Children's HSPN

With the change in recent years, pediatric spectrum of disease, kidney disease was arelative increase in trend. Nephritis, is quietly attacks on children.
Child disease is allergic to certain factors, causing systemic vascular inflammatorylesions, skin manifestations point as a red rash, which is called purpura, kidney damage to the called purpura nephritis. Purpura nephritis may be associated with infection andallergy. In some cases before the onset of infection, the most common upper respiratory tract infection (non-specific or streptococcal infection), such as chlamydia, chicken poxand parasites, and so on. Many cases of disease, drugs (antibiotics, iodine and amines, salicylates, barbiturates, and iodide) or food (dairy, fish, shrimp, crabs and clams, etc.)allergies.
Purpura nephritis, purpura and rash, a part of the main leg front, knee, near the ankle andhip, and of varying sizes, different shapes, often symmetry. Purpura slightly higher than the leather, the pressure does not fade, with a slight itching. Began to bright red, laterbecome dark red, brown. The small number of patients also can be expressed asurticaria, angioedema, erythema multiforme, and even ulcers, necrosis. Purpura can also be integrated into the film, often in batches repeatedly, and some may be associated with localized or diffuse edema of the head, face, eyelids.
Children suffering from purpura nephritis and extrarenal symptoms include skin purpura, abdominal pain, blood in the stool. Some sick child very severe pain, severeintussusception, intestinal perforation, intestinal bleeding. General there are knee, ankle, wrist or elbow pain. Renal symptoms of view, generally two weeks to two months after theskin purpura, there will be hematuria, oliguria, edema, high blood pressure.
To remind parents that this happens, do not blindly give a child medication according todoctor's diagnosis and the child's symptomatic treatment.

Mesangial proliferative glomerulonephritis is caused by what

(A) causes
Membranoproliferative glomerulonephritis according to their clinical and laboratorycharacteristics are divided into primary and secondary glomerular disease.
Primary membranoproliferative glomerulonephritis of unknown etiology, is generally believed that type Ⅰ immune complex disease; type II immune complexes andautoantibodies in disease, may be related to heredity.
Secondary mixed cryoglobulinemia, membranoproliferative glomerulonephritis, there arethree kinds of subtypes. Type Ⅰ cryoglobulinemia monoclonal peaks globulin, usually amyeloma protein. Type Ⅱ usually a combination of IgG monoclonal peak of IgM globulin, also known as anti-IgG rheumatoid factor, and type Ⅲ is a multi-strain peakimmunoglobulin. Type Ⅱ and Ⅲ cryoglobulinemia prone to kidney damage. Itspathological features proliferated mesangial cells, white blood cells especiallymononuclear cell infiltration, glomerular basement membrane thickening of the double-track phenomenon. About 1/3 cases of small and medium-sized arteritis, capillarymicrothrombosis. The etiology and pathogenesis of MPGN is not very clear. Type ⅠMPGN immune complex disease, repeatedly sustained by the relatively large insolubleimmune complex deposition. Patients with type II MPGN serum immune complexes,cryoglobulin, complement abnormalities, sustained reductions in serum C3. Promptimmune complexes in the type of MPGN II. Can be detected in patients with type II MPGNserum C3 nephritis factor (C3NeF), C3NeF, C3bBb converting enzyme autoantibodies,C3bBb role to strengthen, leading to sustained activation of the complement bypass, resulting in the degeneration of sustained hypocomplementemia and basement membrane. Complement metabolic disorder as the central link.
In addition, the type II MPGN kidney transplantation often relapse may be due to materialdeposition can cause abnormal glycoproteins in the basement membrane nephritis inserum.
The disease may be related to inheritance, type II MPGN often in patients with HLA-B7.Most of type Ⅰ MPGN patients with a special B-cell alloantigen.

Clinical manifestations of membranous glomerulonephritis

Idiopathic membranous nephropathy can occur at any age, more common in adults, average age 35 years old, male to female ratio of about 1.5 to 2:1. Insidious onset, a small number of precursor infection after the onset. The first symptom of 15% to 20% of asymptomatic proteinuria, 80% with nephrotic syndrome, non-selective proteinuria.Microscopic hematuria in adults about 60% of children with gross hematuria, but rarely see the red tube. Early blood pressure more than normal, with about 50 percent of the progression of high blood pressure, relax and disappear with kidney disease. In the early days, the renal function is normal. 80% have varying degrees of edema, severe chest, ascites, and other body cavity effusions, the mechanism is multifactorial. There are two serious complications of idiopathic membranous nephropathy: ① high coagulation disorder and renal vein thrombosis: increased levels of blood coagulation factor due to nephrotic syndrome, enhanced platelet adhesion and cohesion, antithrombin Ⅲ Kangxian plasmin activity increased, resulting from high-blood clotting disorder.Dexamethasone can promote coagulation. This disease is about 50% of the incidence of renal vein thrombosis, no obvious symptoms, but the nephrotic syndrome increase the more common chronic form. Acute type can show the sudden appearance of low back pain, often more severe, accompanied by the kidney area, hit pain, hematuria, often gross hematuria, white blood cells in urine, a sudden increase in proteinuria, hypertension and acute renal dysfunction, bilateral renal vein thrombosis even oliguria and acute renal failure, the kidneys were increased. Chronic type of renal tubular dysfunction in performance such as: renal glucosuria, amino acids, urine, and renal tubular acidosis. In addition, it may be complicated by pulmonary embolism. Can also occur such as: brain, heart, legs, and extra-renal thrombosis. Clear diagnosis of the need for renal vein or renal artery angiography, radioactive renography and CT are also helpful in the diagnosis. ② combined anti-GBM crescentic glomerulonephritis: the basement membrane damage, membrane antigen exposure or release can lead to the formation of anti-basement membrane antibodies. May be detected in the serum anti-basement membrane antibodies, anti-neutrophil antibodies (ANCA). Therefore, if medically stable patients with rapid renal dysfunction and rapidly progressive glomerulonephritis-like performance, should be highly alert to the possibility of complications.