Renal disease due to allergic vasculitis (Part 2)

The article was written by Doctor of Emergency Department - Vinmec Phu Quoc International General Hospital

Renal disease usually manifests several days after the onset of clinical symptoms of allergic vasculitis. Typically microcytic erythrocytosis and moderate proteinuria without clinical symptoms during active disease. Some patients may experience edema, increased blood pressure, and slightly increased blood creatinine levels.

4.1. Skin lesions The histopathological manifestation of skin biopsy on skin biopsy is leukocytosis vasculitis. Perivascular accumulation of inflammatory cells, mostly polymorphonuclear leukocytes and monocytes, occasionally eosinophils, perivascular leukocytes and retrocapillary veins. Escaping of red blood cells through capillaries causes hemorrhage. Fibrinous necrosis, leukocyte and platelet thrombosis were seen in the lesions, but only in blood vessels surrounded by infiltrating leukocytes. Immunofluorescence staining showed IgA, complement C3 and fibrin/fibrinogen in vessel wall and connective tissue, no C1q and C4.
4.2. Other organs The authors reported that histopathological lesions occurred in many different organs, including the lungs, and different segments of the gastrointestinal tract. Damage to these organs is similar to damage to the skin.
4.3. Kidney damage 4.3.1. Optical microscopy Renal histopathology of allergic vasculitis was described by Heptinstall and Habib 1983. The glomerular injury is characterized by focal and segmental proliferative glomerulonephritis. Proliferation is mainly seen in the proliferation of mesangial cells. In severe cases, polymorphonuclear leukocyte infiltration and extracapillary epithelial cell proliferation are seen, leading to sickle formation. The ratio of lymphocytes, monocytes/macrophages increased, and also T-CD4 and T-CD8 cells were increased, similar to type 1 proliferative membranous glomerulonephritis. In primary IgA nephropathy, not seen. proliferation of any cell type. Some patients present with minimal glomerular damage, while others present with necrotizing glomerulonephritis with large crescent formation in 100% of the glomeruli. The crescent appears adjacent to the mesangial and endothelial cell proliferation areas of the capillary cluster. Glomerular fibrosis may be seen on biopsy specimens in the late stages of the disease, often associated with Bowman's cyst. This is the fibrosis result of the previous proliferative lesion rather than the primary process. The International Study of Kidney Disease in Childhood (ISKDC) has classified renal histopathology in allergic vasculitis into six classes (1977).
+ Grade I: minimal glomerulonephritis
+ Grade II: simple vasodilating lesion
a/ focal lesion
b/ diffuse lesion
+ Grade III: mesangial proliferative glomerulonephritis with less 50% of glomeruli have crescent-shaped lesions
a/ Focal lesions
b/ Diffuse lesions
+ Grade IV: mesangial proliferative glomerulonephritis with 50-75% sickle-shaped glomeruli.
a/ Focal lesion
b/ Diffuse lesion
+ Grade V: mesangial proliferative glomerulonephritis with more than 75% of glomeruli with crescent shape
a/ Focal lesion
b/ Diffuse lesion
+ Class VI: proliferative membranous glomerulonephritis (capillary mesangial glomerulonephritis)
4.3.2. Electron microscopy In addition to the changes seen in optical microscopy, electron microscopy showed dense electron deposition in the mesangial region, and in the enlarged mesangial region. A small amount of deposition was seen below the epithelial cells. The majority of patients found the deposition in the mesangial region, half of these patients saw the deposition even under the endothelial cells, a few patients saw the deposition even under the epithelial cells. Some deposited on both sides of the capillary basement membrane.
4.3.3. Immunofluorescence technique Immuno-precipitated deposition of IgA in the glomerular mesangium and spread to the capillary wall. The deposits seen in the glomerulus were IgA in 90% of patients, IgG in 69% of patients, and IgM in 30% of patients. Complement deposition of C3 was found in 80% of patients, C1q in 69% of patients, C4 in 2% of patients. Fibrin deposition was observed in 74% of patients, and IgA was deposited in the glomerular mesangium mostly under the IgA1 layer, with a small amount of IgA2 in the mesangial area and capillary wall.

5.1. General clinical presentation of allergic vasculitis 5.1.1. Skin lesions The purpura occurs spontaneously, initially as small petechiae, usually concentrated on the outer surfaces of the arms and legs, particularly around the ankles, buttocks, and elbows. The board has a bilateral symmetry. Abdominal and thoracic areas are usually sparse. One to two days later, the lesion becomes more obvious, the petechiae becomes darker and larger, the skin tightening shows that the hemorrhagic nodule does not go away, the hemorrhagic nodule is usually less than 1 cm in diameter. Sometimes there is itching associated with skin necrosis, later scarring. The hemorrhagic nodule gradually becomes brown and disappears after two weeks. During the acute phase of the disease, bleeding may occur with minor trauma, such as blood pressure measurements. The duration of an acute phase lasts an average of 4 weeks, 1/3 of the patients are less than 2 weeks, 1/3 of the patients are from 2-4 weeks, the remaining 1/3 of the patients are more than 4 weeks. Skin purpura occurs in more than half of patients.
5.1.2. Manifestations in joints Arthralgia occurs in 2/3 of patients, usually pain in large joints, especially ankle and knee joints. It is possible for several joints to be painful, but it is also possible for only one joint to be painful. Pain can be mild to severe resembling acute arthritis. Rarely, joint swelling, if present, is due to periarticular edema, without joint facet changes. The duration of joint pain is usually shorter than the duration of the skin rash.
5.1.3. Abdominal symptoms Abdominal symptoms occur in approximately 78% of patients. Manifestations are abdominal pain, intestinal obstruction, black stools, vomiting blood, or a combination of the above symptoms. Abdominal pain is often severe, resembling a surgical emergency, especially when it is the first symptom of the disease. Gastrointestinal bleeding may occur in up to 80% of patients. The extent of GI bleeding varies, from erythropoiesis with no clinical symptoms, to bleeding requiring blood transfusion. Chronic intestinal obstruction has also been reported in patients with allergic vasculitis, possibly as a result of inflammation or hemorrhagic lesions leading to fibrosis of the intestinal wall. Another manifestation of abdominal symptoms is pancreatitis, possibly due to pancreatic edema.
5.1.4. Renal disease Manifestation of kidney disease is acute glomerulonephritis syndrome. Hematuria, edema, hypertension, and decreased glomerular filtration rate. Hematuria is often the earliest symptom of kidney damage. Some patients may experience nephrotic syndrome. Some patients may lead to end-stage renal failure. The severity of renal injury was not associated with the severity of extrarenal symptoms. The rate of kidney damage is only seen in 30-60% of patients, presenting mainly with erythrocytosis and/or proteinuria.
5.1.5. Nervous system Neurological symptoms may occur in some patients, usually children, such as headache, behavioral changes, cerebral hemorrhage. Most neuropathy is transient. Neurological symptoms occur with vasculitis of the nervous system, hypertension and metabolic disorders
5.1.6. Edema Some patients have edema, usually in the legs around the ankles. Edema may be due to increased vascular permeability due to vasculitis.

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