Page 245 - Medicine and Surgery

P1: KPE
BLUK007-06 BLUK007-Kendall May 25, 2005 18:6 Char Count= 0

Chapter 6: Disorders of the kidney 241

Bowman's space
(urinary lumen)
Bowman's capsule
Proximal tubule Podocyte
(epithelium)
Basement
Bowman's capsule membrane
Endothelium
Capillary loops
Capillary
Bowman's space lumen
(urinary lumen)
Red blood
cell
Blood in Mesangium
Blood out
Mesangial cell

Figure 6.7 Structure of the glomerulus.

The type of damage caused to the structure of the Fibrinoid necrosis, where fibrin is deposited in the
glomerulus determines the pathological appearance, has necrotic vessel walls. Crescents are formed when
abroad relationship to the effect on renal function and necrotic vessel walls leak blood and fibrin, so that
hence the clinical presentation. The disease process may macrophages and proliferating epithelial cells invade
be diffuse affecting all the glomeruli, or focal affecting the Bowman’s space, crushing the glomerulus. If there
only some of the glomeruli. Affected glomeruli may be arecrescentsinmostoftheglomeruli,thetermrapidly
completelydamaged(global),oronlyapartmaybedam- progressiveglomerulonephritisisused,assevererapid
aged (segmental). Most glomerular diseases are either onset acute renal failure usually results.
diffuse global or focal segmental. Almost all forms of glomerulonephritis have a cellular
Within the glomerulus itself, there are different or humoral immunological basis:
appearances: Humoral response: Immune deposits (antibodies or
Proliferation of endothelial cells and mesangial cells antibody–antigen complexes) in the glomerulus fix

is common in diseases that cause nephritic syndrome and activate complement and a variety of other in-
(see Fig. 6.8). Endothelial cell proliferation leads to flammatory mediators such as antioxidants, proteases
occlusion of the capillary lumen, reduced blood flow, and cytokines. The sites, number and type of deposits
oliguria and acute renal failure. Mesangial cell pro- determine the type and extent of damage caused.
liferation, which is usually associated with increased Mesangial deposits cause mesangial cell prolifera-
production of mesangial matrix, can lead to scarring tion and increased mesangial matrix. Subendothe-
(sclerosis) of all or part of the glomerulus. Increased lial deposits are close to the glomerular capillary lu-
matrix can lead to reduced blood flow and/or protein- men, so excite marked inflammation which can lead
uria. to rapidly progressive glomerular nephritis, whereas
GBM thickening, which can be due to a number of subepithelial deposits excite less of an inflammatory

mechanisms, tends to cause nephrotic syndrome, and response, because the glomerular basement mem-
can be due to a number of mechanisms (often co- brane prevents the influx of cells from the capillar-
existent) including deposition of immune complexes, ies. Circulating immune complexes filtered by the kid-
over-synthesis of basement membrane material and ney tend to cause less injury than complexes formed
in-growth of mesangium. de novo in the glomerulus.
More severe patterns may occur when the glomeru- Cellular response: Some glomerular diseases (such

lar capillary walls are acutely and severely damaged. as minimal change nephropathy and focal segmental