What is the relationship between vasculitis and kidney damage?

*It is only for medical professionals to read for reference.
Will these vasculitis affect the kidneys? learned! Systemic vasculitis is a large class of autoimmune diseases with multiple system damage characterized by inflammation of blood vessel walls.

Primary vasculitis mainly includes three types of large, medium and small vasculitis according to the size of the involved blood vessels.

Macrovasculitis includes giant cell arteritis and aortic arteritis.
Medium vasculitis is mainly polyarteritis nodosa and Kawasaki disease.
Small vasculitis includes antineutrophil cytoplasmic antibody (ANCA)-related vasculitis (including microscopy).
Lower polyangiitis, granulomatous polyangiitis, eosinophilic granulomatous polyangiitis) and immune complex deposition of small vasculitis (including cryoglobulinemia small vasculitis, allergic purpura and hypocomplement blood Urticaria vasculitis).

The kidney has a complex vascular structure, which makes it the most commonly affected organ in systemic vasculitis.

Tracing back to the source, the size of the blood vessels involved is different, and the manifestations of kidney involvement are also diverse.

Next, this article will share with you the clinical features, pathogenesis and treatment status of the following three types of vasculitis-related kidney disease.

Aortic arteritis (TA) is a non-specific full-thickness arteritis mainly involving media damage, which mainly affects the aorta and its branches.
Due to immune inflammation, the entire thickness of the artery is diffusely and irregularly thickened and fibrosis.
And lead to ischemic necrosis of blood supply tissues and organs.

Kidney involvement in TA is more common in the main, renal artery and mixed types, with renal artery stenosis or even occlusion, renal atrophy, but rare renal artery dilation and aneurysm.

The most important renal problem caused by TA is renal artery stenosis, which in turn causes renal vascular hypertension and ischemic nephropathy, which is one of the poor prognostic factors and early death causes of TA.

Renal artery stenosis exists in 24% to 68% TA, mostly bilateral proximal, usually accompanied by perrenal aortic stenosis.
The cause is related to the concentration of arterial stress near the main trunk opening caused by hemodynamics.

Patients with TA renal artery involvement often present with hypertension at onset, especially unexplained hypertension under the age of 40 with abdominal auscultation murmurs, unexplained renal atrophy or renal dysfunction.
Imaging tests are needed to screen for There is TA.

Once TA is diagnosed, early vascular ultrasound is needed to assess whether there is renal vascular involvement.

In addition, there are a small number of clinical reports showing that TA can also be manifested as glomerular or tubular interstitial damage, but acute renal insufficiency is rarely seen.
The pathological manifestations are mainly mesangial hyperplasia, or focal segmental kidney.
Glomerulosclerosis, diffuse glomerulosclerosis, etc.

In treatment, glucocorticoids or combined immunosuppressants such as cyclophosphamide, azathioprine, methotrexate and mycophenolate mofetil, and glucocorticoids combined with immunosuppressants can significantly increase the TA remission rate.

For a few refractory cases, biological agents can be used for treatment.

The choice of antihypertensive drugs is also very important.
For unilateral renal artery stenosis, consider the use of angiotensin converting enzyme inhibitors/angiotensin II receptor antagonists (ACEI/ARB) on the basis of monitoring renal function and blood potassium.
In some cases, it is necessary Use with caution.

In addition, surgical intervention can be performed when necessary, including two types of endovascular treatment and open surgery, percutaneous angioplasty and stent implantation.

Polyarteritis nodosa Polyarteritis nodosa (PAN) is a non-granulomatous vasculitis characterized by segmental inflammation and necrosis of small and medium arteries.

It mainly invades small and medium muscular arteries, which are distributed in segments, which are prone to occur at the bifurcation of the artery and spread to the distal end.

The etiology of PAN is unknown, and may be related to infection, drugs and serum injections, especially hepatitis B virus infection.

The histological changes are the most obvious in the middle layer of the vessel.
In the acute phase, the polymorphonuclear leukocytes ooze out to the various layers of the vessel wall and the area around the vessel, the tissue is edema, and the lesion spreads to the outer membrane and the inner membrane, resulting in full-thickness necrosis of the vessel wall.

Subacute and chronic processes include hyperplasia of the vascular intima, degenerative changes in the vascular wall with fibrin exudation and fibrinoid necrosis, thrombosis in the lumen, and severe cases can cause vascular occlusion.

The clinical manifestations of PAN include systemic symptoms such as fever, headache, and fatigue.
It can also involve multiple organ systems such as the kidneys, bones, muscles, nervous system, gastrointestinal tract, skin, heart, and reproductive system.
Lung involvement is rare.

In classic PAN, 63% to 76% of patients have kidney involvement, mainly renal vascular damage, visible or microscopic hematuria, moderate proteinuria, slowly progressive renal failure and hypertension.

The underlying mechanism is vasculitis of the renal arteries and interlobular arteries, leading to the formation of microaneurysms, followed by tissue infarction or hematoma.

30% of patients with PAN have asymptomatic renal infarction and have slow progressive renal insufficiency.

Acute renal failure is mostly the result of multiple kidney infarctions, which can cause renal malignant hypertension.

Renal angiography often shows multiple small aneurysms and infarctions.
Unilateral or bilateral ureteral stenosis may occur due to periureteral vasculitis and secondary fibrosis.

In terms of treatment, the treatment plan is determined according to the condition.
The main medication is hormone combined with immunosuppressive agents.
Immunosuppressive agents include cyclophosphamide, azathioprine, and methotrexate.

Pay attention to adverse drug reactions during medication, and regularly check blood, urine routine, and liver and kidney function.

Actively control blood pressure for hypertensive patients.

If vascular occlusive disease occurs, use vasodilators and anticoagulants.

For patients with hepatitis B infection, antiviral drugs should be added.

Polyangiitis under the microscope Polyangiitis under the microscope (MPA) is a systemic necrotizing vasculitis that mainly affects small blood vessels, which can invade the small arteries, arterioles, capillaries and tiny veins of the kidneys, skin, and lungs.
.

Often manifested as necrotizing glomerulonephritis and pulmonary capillary vasculitis.

MPA may have an acute onset, manifested as rapidly progressive glomerulonephritis and pulmonary hemorrhage, and some may also have an insidious onset, manifested as intermittent purpura, mild kidney damage, intermittent hemoptysis, etc.

Renal damage is the most common clinical manifestation of MPA, with an incidence of more than 90%.
Most patients have proteinuria, hematuria, various casts, edema and renal hypertension, etc.
Some patients have renal insufficiency, which may be progressively worsened.
Renal Failure.

However, a very small number of patients have no renal disease.

The kidney pathology is necrotizing glomerulonephritis, which is characterized by segmental necrosis with crescent formation, and little or no capillary endothelial cell proliferation.

The current treatment of ANCA-related vasculitis includes remission induction and maintenance therapy.

First, sufficient glucocorticoids combined with cyclophosphamide or mycophenolate mofetil to induce remission, hormone reduction after the disease is stable, combined with mycophenolate mofetil, leflunomide or azathioprine for maintenance, for refractory or multiple relapses Patients can consider applying biological agents.

In addition, pay attention to strictly control blood pressure and so on.

Conclusion: Various vasculitis diseases involve blood vessels of different sizes, and also correspond to different kidney diseases: large and medium vasculitis is mainly manifested by renal artery stenosis or aneurysm in ischemic nephropathy, and small vasculitis is mostly manifested as renal involvement Necrotizing glomerulonephritis, membranous nephropathy, or crescent formation, etc.

The clinical manifestations are diverse, with varying degrees of severity, and more accompanied by other systemic manifestations, which may be clues to early diagnosis and often a factor of poor prognosis.

In clinical work, we need to start with the pathogenesis and clinical characteristics of vasculitis, so that kidney involvement can be diagnosed and treated early, and the prognosis can be improved.

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[3]Chinese Medical Association Rheumatology Branch.
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Chinese Rheumatology Chinese Journal of Rheumatology,2011,15(4):259-261.
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