Pathogenesis of kidney damage with nodular periarteritis

The causes of nodular polyarteritis are not exactly established.

• In a number of cases, the disease is preceded by the administration of medications: sulfonamides, iodine preparations, vitamins, especially group B.
• Recently, the development of nodular polyarteritis is increasingly associated with a viral infection. As the main etiological factor, HBV is considered. However, the frequency of detection of markers of HBV infection with nodular periarteritis in different regions varies. In countries with a low overall infection rate (France, the USA), it is low and continues to decline, due to the active vaccination of the population against viral hepatitis B. According to E.N. Semenkovoy, more than 75% of patients with nodular polyarteritis, identify markers of viral hepatitis B in the blood. Among persons infected with HBV, nodular polyarteritis is noted in about 3% of cases. In addition to HBV, discuss the role of hepatitis C viruses, herpes simplex, cytomegalovirus, and recently HIV in the etiology of the disease. The main pathogenetic mechanism of nodular polyarteritis development is immunocomplex. The deposition of immune complexes in the vascular wall leads to activation of the complement system and neutrophil chemotaxis, induces damage and fibroid necrosis of the arterial wall. It is believed that the smallest infrared size, containing HBsAg and antibodies to it, has the greatest damaging effect. Recently, the important role of cellular immune responses in the pathogenesis of nodular polyarteritis has also been discussed.

[1], [2]

Pathomorphology of kidney damage with nodular periarteritis

Nodular polyarteritis is characterized by the development of segmental necrotizing vasculitis of middle and small caliber arteries. Vascular injury is characterized by frequent involvement of all three layers of the vessel wall (panvasculitis), which leads to the formation of aneurysms due to transmural necrosis, and the combination of acute inflammatory changes with chronic (fibrinoid necrosis and inflammatory infiltration of the vascular wall, proliferation of myointimal cells, fibrosis, sometimes with occlusion of the vessel ), reflecting the undulating course of the process.

In the overwhelming majority of cases, renal pathology is represented by a primary vascular lesion - vasculitis of the middle-caliber internal arteries (arches and their branches, interlobar) with the development of ischemia and infarction of the kidneys. The defeat of glomeruli with the development of glomerulonephritis, including necrotizing, is not characteristic and is noted only in a small part of patients.

Macroscopically, the kidneys look different depending on the nature of the process (acute or chronic). In acute form of the disease, the kidneys, as a rule, have normal dimensions, while in chronic form they are significantly reduced. In both cases, their surface is tuberous, which is associated with the alternation of areas of normal and infarcted parenchyma. On a section, it is possible to observe foci of aneurysmal enlargement and arterial thrombosis, most often in the corticomedullary zone. In a number of cases aneurysms of the main renal artery in the kidneys are noted, the rupture of which is accompanied by the formation of large perirenal or subcapsular hematomas.

The segmental vasculitis of the intrarenal arteries with alternation of affected and uninfected sections of the vessel is light-optically detected. In most cases, an eccentric lesion of the vascular wall is detected. A characteristic feature of the defeat of the intrarenal arteries with nodular polyarteritis is the presence of simultaneously acute and chronic vascular changes. Acute disorders are represented by fibrinoid necrosis of the vascular wall and inflammatory infiltrates, consisting mainly of neutrophils. In the case of extensive transmural necrosis, aneurysms of the affected arteries, more often of interlobar and arc, are formed. As the reparative processes develop, the changes in the nature of the inflammatory infiltrate (replacement of neutrophils by mononuclear cells), concentric proliferation of myointimal cells, replacement of foci of necrosis with fibrous tissue, which ultimately leads to complete occlusion or significant narrowing of the lumen of the vessel.

In the classical form of the disease, glomerular lesion is rarely observed. Although a number of glomeruli indicate ischemic collapse of the vascular loops, sometimes in combination with the sclerosis of the capsule, most glomeruli do not have histological changes. Hyperplasia and hypergranulation of the epithelioid (renin-containing) cells of the juxtaglomerular apparatus are often noted. In some cases, a morphological picture of necrotizing glomerulonephritis with half-moon is revealed.

Changes in interstitium are mainly related to the development of heart attacks. Note moderate inflammatory infiltration and fibrosis interstitium.