If we recall the structure of the kidney, we find that it is made of different sections (Figure 1), the functional unit of the kidney (Figure 2) and the main filtration ‘machinery’ (Figure 3, i).
Figure 1: The structure of the kidney – The kidney is surrounded by the renal capsule and split into 3 sections, the medulla, the cortex and then the renal pelvis. Each kidney is supplied with oxygenated blood, by the renal artery and removes deoxygenated blood via the renal vein. Once the kidneys carry out their filtration mechanism, they empty their waste product, 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
Figure 2: A single nephron – The nephron is the functional unit of the kidney and over a million of these are found within each kidney allowing it to carry out its function. Notice how it spans across the different kidney sections.
Taken from www.uptodate.com/patients/content/image.do
Figure 3: The Juxtaglomerular Apparatus – (i) The juxtaglomerular apparatus is the main filtration of blood occurs in nephrons and this is where the glomerulus and Bowman’s capsule interact.
(ii) The mesengial cells are found closely associated with the filtration part of the juxtaglomerular apparatus and their position links with their role in causing inflammation in glomeruli.
(iii) The Podocytes are also found near glomerular capillaries and these may fuse together and influence the filtration of the glomerulus, causing Hodgkins disease. This disease is a type of swelling due to the diversion of accumulating products, which are not filtered and so deposited to other parts of the body.
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 mainly associated with the glomeruli in the kidneys, becoming inflamed (NHS Choices 2009) and there can be different types of the disease which may be proliferative or non-proliferative.
The main cause of the disease is not precisely known but, there are many possible explanations. The most common explanation for proliferative GN is due to an immune system response, where inflammatory cells like platelets or macrophages become trapped in the glomeruli (Couser 1999). Here they circulate and accumulate, initiating a mechanism that leads to inflammation of the glomeruli (Couser 1999). This is the mechanism for the most common form of proliferative GN, known as Immunoglobulin A (IgA) nephropathy (D’Amico 1987). This is when IgA proteins, which fight infections, build up within the glomeruli and therefore inflammation (Geeky Medics 2010). Another immune system response involves antibodies interacting with antigens, formed by the glomerular basement membrane, which can also trigger inflammation (Watson and Royle 1987).
Another possible explanation for proliferative GN is infection-related, following invasion by bacteria of the Streptoccoci strain (Ryan and Ray 2004), which targets the skin or pharyngeal tissue (Watson and Royle 1987). This results in post-infectious GN which can also be associated with other infections like bacterial endocarditis or HIV (Mayo Clinic 2009).
In addition, it is also suggested that vasculitic disorders, like Wegeners Granulomatosis can result in crescentic GN (Geeky Medics 2010) (Figure 4).
Figure 4: Crescentic GM – In Wegener’s Granulomatosis, blood vessels become inflamed, having an effect on the filtration rate of the glomerulus and leads to the formation of crescent shaped scars.
Taken from http://uk.ask.com/wiki/Glomerular_crescent
Non-proliferative GN can be idiopathic, such as membranous GN, or may just simply be genetically linked like focal segmental GN (Geeky Medics 2010).
When looking at GN (mainly proliferative) we need to also consider the mesengial cells (Figure 3, ii). GN can be recognised by an increase in the number of mesengial cells and their intracellular contents (Churg 2006). They rapidly multiply, increasing the thickness of this layer and press against the glomerular capillaries (Churg 2006) (Figure 5).
Figure 5: Histology of proliferative GN – As the mesengial cells multiply, they increase in number and compress against the glomerular capillary and contribute towards the glomerulus increasing in circumference. Taken from (Churg 2006).
In some cases, the mesengial cells may even invade the glomerular capillaries and sit in between the filtration part of the nephron, made up of endothelial cells and the basement membrane (Figure 6) (Churg 2006). Hence, the basement membrane appears split, disrupting renal filtration and therefore resulting 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 basement membrane, disrupting glomerular filtration and leading to GN. Taken from www.uncnephropathology.org/jennette/ch1.htm
The glomerular capillaries are also where proteins from the immune system may be trapped between the basement membrane and the epithelial cells, which accumulate and form ‘humps’ in the glomerular capillary walls (Churg 2006), resulting in membranous GN (Hope et al. 1993).
Specifically in crescentic GN, which is infection related, there is an increase in epithelial cells which compress the glomerulus and causes scars, described as ‘crescent shaped’ (Malvinder 2008) (Figure 4).
However there can be milder forms of GN, with the most common being minimal change GN, caused by the fusion of podocytes (Hope et al. 1993) (Figure 3, iii).
When looking at post-infectious GN, we find that it is normally the group A beta-haemolytic streptococcus bacteria which causes infection (Watson and Royle 1987) and brings about acute post-streptococcal GN (APSGN) (Duvuru 2010). The activity of this bacterium is thought to be associated with the accumulation of streptococcal antigens, binding to the immune antibodies, which are then deposited on the glomerulus basement membrane (Field et al. 2010) (Figure 7).
Figure 7: APSGN – (Arrows show where the antigen-antibody complexes have been deposited.) As the antigen is bound to the antibodies, it prevents the antibodies from inflicting a defence mechanism and leads to modification of the glomerular basement membrane (Field et al. 2010).
Taken from www.ndt-educational.org/ferrariomgp.asp