Constitutes renal damage related to mild or moderate hypertension, characterized
by diastolic blood pressure values above 95 mmHg. Similar morphological
lesions, albeit of modest size, are also found in about half of the subjects
over the age of 60 without anamnestic evidence of hypertension.
It is estimated that 10-15% of subjects show a reduction in renal function that
can also reach IRC. The most severe manifestations and the most unfavorable
developments are reported in black people in whom hypertensive nephrosclerosis
is among the major causes of terminal IRC.
The lesions are of varying severity, especially in relation to the duration of hypertension. In the phase of the state, the kidneys are symmetrically reduced in volume, with a capsule adhering to the parenchyma and a finely granular surface.
Coarser patches due to atherosclerotic lesions of larger vessels are only occasional. On the cutting surface, the cortex appears thinened by atrophy and increases in consistency due to fibrosis, while the medullary bone is poorly damaged.
The arched and interlobar arteries have thickened and rigid walls.
The survey m.o. shows lesions on vessels, glomeruli, interstitium and tubules.
The most precocious alterations occur on the arterioles afferent with deposition
of hyaline material, PAS-positive, first below the endothelium and then
progressively in the thickness of the wall with subsequent atrophy of the smooth
muscle cells of the medium tunic (hyaline arteriolesclerosis : The arciform and
interlobar arteries undergo atherosclerotic lesions, with myofibroblastic
proliferation, collagen deposition intimal fibrosis and reduplication of the
internal elastic lamina.Atteromasic alterations are scarce or completely absent.
Changes in arteries and arterioles result in narrowing of the vessel lumen
and reduction of blood supply with progressive development of the glomerular
ischemia pattern. In the early stages the floccule tends to collapse due to
hypoperfusion, with folding and thickening of the m.b.g. In more advanced phases
there is the transformation of the floccule into an acellular hyaline mass and
the urination of the uriniferous space by collagen type I I (so-called
glomerulus ischemia)
The tubules are prey to atrophy and the interstitium is amplitude increased and
more or less infiltrated by elements of chronic inflammation. For the reasons
mentioned above, morphological alterations are more evident in the subcapsular
peripheral areas of the cortex.
The severity and extent of damage are related to the duration of hypertension
and correlate with the degree of functional impairment. Renal damage may also be
responsible for mild proteinuria.
It develops in the course of severe forms of hypertension (with diastolic
pressure values above 120 mmHg) accompanied by changes in the fundus of the
eye and a tumultuous clinical course. Renal involvement is constant and the
functional consequences are serious, so much so as to lead to IR in a short time
(on the order of months).
Malignant hypertension can damage normal kidneys in initially normotensive
subjects, but more frequently occurs on kidneys already damaged by other
diseases (hypertensive nephrosclerosis in about half of the cases, or chronic
kidney disease).
The macroscopic finding is complex because, in most cases, the aspects proper to
this pathological condition overlap with the pre-existing ones. The kidneys
appear enlarged, tumors and diffuse subcapsular and intraparenchymal hemorrhagic
foci.
Malignant hypertensive nephropathy presents common histological pictures with
thrombotic microangiopathy. Vascular injury involves the smallest vessels of the
arterial bed (arterioles, interlobular and sometimes arciform arteries), while
interlobar ones are generally spared. The arterioles are prey to phenomena of
fibrinoid necrosis often extended to the glomeruli, while the arteries of
smaller caliber present hyperplastic phenomena on the wall (productive
endoarteritis).