (excitatory) synapses from mossy fibers onto Golgi cells. Each glomerulus contains approximately 50 granule cell dendrites, 210 total dendritic digits and 230 synaptic junctions. "Velate astrocytes" are glia that sheath the glomeruli. They are protoplasmic astrocytes with extremely thin veil-like processes that spread out and overlap each other. Researchers Sanford Palay and Victoria Chan-Palay noted that the sheath does not penetrate into the deeper part of the

neg: Kidney disease 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

neg: Diuresis with cellular matter, particularly necrotic sloughing of dead cells. This debris obstructs the flow of filtrate, which results in reduced output of urine. The arterial supply of the nephron is linked to the filtration apparatus (glomerulus), and reduced perfusion leads to reduced blood flow; usually this is the result of pre-renal pathology. The kidney's resorptive mechanisms are particularly energetic, using nearly 100% of the O supplied. Thus, the kidney is particularly sensitive to reduction in blood supply. This phenomenon occurs because renal flow is restored prior to the normal resorption function of the renal tubule. As you can see in

neg: Glomerulonephritis the urine (especially Red blood cell casts with dysmorphic red blood cells) and a decrease in the amount of urine in the presence of hypertension. In this syndrome, inflammatory damage to cells lining the glomerulus are thought to result in destruction of the epithelial barrier, leading to blood being found in the urine. At the same time, reactive changes, e.g. proliferation of mesangial cells, may result in a decrease in kidney blood flow, resulting in a decrease in the production of urine. The renin–angiotensin system may be subsequently activated, because of the decrease in perfusion of juxtaglomerular apparatus, which may

neg: Renal corpuscle collected in the Bowman's capsule to form "glomerular filtrate", which is then further processed along the nephron to form urine. A renal corpuscle is also known as a "Malpighian corpuscle", named after Marcello Malpighi (1628–1694), an Italian physician and biologist. This name is no longer widely used, probably to avoid confusion with a Malpighian corpuscle in the spleen. Renal corpuscle A renal corpuscle is the blood-filtering component of the nephron of the kidney. It consists of a glomerulus - a tuft of capillaries composed of endothelial cells, and a glomerular capsule known as Bowman's capsule. The renal corpuscle is composed

neg: American flamingo body size. As food and saltwater are ingested, sodium and water absorption begins through the walls of the gut and into the extracellular fluid. Sodium is then circulated to the kidney, where the plasma undergoes filtration by the renal glomerulus. Although birds' kidneys tend to be larger in size, they are inefficient in producing concentrated urine that is significantly hyperosmotic to their blood plasma. This form of secretion would cause dehydration from water loss. Therefore, sodium and water are reabsorbed into the plasma by renal tubules. This increase in osmotic plasma levels causes extracellular fluid volume to increase, which triggers

neg: Excretory system such as tumors. The consequences of this depend on the site of blockage and how long it goes on for. There is inflammation of the ducts due to the irritation from the bile acids and this can cause infections. If rupture of the duct takes place it is very traumatic and even fatal. Within the kidney, blood first passes through the afferent artery to the capillary formation called a glomerulus and is collected in the Bowman's capsule, which filters the blood from its contents—primarily food and wastes. After the filtration process, the blood then returns to collect the food nutrients

neg: Macula densa Macula densa In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the distal tubule, at the point where the thick ascending limb meets the distal convoluted tubule. The macula densa is the thickening where the distal tubule touches the glomerulus. The cells of the macula densa are sensitive to the concentration of sodium chloride in the distal convoluted tubule. A decrease in sodium chloride concentration initiates a signal from the macula densa that has two effects: (1) it decreases resistance to blood flow in the afferent arterioles, which raises glomerular hydrostatic

neg: Laminin, beta 2 molecules are largely unknown, but some of the chains have been shown to differ with respect to their tissue distribution, presumably reflecting diverse functions in vivo. This gene encodes the beta chain isoform laminin, beta 2. The beta 2 chain contains the 7 structural domains typical of beta chains of laminin, including the short alpha region. However, unlike beta 1 chain, beta 2 has a more restricted tissue distribution. It is enriched in the basement membrane of muscles at the neuromuscular junctions, kidney glomerulus and vascular smooth muscle. Transgenic mice in which the beta 2 chain gene was inactivated by

neg: Diuretic increase osmolarity but have limited tubular epithelial cell permeability. They work primarily by expanding extracellular fluid and plasma volume, therefore increasing blood flow to the kidney, particularly the peritubular capillaries. This reduces medullary osmolality and thus impairs the concentration of urine in the loop of Henle (which usually uses the high osmotic and solute gradient to transport solutes and water). Furthermore, the limited tubular epithelial cell permeability increases osmolality and thus water retention in the filtrate. It was previously believed that the primary mechanism of osmotic diuretics such as mannitol is that they are filtered in the glomerulus, but cannot

neg: Filtration When left in sealed containers the filtered water takes longer to go foul, demonstrating that very small items (such as bacteria) can be removed from fluids by filtration. In the kidney, renal filtration is the filtration of blood in the glomerulus, followed by selective reabsorption of many substances essential for the body to maintain homeostasis. Filtration Filtration is any of various mechanical, physical or biological operations that separate solids from fluids (liquids or gases) by adding a medium through which only the fluid can pass. The fluid that passes through is called the filtrate. In physical filters oversize solids in

neg: Podocin N- and C-terminus, the latter of which interacts with the cytosolic tail of nephrin, with CD2AP serving as an adaptor. Podocin is localized on the membranes of podocyte pedicels (foot-like long processes), where it oligomerizes in lipid rafts together with nephrin to form the filtration slits. Podocin Podocin is a protein component of the filtration slits of podocytes. Glomerular capillary endothelial cells, the glomerular basement membrane and the filtration slits function as the filtration barrier of the kidney glomerulus. Mutations in the podocin gene NPHS2 can cause nephrotic syndrome, such as focal segmental glomerulosclerosis (FSGS) or minimal change disease (MCD).

neg: Podocyte Podocyte Podocytes are cells in the Bowman's capsule in the kidneys that wrap around capillaries of the glomerulus. The Bowman's capsule filters the blood, retaining large molecules such as proteins while smaller molecules such as water, salts, and sugars are filtered as the first step in the formation of urine. Although various viscera have epithelial layers, the name visceral epithelial cells usually refers specifically to podocytes, which are specialized epithelial cells that reside in the visceral layer of the capsule. Podocytes are found lining the Bowman's capsules in the nephrons of the kidney. The foot processes known as "pedicels" that

neg: Mesangium separated from the lumen of the capillaries by endothelial cells. Mesangium In the glomerulus of the kidney, the mesangium is a structure associated with the capillaries. It is continuous with the smooth muscles of the arterioles. It is outside the capillary lumen, but surrounded by capillaries. It is in the middle (meso) between the capillaries (angis). It is contained by the basement membrane, which surrounds both the capillaries and the mesangium. This term is often used interchangeably with mesangial cell, but in this context refers specifically to the intraglomerular mesangial cells. These cells are phagocytic and secrete the amorphous basement

neg: Mesangium Mesangium In the glomerulus of the kidney, the mesangium is a structure associated with the capillaries. It is continuous with the smooth muscles of the arterioles. It is outside the capillary lumen, but surrounded by capillaries. It is in the middle (meso) between the capillaries (angis). It is contained by the basement membrane, which surrounds both the capillaries and the mesangium. This term is often used interchangeably with mesangial cell, but in this context refers specifically to the intraglomerular mesangial cells. These cells are phagocytic and secrete the amorphous basement membrane-like material known as the "mesangial matrix". They are typically

neg: Endothelium filtration, such as in the glomerulus of the kidney, blood vessel tone, hemostasis, neutrophil recruitment, and hormone trafficking. Endothelium of the interior surfaces of the heart chambers is called endocardium. Endothelium is mesodermal in origin. Both blood and lymphatic capillaries are composed of a single layer of endothelial cells called a monolayer. In straight sections of a blood vessel, vascular endothelial cells typically align and elongate in the direction of fluid flow. The foundational model of anatomy makes a distinction between endothelial cells and epithelial cells on the basis of which tissues they develop from, and states that the presence

neg: IgA nephropathy glomerulus. There are other diseases associated with glomerular IgA deposits, the most common being IgA vasculitis (formerly known as Henoch–Schönlein purpura [HSP]), which is considered by many to be a systemic form of IgA nephropathy. IgA vasculitis presents with a characteristic purpuric skin rash, arthritis, and abdominal pain, and occurs more commonly in young adults (16–35 years old). HSP is associated with a more benign prognosis than IgA nephropathy. In non-aggressive IgA nephropathy there is traditionally a slow progression to chronic kidney failure in 25–30% of cases during a period of 20 years. The classic presentation for the non-aggressive form

neg: Alport syndrome by mutations in "COL"4A3, "COL4A4", and "COL4A5", three of six human genes involved in basement membrane (type IV) collagen biosynthesis. Mutations in any of these genes prevent the proper production or assembly of the specialised type IV collagen '345' network found in the glomerulus, which is an important structural component of basement membranes in the kidney, inner ear, and eye. It is also found in other locations, including the alveoli of the lungs. Basement membranes are thin, sheet-like structures that separate and support cells in many tissues. Type IV collagen '112' type is found in both vertebrates and invertebrates, and

neg: Organ-on-a-chip of the nephron’s glomerulus, proximal convoluted tubule and loop of Henle. Each part of the device has its unique design, generally consisting of two microfabricated layers separated by a membrane. The only inlet to the microfluidic device is designed for the entering blood sample. In the glomerulus’ section of the nephron, the membrane allows certain blood particles through its wall of capillary cells, composed by the endothelium, basement membrane and the epithelial podocytes. The fluid that is filtered from the capillary blood into Bowman’s space is called filtrate or primary urine. In the tubules, some substances are added to the

neg: Glomerulus (olfaction) Glomerulus (olfaction) The glomerulus (plural glomeruli) is a spherical structure located in the olfactory bulb of the brain where synapses form between the terminals of the olfactory nerve and the dendrites of mitral, periglomerular and tufted cells. Each glomerulus is surrounded by a heterogeneous population of juxtaglomerular neurons (that include periglomerular, short axon, and external tufted cells) and glial cells. All glomeruli are located near the surface of the olfactory bulb. The olfactory bulb also includes a portion of the anterior olfactory nucleus, the cells of which contribute fibers to the olfactory tract. They are the initial sites for synaptic

neg: Nephron convoluted section the proximal convoluted tubule followed by a straight section (proximal straight tubule); the loop of Henle, which has two parts, the descending loop of Henle ("descending loop") and the ascending loop of Henle ("ascending loop"); the distal convoluted tubule ("distal loop"); the connecting tubule, and the collecting ducts. Nephrons have two lengths with different urine concentrating capacities: long juxtamedullary nephrons and short cortical nephrons. The four mechanisms used to create and process the filtrate (the result of which is to convert blood to urine) are filtration, reabsorption, secretion and excretion. Filtration occurs in the glomerulus and is largely

neg: Shiga-like toxin The vascular endothelium has to continually renew itself, so this killing of cells leads to a breakdown of the lining and to hemorrhage. The first response is commonly a bloody diarrhea. This is because Shiga toxin is usually taken in with contaminated food or water. The toxin is effective against small blood vessels, such as found in the digestive tract, the kidney, and lungs, but not against large vessels such as the arteries or major veins. A specific target for the toxin appears to the vascular endothelium of the glomerulus. This is the filtering structure that is a key to

neg: Marilyn Farquhar due to the recent innovation of the electron microscope. George Palade was working on the kidney glomerulus at the time and provided Farquhar with formal training in the field of cell biology. Together Farquhar and Palade named tight junctions and adherens junctions. Since then, Farquhar has continued to study junctions in the podocytes. After leaving Rockefeller in 1962, she established her own laboratory at the University of California, San Francisco where she became a Professor of Pathology. Her lab focused on using tracers and cytochemistry to investigate the secretory process in pituitary cells and leukocytes. This work yielded the first

neg: Nephrotic syndrome 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

neg: Glomerulus (olfaction) epithelium of fish consists of three cell types, like other vertebrates. These three cell types are the receptor cells, supporting cells and basal cells. Fish glomerulus differs from the mammalian glomerulus in terms of the number of dendrites that it receives from the mitral cells. In a mammalian olfactory system, a single dendrite from a mitral cell enters a single glomerulus. However, in fish, one or more dendrites from mitral cells enter one or more glomerulus. Glomerulus (olfaction) The glomerulus (plural glomeruli) is a spherical structure located in the olfactory bulb of the brain where synapses form between the terminals

neg: Elimination (pharmacology) from the kidney by glomerular filtration and by active tubular secretion following the same steps and mechanisms as the products of intermediate metabolism. Therefore, drugs that are filtered by the glomerulus are also subject to the process of passive tubular reabsorption. Glomerular filtration will only remove those drugs or metabolites that are not bound to proteins present in blood plasma (free fraction) and many other types of drugs (such as the organic acids) are actively secreted. In the proximal and distal convoluted tubules non-ionised acids and weak bases are reabsorbed both actively and passively. Weak acids are excreted when the

neg: Glomerulonephritis is usually mild and overall prognosis is excellent. Proliferative glomerulonephritis is characterised by an increased number of cells in the glomerulus. These forms usually present with a triad of blood in the urine, decreased urine production, and hypertension, the nephritic syndrome. These forms usually progress to end-stage kidney failure (ESKF) over weeks to years (depending on type). IgA nephropathy, also known as "Berger's disease", is the most common type of glomerulonephritis, and generally presents with isolated visible or occult hematuria, occasionally combined with low grade proteinuria, and rarely causes a nephritic syndrome characterised by protein in the urine, and visible

neg: Agkistrodon purposes. Researchers have found that this venom contains protease activity, meaning it attacks and degrades intra- and extracellular proteins. If injected into mice, within 2 hours the venom begins a process known as mesangiolysis (the degeneration and death of cells that line the inner layer of the glomerulus and regulate glomerular filtration in the kidney). Eventually, the kidneys no longer function and the mouse dies. Although "Agkistrodon" venom is lethal to both prey and humans "in vivo", when controlled, the venom has some clinical application. "D. acutus" snake venom contains a protein called ACTX-6. This protein was shown to induce

neg: Efferent arteriole mammalian kidney about 15% of glomeruli lie close to the boundary between the renal cortex and renal medulla and are known as juxtamedullary glomeruli. The rest are simply undifferentiated cortical glomeruli. The efferent arterioles of the undifferentiated cortical glomeruli are the most complex. Promptly on leaving the glomerulus they break up into capillaries and become part of a rich plexus of vessels surrounding the cortical portions of the renal tubules. The efferent arterioles of the juxtamedullary glomeruli are much different. They do break up, but they form bundles of vessels (arteriolae recti) that cross the outer zone of the medulla

neg: Bowman's capsule 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)

neg: Interlobular arteries From each glomerulus, the corresponding efferent arteriole arises and then exits the capsule near the point where the afferent arteriole enters. Distally, efferent arterioles branch out to form dense plexuses (i.e., capillary beds) around their adjacent renal tubules. For cortical nephrons, a single network of capillaries, known as the peritubular capillaries, surrounds the entire renal tubule, whereas for juxtamedullary nephrons, the peritubular capillaries surround only the proximal and distal convoluted tubules, while another network branching from the efferent arteriole, known as the straight arterioles of kidney, surrounds the nephron loop (of Henle). Interlobular arteries Interlobular arteries (or cortical radiate arteries

neg: Apical dendrite receive extrinsic inputs, which the corresponding proximal dendrites receive intrinsic inputs. In each glomerulus the axons of the receptor neurons contact the apical dendrites of mitral cells, which are the principal projection neurons in the olfactory bulb. Cell bodies of mitral cells are located in a distinct layer deep in the olfactory glomeruli. Each mitral cell extends a primary dendrite to a single glomerulus, where the dendrite gives rise to an elaborate tuft of branches onto which the primary olfactory axons synapse. Each glomerulus in the mouse model, for example, contains approximately 25 mitral cells which receive innervation from approximately

neg: Kidney development cranial-to-caudal direction. As it elongates caudally, the pronephric duct induces nearby intermediate mesoderm in the thoracolumbar area to become epithelial tubules called mesonephric tubules. Each mesonephric tubule receives a blood supply from a branch of the aorta, ending in a capillary tuft analogous to the glomerulus of the definitive nephron. The mesonephric tubule forms a capsule around the capillary tuft, allowing for filtration of blood. This filtrate flows through the mesonephric tubule and is drained into the continuation of the pronephric duct, now called the mesonephric duct or Wolffian duct. The nephrotomes of the pronephros degenerate while the mesonephric duct

neg: Podocin Podocin Podocin is a protein component of the filtration slits of podocytes. Glomerular capillary endothelial cells, the glomerular basement membrane and the filtration slits function as the filtration barrier of the kidney glomerulus. Mutations in the podocin gene NPHS2 can cause nephrotic syndrome, such as focal segmental glomerulosclerosis (FSGS) or minimal change disease (MCD). Symptoms may develop in the first few months of life (congenital nephrotic syndrome) or later in childhood. Podocin is a membrane protein of the band-7-stomatin family, consisting of 383 amino acids. It has a transmembrane domain forming a hairpin structure, with two cytoplasmic ends at the

neg: John Savill Savill is active in acute general medicine and is an Honorary Consultant Physician and Nephrologist with the Lothian University Hospitals Division. He is a member of the Lothian Health Board and chairs its Service Redesign Committee. Savill has extensive experience in peer review and has a particular interest in research and development, and the career structures necessary for this, having chaired the Academy of Medical Sciences Working Party on Clinical Academic Careers. John Savill's research interests revolve around the role of cell death and macrophages in resolution and repair of inflammation, especially inflammatory disorders of the kidney glomerulus (glomerulonephritis) and