Other parts (Hicks 2009). Respiratory problems related to sympto
There are many signs and symptoms associated with GN, which can vary between the different forms 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 therefore this blood passes out into the urine (Watson and Royle 1987). The urine may also be described as 'cloudy' and this is due to proteinuria. This is when excess serum proteins are passed out, in the urine (Nordqvist 2009) due to the impaired filtration mechanism (Field et al. 2010) . This excess serum may also be linked with symptoms of nausea and vomiting, which are also associated with GN (Unanue 2011). The urine may also be described as, haematuria, where red blood cells are lost, triggering anaemia in GN sufferers (Watson and Royle 1987). Another common symptom is swelling, as there is a diversion of accumulating products, which are not filter, to other parts of the body (Hicks 2009). Symptoms related to respiratory problems such, a sore throat or skin rash would be more significant in post-infectious GN due to streptococci bacteria infecting the pharyngeal tissue and the skin (Feldon et al. 2010). Another common symptom is hypertension, caused by salt and water preservation 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 accumulation of water and salt, the circulating volume also increases and activates RAS. RAS then vasoconstricts blood vessels, causing an increase in blood pressure, 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 find the presence of blood and proteins in the urine (Haggerty 2002). Also a blood test can be taken and if there is an accumulation of waste products, such as creatinine or urea-nitrogen then this can indicate GN (Haggerty 2002). The blood can also be checked for anti-streptolysin titre, due to reactions by streptococci bacteria and another indication of GN (Brunner and Suddarth 1990). Otherwise a much simpler swab of the throat could be used to detect the streptococcal infection, which is used widespread (Hicks 2009). A final diagnostic evaluation is by carrying out a renal biopsy in order to view the inflamed glomeruli and accumulation of cells surrounding the glomerular capillaries (Brunner and Suddarth 1990).These tend to be the most common diagnostic procedures but investigations can be made by means of other methods, like in radiology, where a renal ultrasound is used (Hope et al. 1993).
Treatments on GN sufferers can range and depends on the type of GN that they suffer from, but the main aim of treatment is to promote kidney function and reduce symptoms of GN (Hicks 2009). By simply getting plenty of rest, until the urine becomes clear and levels of nitrogenous waste products regularize, can encourage the regain of renal function and a reduction of the other symptoms associated with GN (Hope et al. 1993). Another treatment used is by regulating the diet and fluids of the GN sufferer, for example, by placing restrictions on dietary proteins and compensating for fluid loses by drinking plenty of fluids (Hope et al. 1993). It has been predicted that drugs which block the Angiotensin II receptors or ACE inhibitors may be a form of treatment, for reducing the effects of GN, but this is still being investigated (McMillan 2010). As there are different forms of the disease, different drugs may be used to treat each form, for example in GN caused by immune response, corticosteroids or immunosuppressant may be used, but this is not a definite treatment for GN (McMillan 2010). Treatment of vasculitic disorders like Wegener's granulomatosis, can be a form of treatment, which found that plasma exchange can be used to minimise the effects of immune antibodies which lead to the development of GN (Casian 2011).
Current novel methods being researched, investigate pathological mechanisms of GN, to possibly produce a drug to reverse this mechanism. One interesting study identified that the voltage-gated potassium channel, Kv1.3 was found in the glomeruli and tubules of rats, with GN (Hyodo et al. 2010).They suggest that Kv1.3 targets and restrain memory T cells, which act like an immune response by recognising foreign bodies (Hyodo et al. 2010). After using a Kv1.3 blocker drug, they found that the rats produced less proteinuria and their glomeruli had less scarring (Hyodo et al. 2010). The study concluded that this Kv1.3 could be the cause of GN and could be a useful finding to potentiate a cure for GN in humans, which is still being investigated (Hyodo et al. 2010).
Another study suggested that kidney disease may be linked with bone morphogenetic proteins (BMPs), which are growth factors that are important in the regulation on kidney function (Suh et al. 2011). As they interact with binding sites found in the epithelial cells, this study investigated whether polymorphism of the gene for BMP, may play a role in GN (Suh et al. 2011). The study concluded that mutations in this gene may cause children to become susceptible to IgA nephropathy, which is currently being investigated and could mean a possible treatment mechanism (Suh et al. 2011).
One other study investigated the presence of myleoperoxidase-associated anti-neutrophil cytoplasmic antibody (MPO-ANCA) and anti-glomerular basement antibodies (anti-GBM Ab) as a possible cause of the crescent shaped scars in rapid progressive GN (RPGM), but this is also still being investigated (Nakabayashi et al. 2011).
To conclude GM, is a diverse renal disease, which can be acute or chronic in terms of its causes and consequences. The disease is still being thoroughly investigated today as no definite treatment has been found.