FIGURE 13.1

The renal parenchyma in end-stage renal failure is characterized by extensive glomerulosclerosis, tubular atrophy and hypertrophic and hyaline changes in the arteries and arterioles. Virtually no functioning renal parenchyma remains.

FIGURE 13.2

Autosomal dominant polycystic kidney disease. In this disease the kidney is enormously enlarged with cysts throughout the renal parenchyma. Many of these cysts will be up to several centimetres in diameter. Haemorrhage and infection within cysts is common.

FIGURE 13.3

Histological examination of a kidney with autosomal dominant polycystic kidney disease shows cysts developing from all parts of the nephron. Intervening parenchyma is compressed and shows progressive ischaemia and hypertensive damage.

FIGURE 13.4

In Alport’s syndrome there is a genetic abnormality of type IV collagen, which is an essential part of the glomerular basement membrane. As a consequence there is a failure of the basement membrane assembly with the appearance of multilayering and fragmentation.

FIGURE 13.5

The glomerulus is a specialized capillary bed with close approximation of the endothelium and the epithelium (podocytes) separated only by a thin glomerular basement membrane (GBM). The endothelium is fenestrated to allow the free passage of macromolecules. The glomerular basement membrane is a product of both the endothelial and epithelial cells. The podocytes have specialist filtration structures called foot processes which align themselves on the glomerular basement membrane. This specialized capillary bed is supported by modified smooth muscle cells called mesangial cells. The latter are also phagocytic and have a major role in determining the intraglomerular pressure. Filtration occurs from the capillary lumen into the urinary filtration space.

FIGURE 13.6

(A) Normal glomeruli. (B) These glomeruli show an increase in cellularity due to proliferation of endogenous glomerular cells, predominantly mesangial cells, and infiltration of the glomerulus by inflammatory cells.

FIGURE 13.7

(A) Normal glomerular basement membrane shown by electron microscopy. (B) The glomerular basement membrane here shown by light microscopy is markedly thickened, a feature seen in a variety of diseases including  membranous glomerulonephritis and diabetic nephropathy.

FIGURE 13.8

A crescent is a proliferation of macrophages and epithelial cells within Bowman’s space but outwith the glomerular capillary bed.

FIGURE 13.9

In minimal change nephropathy the light microscopic appearance of the glomerulus is normal. On examination by electron microscopy there is loss of the normal glomerular epithelial foot processes, known as foot process fusion, and there may be some vacuolation of the epithelium. No other abnormalities are seen in this disease.

FIGURE 13.10

Focal segmental glomerulosclerosis is a disease in which there is fibrosis of part of the glomerular tuft with only a proportion of the glomeruli affected. Within the affected segment there is obliteration of the capillary spaces, extracellular matrix accumulation and sometimes the presence of foamy macrophages.

FIGURE 13.11

(A) Membranous nephropathy is characterized by thickening of the glomerular capillary walls but with normal cellularity. The thickened capillary walls exhibit a spiky appearance on silver stained preparations. (B) Immunofluorescence staining reveals the presence of immune complexes, in this case IgM, within the capillary walls as granular deposits. (C) Electron microscopic examination reveals the presence of subepithelial electron dense immune complexes.

FIGURE 13.12

Mesangiocapillary glomerulonephritis, also known as membranoproliferative glomerulonephritis, is characterized by a combination of hypercellularity and capillary wall thickening. (A) At the light microscopy level the hypercellularity is seen clearly with accentuation of the glomerular) lobular architecture and a reduction in the capillary luminal space. Thickening of the glomerular capillary wall is also evident. (B) Immunofluorescence staining in cases of mesangiocapillary glomerulonephritis reveals the deposition of granules of immune complexes within capillary walls and within mesangial regions in most cases. In the example illustrated here the immunofluorescence reactivity demonstrates IgG deposition within the glomerulus. (C) Examination of cases of mesangiocapillary glomerulonephritis by electron microscopy reveals different patterns of deposition. In one form there is electron-dense thickening of the glomerular basement membrane itself. This form is known as dense deposit disease. The presence of focal electron dense deposits in the subendothelial space as shown here is the much more common form.

FIGURE 13.13

On occasion proliferative glomerulonephritis is focal and segmental. In these instances the hypercellularity is limited to a portion of the glomerular tuft with obliteration of capillaries and occasionally foci of necrosis.

FIGURE 13.14

(A) In diffuse proliferative glomerulonephritis there is marked hypercellularity often with an influx of neutrophil polymorphs and obliteration of the capillary spaces. The glomerular capillary walls are difficult to identify within this hypercellular glomerulus. (B) Immunofluorescence in these instances reveals the granular deposition of immune complexes in the capillary walls. (C) The electron microscopic findings in diffuse proliferative glomerulonephritis are highly characteristic. In the subepithelial space there are large ‘hump’-shaped electron dense deposits.

FIGURE 13.15

(A) In Goodpasture’s syndrome there is a focal proliferative and necrotizing glomerulonephritis usually accompanied by crescent formation. (B) Immunofluorescence staining of renal biopsies demonstrates a linear pattern of deposition of IgG and C3 diagnostic of antiglomerular basement membrane antibodies.

FIGURE 13.16

In diabetic nephropathy there is a nodular expansion of the mesangial matrix with thickening of the glomerular capillary walls but with no hypercellularity. Immunofluorescence staining in diabetic nephropathy is negative.

FIGURE 13.17

In amyloidosis there is marked expansion of the extracellular matrix of the glomerulus with obliteration of the capillary spaces – these features may also affect the larger blood vessels, the tubules and the interstitium of the kidney. The amyloid material stains with the Congo Red stain.

FIGURE 13.18

In a true tubular necrosis there is a flattening of the epithelial cells and many of the tubules contain cellular or acellular debris. The interstitium is oedematous but there is no significant inflammatory infiltrate.

FIGURE 13.19

Patients with myeloma excrete large amounts of light chains in their urine. These light chains may precipitate as casts eliciting a tubular epithelial response and inflammation in the adjacent renal parenchyma – so-called cast nephropathy. This cast nephropathy is one of the forms of kidney involvement in multiple myeloma.

FIGURE 13.20

Hypertension affects the small arteries and arterioles of the kidney. There is a marked hyaline deposition within arteriolar walls with loss of smooth muscle cells. This leads to progressive glomerular ischaemia and glomerular fibrosis.

FIGURE 13.21

(A) In malignant hypertension more severe and acute vascular changes are seen in the arterioles. (B) This is characterized by fibrin deposition, platelet activation and transmural necrosis of the arteriolar wall, a constellation of features known as fibrinoid necrosis. There is little inflammatory infiltrate in fibrinoid necrosis.

FIGURE 13.22

Vasculitis frequently affects the kidney and is characterized by a transmural inflammatory infiltrate causing localized damage with focal cellular necrosis in the blood vessel wall. Eventually this leads to ischaemia of the renal parenchyma and scarring in the blood vessel wall.

FIGURE 13.23

In the haemolytic uraemic syndrome there is fibrinoid necrosis of arterioles with fibrin and platelet deposition within glomeruli.

FIGURE 13.24

Wilms’ tumour shows a triphasic appearance. The three histological elements comprise the undifferentiated blastema, immature epithelium and stromal connective tissue. The relative contribution of these elements varies enormously between individual cases of Wilms’ tumour.

FIGURE 13.25

The most common form of renal cell carcinoma is characterized by a solid architecture composed of clear cuboidal cells supported by a rich vascular stroma. Other variants include the papillary, chromophobe and collecting duct types.