We distinguish a primitive and secondary wrenkled kidney.
Kidney wrinkled primitive or vascular or genuine or small red kidney.
The primitive or arteriosclerotic wrenkled kidney characterized by a vascular hyaline
arteriosclerosis, into the afferent arterioles, is a typical pathology of the
elderly, with reduction of blood supply to the glomerulus, which goes against
obsolescence, also characterized by deposit of hyaline material into the glomerulus,
that becomes a fibrous mass. The surface of the kidney is grainy and irregular, due to the
alternation of whitish dark and hypertrophic retracted areas. The dark areas are
the degenerate, obsolescent nephrons, the clear ones are represented by the
victorious glomeruli. The calicopielici spaces are filled with adipose tissue,
the capsule becomes adherent to the kidney and does not escape and the kidney
becomes smaller and smaller, weighing up to 30g, from 150 grams of origin.
Arteriosclerosis is in general a process that causes hardening of the arteries
due to thickening and loss of elasticity; is characterized by an increase in the
consistency of the vessel wall which represents the outcome in sclerosis of
various pathological processes.
Under this name are included various morbid forms that can be found associated or isolated and that however all have as a final effect a more or less high reduction of the elasticity of the arterial wall with consequent infarction (coronary arteries) or thrombosis (arteries of the ari). These forms are: 1) arteriosclerosis of small vessels (arteriolesclerosis); 2) hyperplastic arteriosclerosis; 3) arteriosclerosis of the average tunic; 4) atherosclerosis.
Arteriolesclerosis, on the other hand, affects the larger
vessels, only the arterioles of the organs and is well documented especially in
the kidneys, where it causes a wrinkling (renal wrenkled) known as benign
nephrosclerosis. In the affected arterioles there is a homogeneous thickening
due to deposits of hyaline substance (v. Lalynosis) with loss of cellular
infrastructures. The hyperplastic form is due to proliferation of the muscle
cells that restrict the lumen; it also frequently affects the renal arterioles
and is found in cases of severe hypertension sustained by a severe impairment of
the kidneys (malignant nephrosclerosis).
The arteriosclerosis of the middle tunic is characterized by regressive phenomena of the muscular and elastic tissues of the medium tunic, to which fibrosclerolic tissue is substituted; from this comes not so much a deformation of the vessel as a significant loss of its elasticity.
In juveniles the primitive wrenkled kidney is due to malignant nefroangiosclerosis with myintimal hyperplasia, with thickening of the onion bulb artery, with hypertensive phenomena and hypertensive nephropathy. These patients do not present with slow evolution on an arteriosclerotic basis, but rapid evolution occurs, with fibrinoid necrosis of the arterioles and abrupt hypoafflexion and this causes renal infarction, with necrosis of a portion of the wedge-shaped renal parenchyma, with apical towards the occluded vase.
|
Appearance to "onion bulb" of medium-sized vessels |
The rapid rise in blood pressure is responsible for endothelial damage, which
causes alteration of vascular permeability, facilitating the entry of plasma
components into the thickness of the vessel wall. To this is added fibrinoid
necrosis which intervenes in the inner layers of the vessel wall, just below the
endothelium. The result of these processes is a narrowing of the vessel lumen;
this results in a reduced blood supply to the kidney, which is detected by the
juxtaglomerular apparatus, leading to an increase in renin release. This enzyme
in turn determines the production of angiotensin and finally of aldosterone,
substances responsible for a further increase in blood pressure. This happens
because the normal function of the juxtaglomerular apparatus is to respond to a
drop in blood pressure (which manifests itself by reducing the blood supply to
the kidney) triggering the production of vasoconstrictive and sodioritentive
substances. Thus a sort of "vicious circle" (positive feedback) is established,
for which the increase in blood pressure results in vascular damage, which in
turn induces pressure increase.
Renal biopsy performed in affected individuals shows, in the medium-caliber
arteries observed in cross section, a characteristic "onion bulb" appearance due
to the remarkable lamellar hyperplasia of the wall; in the afferent and
intralobular arterioles, on the other hand, aspects of fibrinoid necrosis and
thickening of the intimate tunic are observed.
We have the forms of kidney wrenkled secondary to:
- bilateral chronic pyelonephritis with asynchronous onset
- LES (>> lupus)
- Amiloidosico
- tubercular
- papillary necrosis
- chronic glomerulonephritis
It leads to chronic renal failure. In chronic pyelonephritis there will be
interstitiopathy, with unilateral onset and with asynchronous evolution, which
eventually becomes bilateral. The kidney wrenkled by chronic glomerulonephritis
leads to destruction of the glomeruli, with irreversible aggression of all the
glomerulus, for lesions e.g. as a result of membrano-proliferative
glomerulonephritis or lead to sclerosing glomerulonephritis, with tubular
atrophy and interstitial fibrosis. The small gray kidney is determined. The
chronic pyelonephritic wrenkled kidney, in the presence of a pyelonephritis, due
to infection due to germs, e.g. in one diabetic, one of the two kidneys evolves
up to the picture of acute renal failure and the other vicar, but also the other
vicariating kidney, soon, will be involved, in a more or less long time. The
kidney becomes loose, calcium is deposited and the renal pelvis narrows up to
hydronephrosis and urolithiasis, due to accumulation of necrotic and purulent
material with consequent calcification. In the case of diabetics, moreover,
infections and especially if they use analgesics, can be have papillary necrosis
that plays a major role in the anatomy of the kidney, with loss of the renal
medulla architecture, which is less, as a result of degeneration.
Renal manifestations. Renal involvement results in a lupic nephropathy with
nephritic and/or nephrotic syndrome pictures that turn to acute renal failure.
From the histological point of view we will have the picture of a) mesangial
glomerulonephritis: with the increase of the mesangial component and the
deposition of immune complexes; b) membranous glomerulonephritis: with rigid
loops and thickening of the glomerular basement membrane with deposits of
immunoglobulins and of complement to which proteinuria follows c) glocalulphite
proliferative focal: proliferation of some glomerular loops, proliferation of
endothelial cells and thickening of the basement membrane and deposition of
immune complexes (IgG) and complement (C3); d) Proliferative proliferative
glomerulonephritis, characterized by an intense proliferation that covers 50% of
the glomeruli in the subendothelial site and in the mesangium, with areas of
proliferative sclerosis that turns towards the picture of renal failure.
Increased in volume, the kidney is pale, with replacement of the entire renal
parenchyma, with destruction of vessels, glomeruli and tubules, whereby the
whole kidney is filled with amyloid, visible with polarized light, while for the
histochemical demonstration we can use the technique of coloring with red congo;
it can occur in multiple myeloma, chronic osteomyelitis and chronic degenerative
affections.
The tuberculous condition can result in a wrenkled kidney, which appears, however, in the ascending infection. in fact, in widespread miliary tuberculosis, when Koch's bacilli are in circulation, the lesions are descending. The fundamental condition is like a descending pyelonephritis, ie the bacilli from the bloodstream lead to the cortical of the kidney, where there are tuberculous lesions. The mechanism correlates with tuberculous cystitis, in this case, ie infection of the bladder and ascending mechanism, called pyelonephritis by ascending route. Acidic micropiuria is determined. Koch's bacillus rises and infects the pelvis and will be found in the renal calyxes destroying the renal parenchyma by caseous necrosis. Then the bacillus will be brought from the glasses into the bladder together with the caseous material: a tuberculosis ureterite will be determined and the kidney becomes functionally excluded. The kidney will turn into a caseous mass called the "glassy kidney of the glassmakers".
index nefrology