Kidney involvement

Introduction Allergic purpura, also known as hemorrhagic capillary venom, is a capillary allergic hemorrhagic disease associated with autoimmune damage to blood vessels. Clinically, the renal involvement caused by allergic purpura is called allergic purpura nephritis. Clinical features In addition to purpura, there are often rashes and angioedema, arthritis, abdominal pain and nephritis. The disease can occur at any age, more common in children and adolescents, with the highest incidence rate of 6 to 13 years old, followed by 14 to 20 years old, the first time is more than 20 years old. It happens in the cold season.

Cause

The exact cause is not clear and is related to allergic reactions caused by:

1. Infection with bacteria, viruses and schistosomiasis infections or other parasitic infections. Most have pre-respiratory respiratory infections and tonsillitis.

2, drug antibiotics (such as tetracycline, Vancomycine, etc.), sulfonamide, isoniazid, salicylic acid, barbital, quinine, iodide, streptokinase, vaccination (measles vaccine, epidemic cerebrospinal meningitis vaccine, etc.) , tuberculin test, etc.

3, food consumption milk, shrimp, crab, sputum and so on.

4, other pollen or insect bites, cold stimulation. There are also a small number of patients with no obvious incentives. A large amount of data indicates that the disease is an immune complex disease.

an examination

Related inspection

Renal static imaging renal blood flow map

Allergic purpura nephritis must have the characteristics of allergic purpura and nephritis to confirm the diagnosis.

Because the disease has special skin, joint, gastrointestinal and kidney involvement, the kidney has a mesangial proliferative pathological change mainly based on IgA deposition, so it is not difficult to confirm the diagnosis. About 25% of patients have mild renal involvement, and repeated urine tests are needed to detect the main basis of kidney involvement. Confirmation of the diagnosis by renal histopathology if necessary. Serum examination showed that IgA and IgM were mostly elevated, IgG was normal, and in many cases, the amount of cryoglobulin in the blood increased. The pathological changes of the kidney in this disease are similar to those of IgA nephropathy, but the glomerular capillary necrosis and the degree of cellulose deposition are heavier, so it should be distinguished.

Laboratory inspection:

1, blood routine examination of platelets, bleeding time, clotting time, blood clot retraction time and prothrombin time is normal. Severe bleeding can be associated with anemia.

2. Immunological examination showed elevated serum IgA, normal IgG and IgM. IgA began to rise 2 weeks after onset. Most of C3, C4, and CH50 are normal or increased. Interleukin-6 (IL-6) and tumor necrosis factor (TNF-a) are elevated.

3, renal function blood urea nitrogen, creatinine can be increased, creatinine clearance can be reduced.

4, urine examination showed hematuria, proteinuria and tubular urine.

Differential diagnosis

Differential diagnosis of kidney involvement:

1, acute nephritis: the disease and purpura nephritis is the majority of serum C3 decreased, no skin rash, arthritis and intestinal colic performance, skin biopsy and renal biopsy to help identify.

2, lupus nephritis lupus nephritis: rash has characteristic butterfly erythema or discoid erythema, mostly congestive erythema, lupus in addition to joints, rash, abdomen and kidney performance, there are many systemic damage including photoallergies, oral ulcers, Synovitis, nervous system manifestations, abnormal blood system examination, immunological examination showed decreased serum C3, anti-dsDNA positive, anti-Smith antibody positive, antinuclear antibody positive, skin biopsy: lupus positive, renal biopsy: lupus kidney has V type Pathological changes, glomerular capillary wall "Platinum"-like changes, immunofluorescence showed "full hall bright", IgG, IgM, IgA, C3 co-deposited, mainly IgG, IgM.

3, primary vasculitis (micro polyarteritis, Wegener granuloma): clinical manifestations in addition to rash, kidney damage, upper respiratory tract, lung performance is more common. Skin or nodule biopsy showed swelling and hyperplasia of endothelial cells in the vascular wall, medial cell necrosis with inflammatory cell infiltration, and edema. Sometimes accompanied by a large number of lymphocytes, monocytes, multinucleated giant cells and neutrophils infiltration, and even the formation of granulomatous lesions. No immunoglobulin deposition, negative immunofluorescence. Renal biopsy: glomerular segmental necrosis with peripheral inflammatory cell infiltration, and even granuloma formation, may be associated with crescent, most negative immunofluorescence, and sometimes necrotizing arteritis. Anti-leukocyte cytoplasmic antigen autoantibodies (ANCA) can be found in the blood. Mini-polyarteritis is mainly perinuclear PANCA, and the target antigen is myeloperoxidase (MPO). Wegener's granuloma is dominated by cytoplasmic C-ANCA and the target antigen is protease 3 (PR3).

4, IgA nephropathy (IgAN): IgA nephropathy with repeated gross hematuria, rarely rash, joint pain and abdominal performance, gAN incidence is more common in adulthood, pathological examination more common IgA, IgG, IgM deposition, classic complement activation via C4 The /C1q deposition ratio is significantly higher. Allergic purpura nephritis is difficult to distinguish from IgA nephropathy according to changes in renal pathology and immunopathology. Most authors believe that the clinical and pathological processes of renal involvement in allergic purpura nephritis are very similar to IgA nephropathy, so they are considered to be two different manifestations of the same disease. IgA nephropathy is mainly caused by kidney involvement, and allergic purpura nephritis is affected by kidney involvement. There is also damage to the whole body system. Further genetic studies found that the two diseases occurred in the same family, and the homozygous ineffective C4 genetic phenotype frequency increased, both of which showed IgA immunoregulatory abnormalities, such as IgA and macromolecular (poly) IgA increased, both The ratio of IgA plasma cells/IgG plasma cells in the tonsil lymphocytes of patients increased. Allergic purpura nephritis is a systemic vasculitis, also a secondary IgA nephropathy, which is mainly pathological and IgA nephropathy with mesangial lesions, both with crescent formation and glomerular sclerosis, especially IgA Renal patients with recurrent episodes of hematuria, whether in clinical or genetic background, have more similarities than other clinical types of IgA nephropathy and allergic purpura nephritis. However, although there are many similarities between allergic purpura nephritis and IgA nephropathy, there are still significant differences between the two.

5, blood disease caused by purpura: due to allergic purpura nephritis platelet count and bleeding, clotting time is normal, it can be distinguished from blood disease caused by purpura.

6, acute abdomen: due to abdominal allergic purpura prone to nephritis, especially before the appearance of purpura, should be associated with acute appendicitis, hemorrhagic enteritis, intestinal perforation, acute pancreatitis or kidney stones, such as hemoptysis, renal failure Identification with Goodpaschu syndrome.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.