Renal disease due to allergic vasculitis (Part 1)

Article written by Doctor of Emergency Department - Vinmec Phu Quoc International General Hospital

Allergic vasculitis (Henoch-Schonlein purpura) is a term used to describe a syndrome rather than a disease, clinically characterized by symptoms that are: skin rash; gastroenteritis; athritis; and kidney disease.
The first patient reported by Willan in the early 19th century (1808) with a combination of purpura and arthritis was clearly described in 1837. Later in 1874, Henoch described four children with disease combined with purpura in the skin, gastroenteritis, arthralgia. 1899 Henoch added a report adding nephritis to this syndrome, thus completing the disease definition.
The general clinical feature of allergic vasculitis is that the disease occurs at any age and in both sexes, but mainly occurs in children, mostly around 10 years of age, male/female ratio is 2/1 . A recent history is often associated with bacterial infections, most often respiratory tract infections. Although there are 4 groups of symptoms (skin rash, gastrointestinal syndrome, joint pain, kidney disease) but disease manifestations are variable, often not all 4 symptom groups, kidney disease is less common. The most common manifestations of the disease are skin rash, arthralgia, gastrointestinal syndrome, which occurs simultaneously or within a few days. Nephritis is uncommon and usually presents later with urinary abnormalities. The disease is rare in adults, in the UK, the rate of people over 20 years old with this disease is only 1/10 000 000 of the population. There are no clinical differences between children and adults.

Many patients with allergic vasculitis have a history of bacterial infection, usually an upper respiratory tract infection at the time of illness onset or shortly before. Allergies to drugs, foods, and other exogenous agents other than bacteria, have also been reported. In fact, IgA antibodies play a role in the pathogenesis of this disease. Agents such as bacteria, foods, drugs, and others play a role in disease initiation.

Clinical and laboratory features suggest that the pathogenesis of allergic vasculitis is immunological. First, most patients' onset of illness is related to exposure to foreign agents such as drugs, foods, and bacteria. Second, immunoglobulins and components of complement were found to be deposited in the glomeruli and in the skin of these patients. Third, there are changes in circulating IgA levels, rheumatoid factor, and IgA-containing immune complexes present in the serum in a high proportion of patients.
3.1. IgA Immune System Variations Serum IgA levels in half of patients are elevated during the first trimester of illness. Elevated serum IgA is mainly the polymer IgA component. In normal people, serum IgA is mainly a monomer component. IgA-containing immune complexes have been detected in the patient's blood, which have a molecular weight of 106 Da. Cryoglobulin containing IgA and properdin was also found in the patient's serum.

3.2. Presumptive antigens Immunocomplex is a term used to refer to large molecules containing antibodies and antigens. Nonspecific antigens have been isolated from immune complexes in the serum of patients with allergic vasculitis such as α-galactosyl, polyethylene glycol. IgA-antigen complexes have been found to be deposited in blood vessel walls, leading to complement activation, inflammation, and tissue damage. Rheumatoid factor (IgA antibody reacting to the Fc fragment of IgG) was also detected in the serum
of patients with allergic vasculitis. Rheumatoid factor IgA has also been detected in immune complexes deposited in small blood vessels and in patient serum during active disease,
3.3. Role of the complement system Complement concentrations in the serum of patients are normal. However, some authors found an increase in C3d concentration, a decrease in CH50 concentration, and normal serum C1q and C4 concentrations. This week's immune complex contains properlin. This suggests that complement activation occurs mainly by the classical pathway.
3.4. Similarities and differences between allergic vasculitis and primary IgA nephropathy The renal histopathology in allergic vasculitis resembles that of primary IgA nephropathy. Since then, it has been hypothesized that allergic vasculitis and primary IgA nephropathy may be the same, with two different forms of the disease. In other words, IgA nephropathy can be allergic vasculitis without disease manifestations in other organs. Or conversely, allergic vasculitis is primary IgA nephropathy associated with systemic vasculitis. Allergic vasculitis nephropathy has many manifestations of primary IgA nephropathy, with only a few other features.

+ Similarities between the two diseases: glomerular deposition in both diseases is IgA, both J series. Serum IgA levels are elevated in the acute phase in both diseases, as is IgA levels in the washings. throat increases. IgA-containing immune complexes are present in the circulation at similar rates in both diseases. The ratio of IgA/IgG produced by plasmocytes in the tonsils and in lymphoid tissues is increased, seen in both diseases. Anti-α-galactosyl antibodies and immune complexes were present in the serum of patients in both diseases. Patients in both diseases had a similarly high HLA-BW35 ratio.
+ The differences between the two diseases: the two diseases differ in their clinical manifestations. Although allergic vasculitis occurs at any age, it is most common in children, while primary IgA nephropathy is more common in adults. Although the clinical features of nephropathy are similar in both diseases, nephrotic-grade proteinuria is more common in the active phase of allergic vasculitis, whereas primary IgA nephropathy is more common with hematuria may or may not be microscopic and recurrent asymptomatic proteinuria. Importantly, the natural course of the two diseases is different, the renal injury in allergic vasculitis is not associated with other clinical manifestations, but the progression of nephropathy is associated with the histopathological lesion that develops. initial show. While in primary IgA nephropathy, progression of nephropathy is not associated with the primary renal histopathological lesion.
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