Diagnosis And Treatment Of Glomerulonephritis Biology Essay

If we recall the construction of the kidney, we find that it is made of different subdivisions ( Figure 1 ) , the functional unit of the kidney ( Figure 2 ) and the chief filtration ‘machinery ‘ ( Figure 3, I ) .

Figure 1: The construction of the kidney – The kidney is surrounded by the nephritic capsule and split into 3 subdivisions, the myelin, the cerebral mantle and so the nephritic pelvic girdle. Each kidney is supplied with oxygenated blood, by the nephritic arteria and removes deoxygenated blood via the nephritic vena. Once the kidneys carry out their filtration mechanism, they empty their waste merchandise, down the ureter.

Taken from web1.stmaryssen-h.schools.nsw.edu.au/SMSHS/ricks % 20sites/Biology % 20web % 20site/HSC_9_2maintaining % 20a % 20balance/Notes % 20for % 20point % 203/summary % 20notes.html

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Figure 2: A individual uriniferous tubule – The uriniferous tubule is the functional unit of the kidney and over a million of these are found within each kidney leting it to transport out its map. Notice how it spans across the different kidney subdivisions.

Taken from www.uptodate.com/patients/content/image.do

Figure 3: The Juxtaglomerular Apparatus – ( I ) The juxtaglomerular setup is the chief filtration of blood occurs in uriniferous tubules and this is where the glomerulus and Bowman ‘s capsule interact.

( two ) The mesengial cells are found closely associated with the filtration portion of the juxtaglomerular setup and their place links with their function in doing redness in glomeruli.

( three ) The Podocytes are besides found near glomerular capillaries and these may blend together and act upon the filtration of the glomerulus, doing Hodgkins disease. This disease is a type of swelling due to the recreation of roll uping merchandises, which are non filtered and so deposited to other parts of the organic structure.

Taken from www.siumed.edu/~dking2/crr/images/corp5.jpg.

Glomerulonephritis ( GN ) is a type of kidney disease ; where by filtration of the blood is disrupted. It is chiefly associated with the glomeruli in the kidneys, going inflamed ( NHS Choices 2009 ) and there can be different types of the disease which may be proliferative or non-proliferative.

The chief cause of the disease is non exactly known but, there are many possible accounts. The most common account for proliferative GN is due to an immune system response, where inflammatory cells like thrombocytes or macrophages become trapped in the glomeruli ( Couser 1999 ) . Here they circulate and accumulate, originating a mechanism that leads to redness of the glomeruli ( Couser 1999 ) . This is the mechanism for the most common signifier of proliferative GN, known as Immunoglobulin A ( IgA ) kidney disease ( D’Amico 1987 ) . This is when IgA proteins, which fight infections, construct up within the glomeruli and therefore redness ( Geeky Medics 2010 ) . Another immune system response involves antibodies interacting with antigens, formed by the glomerular cellar membrane, which can besides trip redness ( Watson and Royle 1987 ) .

Another possible account for proliferative GN is infection-related, following invasion by bacteriums of the Streptoccoci strain ( Ryan and Ray 2004 ) , which targets the tegument or pharyngeal tissue ( Watson and Royle 1987 ) . This consequences in post-infectious GN which can besides be associated with other infections like bacterial endocarditis or HIV ( Mayo Clinic 2009 ) .

In add-on, it is besides suggested that vasculitic upsets, like Wegeners Granulomatosis can ensue in crescentic GN ( Geeky Medics 2010 ) ( Figure 4 ) .

Figure 4: Crescentic GM – In Wegener ‘s Granulomatosis, blood vass become inflamed, holding an consequence on the filtration rate of the glomerulus and leads to the formation of crescent shaped cicatrixs.

Taken from hypertext transfer protocol: //uk.ask.com/wiki/Glomerular_crescent

Non-proliferative GN can be idiopathic, such as membranous GN, or may merely merely be genetically linked like focal segmental GN ( Geeky Medics 2010 ) .

When looking at GN ( chiefly proliferative ) we need to besides see the mesengial cells ( Figure 3, two ) . GN can be recognised by an addition in the figure of mesengial cells and their intracellular contents ( Churg 2006 ) . They quickly multiply, increasing the thickness of this bed and imperativeness against the glomerular capillaries ( Churg 2006 ) ( Figure 5 ) .

Figure 5: Histology of proliferative GN – As the mesengial cells multiply, they increase in figure and compress against the glomerular capillary and contribute towards the glomerulus increasing in perimeter. Taken from ( Churg 2006 ) .

In some instances, the mesengial cells may even occupy the glomerular capillaries and sit in between the filtration portion of the uriniferous tubule, made up of endothelial cells and the cellar membrane ( Figure 6 ) ( Churg 2006 ) . Hence, the cellar membrane appears split, interrupting nephritic filtration and hence ensuing in a certain type of GN, known as membranoproliferative GN ( Hope et al. 1993 ) .

Figure 6: A Normal Glomerular Capillary – Proliferation of the mesengial cells leads to invasion between the epithelial cells and the cellar membrane, interrupting glomerular filtration and taking to GN. Taken from www.uncnephropathology.org/jennette/ch1.htm

The glomerular capillaries are besides where proteins from the immune system may be trapped between the cellar membrane and the epithelial cells, which accumulate and form ‘humps ‘ in the glomerular capillary walls ( Churg 2006 ) , ensuing in membranous GN ( Hope et al. 1993 ) .

Specifically in crescentic GN, which is infection related, there is an addition in epithelial cells which compress the glomerulus and causes cicatrixs, described as ‘crescent shaped ‘ ( Malvinder 2008 ) ( Figure 4 ) .

However there can be milder signifiers of GN, with the most common being minimum alteration GN, caused by the merger of podocytes ( Hope et al. 1993 ) ( Figure 3, three ) .

When looking at post-infectious GN, we find that it is usually the group A beta-haemolytic streptococci bacteriums which causes infection ( Watson and Royle 1987 ) and brings about acute post-streptococcal GN ( APSGN ) ( Duvuru 2010 ) . The activity of this bacteria is thought to be associated with the accretion of streptococcic antigens, adhering to the immune antibodies, which are so deposited on the glomerulus cellar membrane ( Field et al. 2010 ) ( Figure 7 ) .

Figure 7: APSGN – ( Arrows show where the antigen-antibody composites have been deposited. ) As the antigen is bound to the antibodies, it prevents the antibodies from bring downing a defense mechanism mechanism and leads to alteration of the glomerular cellar membrane ( Field et al. 2010 ) .

Taken from www.ndt-educational.org/ferrariomgp.asp

There are many marks and symptoms associated with GN, which can change between the different signifiers of GN, but there are common symptoms that are found in all types. As the glomeruli are obstructed, filtration is reduced and allows for blood to leak into the tubules and hence this blood passes out into the piss ( Watson and Royle 1987 ) . The piss may besides be described as ‘cloudy ‘ and this is due to proteinuria. This is when extra serum proteins are passed out, in the piss ( Nordqvist 2009 ) due to the impaired filtration mechanism ( Field et al. 2010 ) . This extra serum may besides be linked with symptoms of sickness and emesis, which are besides associated with GN ( Unanue 2011 ) . The piss may besides be described as, hematuria, where ruddy blood cells are lost, triping anemia in GN sick persons ( Watson and Royle 1987 ) . Another common symptom is swelling, as there is a recreation of roll uping merchandises, which are non filter, to other parts of the organic structure ( Hicks 2009 ) . Symptoms related to respiratory jobs such, a sore pharynx or tegument roseola would be more important in post-infectious GN due to streptococci bacteriums infecting the guttural tissue and the tegument ( Feldon et al. 2010 ) . Another common symptom is high blood pressure, caused by salt and H2O saving and therefore activation of the renin-angiotensin system ( Field et al. 2010 ) ( Figure 8 ) .

Figure 8: The Renin-angiotensin ( aldosterone ) system ( RAS ) – As there is an accretion of H2O and salt, the circulating volume besides increases and activates RAS. RAS so vasoconstricts blood vass, doing an addition in blood force per unit area, which is a symptom of GN.

Taken from: www.commons.wikimedia.org/wiki/File: Systeme_renine-angiotensine-aldosterone.png

Diagnosis of GN, tends to be via Urinalysis, in order to happen the presence of blood and proteins in the piss ( Haggerty 2002 ) . Besides a blood trial can be taken and if there is an accretion of waste merchandises, such as creatinine or urea-nitrogen so this can bespeak GN ( Haggerty 2002 ) . The blood can besides be checked for anti-streptolysin titer, due to reactions by streptococcus bacteriums and another indicant of GN ( Brunner and Suddarth 1990 ) . Otherwise a much simpler swab of the pharynx could be used to observe the streptococcic infection, which is used widespread ( Hicks 2009 ) . A concluding diagnostic rating is by transporting out a nephritic biopsy in order to see the inflamed glomeruli and accretion of cells environing the glomerular capillaries ( Brunner and Suddarth 1990 ) .These tend to be the most common diagnostic processs but probes can be made by agencies of other methods, like in radiology, where a nephritic ultrasound is used ( Hope et al. 1993 ) .

Treatments on GN sick persons can run and depends on the type of GN that they suffer from, but the chief purpose of intervention is to advance kidney map and cut down symptoms of GN ( Hicks 2009 ) . By merely acquiring plentifulness of remainder, until the urine becomes clear and degrees of nitrogen-bearing waste merchandises regularize, can promote the regain of nephritic map and a decrease of the other symptoms associated with GN ( Hope et al. 1993 ) . Another intervention used is by modulating the diet and fluids of the GN sick person, for illustration, by puting limitations on dietetic proteins and counterbalancing for fluid loses by imbibing plentifulness of fluids ( Hope et al. 1993 ) . It has been predicted that drugs which block the Angiotensin II receptors or ACE inhibitors may be a signifier of intervention, for cut downing the effects of GN, but this is still being investigated ( McMillan 2010 ) . As there are different signifiers of the disease, different drugs may be used to handle each signifier, for illustration in GN caused by immune response, corticoids or immunosuppressor may be used, but this is non a definite intervention for GN ( McMillan 2010 ) . Treatment of vasculitic upsets like Wegener ‘s granulomatosis, can be a signifier of intervention, which found that plasma exchange can be used to understate the effects of immune antibodies which lead to the development of GN ( Casian 2011 ) .

Current novel methods being researched, look into pathological mechanisms of GN, to perchance bring forth a drug to change by reversal this mechanism. One interesting survey identified that the voltage-gated K channel, Kv1.3 was found in the glomeruli and tubules of rats, with GN ( Hyodo et al. 2010 ) .They suggest that Kv1.3 marks and keep memory T cells, which act like an immune response by recognizing foreign organic structures ( Hyodo et al. 2010 ) . After utilizing a Kv1.3 blocker drug, they found that the rats produced less albuminurias and their glomeruli had less scarring ( Hyodo et al. 2010 ) . The survey concluded that this Kv1.3 could be the cause of GN and could be a utile determination to potentiate a remedy for GN in worlds, which is still being investigated ( Hyodo et al. 2010 ) .

Another survey suggested that kidney disease may be linked with bone morphogenetic proteins ( BMPs ) , which are growing factors that are of import in the ordinance on kidney map ( Suh et al. 2011 ) . As they interact with binding sites found in the epithelial cells, this survey investigated whether polymorphism of the cistron for BMP, may play a function in GN ( Suh et al. 2011 ) . The survey concluded that mutants in this cistron may do kids to go susceptible to IgA kidney disease, which is presently being investigated and could intend a possible intervention mechanism ( Suh et al. 2011 ) .

One other survey investigated the presence of myleoperoxidase-associated anti-neutrophil cytoplasmic antibody ( MPO-ANCA ) and anti-glomerular cellar antibodies ( anti-GBM Ab ) as a possible cause of the crescent shaped cicatrixs in rapid progressive GN ( RPGM ) , but this is besides still being investigated ( Nakabayashi et al. 2011 ) .

To reason GM, is a diverse nephritic disease, which can be acute or chronic in footings of its causes and effects. The disease is still being exhaustively investigated today as no definite intervention has been found.

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