Nephroangiosclerosis

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The term refers to morphological lesions and renal functional impairment associated with chronic hypertension, although it is proven that genetic conditioning is needed. In fact, in some rare cases, there are typical morphological alterations not associated with arterial hypertension; however it refers equally to nefroangiosclerosis, even if the mechanism that caused the injury remains controversial. Injuries of the arterial vessels. High pressure values in the long run cause two types of lesions in the kidney vessels:
1. lesions of the endothelium and consequent increase in permeability with subsequent deposition of plasma proteins and biologically inactive fractions of the complement (C3 b) in the intima of the arterioles;
2. hypertrophy and thickening of the artery wall.
The histological aspect of the two lesions consists respectively in: 1. presence of hyaline material, ie homogeneous, in the intima of the arterioles whose lumen is restricted: it is the so-called arteriolesclerosis or arteriolar hyalinosis; 2. in the thickening of the wall of the arteries, particularly of the intima, in which the component of collagen fibers increases and a slumping or apparent duplication of the internal elastic lamina occurs. Furthermore, a certain degree of hyperplasia of the smooth muscle cells of the media is also considered. Also in this site there is a narrowing of the vessel lumen.

Glomerular lesions

In a first phase of hypertension, the glomeruli are hypertrophic due to glomerular hypertension (due, in turn, to systemic hypertension and loss of self-regulation capacity). The hypertrophy of the glomeruli then hesitates in progressive sclerosis, with a similar mechanism to what we have seen in the congenital oligomeganephronic condition. The lower the number of preserved glomeruli, the more the remainder go into hypertrophy. The ease with which lesions progress more rapidly in African-American patients than in Caucasians towards renal failure is attributed to the reduced number of nephrons present at birth in African-American subjects, a genetic condition that leads to a more precocious hypertrophy.

The hypertension of the glomeruli and their consequent hypertrophy are events that represent an important mechanism of compensation that stands for: also at the base of the progression towards the sclerosis of many nephropathies. On this compensation is based: rationale of many drug therapies: we are looking for not only or not so much to decrease the systemic arterial pressure, but above all to decrease the glomerular saving the residual glomeruli. Drugs that reduce the systemic arterial pressure but do not influence the intraglomerular pressure are not effective to reduce the progression of renal damage to renal failure. In the advanced stages of hypertension, instead, changes in the glomeruli refer mainly to ischemia.

This is not surprising if we remember, once again, that despite the blood pressure increase the blood flow in the glomeruli at some point decreases or stops because of the progressive narrowing of the lumen of the arterial vessels and especially of the arterioles. In the end the convolute of the glomerular capillaries is transformed into a tangled tangle, devoid of light, while in the space of Bowman accumulates amorphous material and collagen.

Tubulointerstitial lesions

In the intertubular interstitium, an interstitial lymphocyte infiltrate associated with tubular atrophy is often observed. While the reasons for tubular atrophy are understandable because they are due to ischemia, a little like in renal artery stenosis, reason; of the inflammatory infiltrate, (lesion which, due to its interstitial localization, can be defined as interstitial nephritis) are unknown. On the basis of experimental data, it has recently been hypothesized that also inflammation is an immune response against tubular antigens, highlighted or exposed by ischemic lesions.

All the histological lesions described: hypertrophy of the mean and intimal sclerosis of the artery, hyalinosis of the arterioles, systemic collapse of the glomeruli, inflammation and fibrosis of the interstitium and tubular atrophy, explain well the macroscopic appearance of the kidneys undergoing nefroangiosclerosis. Because they atrophy; tubules and others remain, the surface of the kidneys becomes finely granular. The inter-tubular vessels are more resistant to ischemia and therefore the color of the kidney (since the tubules disappear and the capillaries remain) are more red than normally. Overall, the kidney is reduced in volume with an increased consistency: in extreme synthesis it takes on the characters of a small red kidney kidney. Although nefroangiosclerosis is a very common disease and causes numerous terminal renal insufficiencies requiring dialysis, the progression is very slow.
The manifestations are devious: next to hypertension there can be only mild proteinuria (which however already documents an initial glomerular damage) and rarely we proceed to renal biopsy to establish the diagnosis.
Particular considerations deserve the nefroangiosclerosis lesions that appear in cases in which the pressure levels are particularly high above 110-120 mmHg in the minimum values).
In these cases, the insurgency in the arteriolar wall and the ialinosis are produced, but serious necrotizing lesions of the arterioles and the glomeruli with the formation of thrombus and proliferation of the cells. In the absence of adequate treatment, severe renal insufficiency occurs: for this reason, this form of nefroangiosclerosis is called malignant, with reference to the serious impairment of renal function. In fact it is not a disease that is distinct from the previous one (called benign nefroangiosclerosis), because it is two phases of the same disease: the malignant phase of hypertension necrosis of the malignant) can appear at any time, both in the subject not previously hypertensive than in that with long history of modest hypertension and benign nephrosclerosis. The area of necrosis of the arterioles wall and part of the glomeruli takes the colors of the ribrin in classical histological methods and is referred to as fibrinoid necrosis. The relationships between morphological (and functional) changes in renal tissue and changes in blood perfusion (hypo- or hyperafflow, hypo- or arterial hypertension, etc.) are very complex. In practice, the kidney is not only sensitive, like all organs, to blood perfusion, but also has the primary function of regulating the circulating blood mass and pressure levels, using a sophisticated system of reabsorption and excretion of salts and water or with the participation of numerous vasopressor hormones. It follows, for example, that a renal disease can cause intraparenchymal ischemia of the kidney, which induces hyperincrement of vasoactive hormones (see S. renin) with increased blood pressure which in turn produces structural damage on the already compromised renal parenchyma: so a vicious circle is established which self-amplifies. The result is that, in medical practice, very often kidney diseases are found that have multiple structural lesions: such primitive changes (congenital malformations glomerulonephritis, infections) that lesions caused by hypertension. Since all the most diverse chronic diseases lead to tissue sclerosis, which presents itself with morphological aspects that are largely overlapping, it often becomes difficult to determine which of the structural lesions of the parenchyma and its functional damage is the real initial aetiology. For the sake of simplicity, we have illustrated the main lesions produced by the altered renal perfusion as they are ideally observed in subjects affected only by obvious circulatory alterations (therefore not complicated or confused with other diseases) or as observed in experimental animals. However, it should be remembered that in reality, many and different reasons of the structural morphological damage in existence often coexist in the kidney.