Pathogenesis of renal damage in periarteritis nodosa

The causes of polyarteritis nodosa are not precisely known.

• In some cases, the disease is preceded by the administration of medications: sulfonamides, iodine preparations, vitamins, especially group B.
• Recently, the development of polyarteritis nodosa has been increasingly associated with a viral infection. HBV is considered the main etiologic factor. However, the frequency of detection of HBV infection markers in periarteritis nodosa varies in different regions. In countries with a low overall infection rate (France, USA), it is low and continues to decline, believed to be due to active vaccination of the population against viral hepatitis B. According to E. N. Semenkova, more than 75% of patients with polyarteritis nodosa have markers of viral hepatitis B in the blood. Among individuals infected with HBV, polyarteritis nodosa is observed in approximately 3% of cases. In addition to HBV, the role of hepatitis C, herpes simplex, cytomegalovirus, and recently HIV in the etiology of the disease is discussed. The main pathogenetic mechanism for the development of polyarteritis nodosa is immune complex. 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 small-sized ICs containing HBsAg and antibodies to it have the maximum damaging effect. Recently, the important role of cellular immune reactions in the pathogenesis of nodular polyarteritis has also been discussed.

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Pathomorphology of kidney damage in periarteritis nodosa

Polyarteritis nodosa is characterized by the development of segmental necrotizing vasculitis of medium and small caliber arteries. The features of vascular damage are considered to be frequent involvement of all three layers of the vessel wall (panvasculitis), which leads to the formation of aneurysms due to transmural necrosis, and a combination of acute inflammatory changes with chronic ones (fibrinoid necrosis and inflammatory infiltration of the vascular wall, proliferation of myointimal cells, fibrosis, sometimes with vascular occlusion), reflecting the wave-like course of the process.

In the overwhelming majority of cases, renal pathology is represented by primary vascular damage - vasculitis of the intrarenal arteries of medium caliber (arc and their branches, interlobar) with the development of ischemia and renal infarctions. Damage to the glomeruli with the development of glomerulonephritis, including necrotizing, is not typical and is observed only in a small proportion of patients.

Macroscopically, the kidneys look different depending on the nature of the process (acute or chronic). In the acute form of the disease, the kidneys are usually of normal size, while in the chronic form, they are significantly reduced. In both cases, their surface is uneven, which is associated with the alternation of areas of normal and infarcted parenchyma. In the section, foci of aneurysmal expansion and thrombosis of the arteries can be observed, most often in the corticomedullary zone. In some cases, aneurysms of the main renal artery are noted in the renal hilum, the rupture of which is accompanied by the formation of large perirenal or subcapsular hematomas.

Light-optical examination reveals segmental vasculitis of the intrarenal arteries with alternating affected and unaffected areas of the vessel. In most cases, eccentric damage to the vascular wall is detected. A characteristic feature of damage to the intrarenal arteries in nodular polyarteritis is the presence of both 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 are formed, most often interlobar and arcuate. As reparative processes develop, a change in the nature of the inflammatory infiltrate is noted (replacement of neutrophils with mononuclear cells), concentric proliferation of myointimal cells, replacement of necrosis foci with fibrous tissue, which ultimately leads to complete occlusion or significant narrowing of the lumen of the vessel.

In the classic form of the disease, glomerular damage is rarely observed. Although ischemic collapse of vascular loops is observed in some glomeruli, sometimes in combination with capsule sclerosis, most glomeruli have no histological changes. Hyperplasia and hypergranulation of epithelioid (renin-containing) cells of the juxtaglomerular apparatus are often observed. In some cases, the morphological picture of necrotizing glomerulonephritis with crescents is revealed.

Interstitial changes are associated mainly with the development of infarctions. Moderate inflammatory infiltration and interstitial fibrosis are noted.