Non-IgA mesangial proliferative nephritis

Introduction to non-IgA mesangial proliferative nephritis Non-IgA mesangial proliferative glomerulonephritis refers to a group of diseases in which pathological changes under light microscopy are caused by diffuse mesangial cell proliferation and/or mesangial matrix broadening. Most of the disease is insidious, some infection history before the onset, the above respiratory infections are more, the pathogen is not clear, the exact role of infection on the disease is still unclear, the pathogenesis of mesangial proliferative nephritis is unknown. Mesangial proliferative glomerulonephritis can occur at any age, but it is more common in adolescents. Males are slightly more than females. About 30% to 40% of patients have infections before onset, mostly upper respiratory tract infections. basic knowledge The proportion of illness: 0.003% Susceptible people: teenagers are more common Mode of infection: non-infectious Complications: nephrotic syndrome

The cause of non-IgA mesangial proliferative nephritis

Most of the disease is insidious, some have a history of infection before the onset, the above respiratory tract infection is more, the pathogen is not clear, the exact effect of the infection on the disease is still unclear, the pathogenesis of mesangial proliferative nephritis is unknown, but immunofluorescence It is suggested that the disease is immune complex disease, the nature of antigen and antibody is still unclear, although the poorly soluble and insoluble immune complex is an important cause of mesangial damage, the exact process is still unclear, the degree of mesangial proliferation can be immune The size, number, charge and shape of the complex affect many factors. When the mesangial function is low or inhibited, immune complexes or macromolecules that cannot be processed or transported may retain the mesangial area, which may lead to mesangial lesions. .

Non-IgA mesangial proliferative nephritis prevention Pay attention to rest, work and rest, life in an orderly manner, and maintaining an optimistic, positive and upward attitude towards life can be of great help in preventing diseases.

Non-IgA mesangial proliferative nephritis complications Complications nephrotic syndrome

Can be complicated by nephrotic syndrome, renal insufficiency, balloon adhesion, glomerular sclerosis, tubular atrophy and interstitial fibrosis.

Non-IgA mesangial proliferative nephritis symptoms common symptoms protein hematuria

Mesangial proliferative glomerulonephritis can occur at any age, but it is more common in adolescents. Males are slightly more than females. About 30% to 40% of patients have infections before onset, mostly upper respiratory tract infections. 20% to 25% of patients with acute nephritis syndrome as onset, about 25% with nephrotic syndrome (37% for children), and often with asymptomatic proteinuria and/or hematuria The onset of the disease, the incidence of hematuria is about 80%, can be repeated episodes, can also be gross hematuria or microscopic hematuria, proteinuria varies, but usually non-selective, about 30% of patients have hypertension at the time of treatment , but often mildly elevated, may have pain in the kidney area, may be unilateral or bilateral, but rare, renal function tests are mostly normal at the time of treatment, a few have been mildly reduced, serum complement components are generally normal The level of blood immunoglobulin is also rarely abnormal, and the anti-streptomycin "O" titer is often normal.

Non-IgA mesangial proliferative nephritis

Under light microscopy, diffuse mesangial cells can be seen, 4 to 5 per mesangial area, and more than 5 in severe cases; endothelial cells can also proliferate, often lighter; proliferating cells may also have infiltrative cells Nuclear cells; increased mesangial matrix; although sometimes segmental aggravation, usually diffuse uniformity; glomerular capillary wall intact, no vascular plexus necrosis; usually without adhesion and hardening changes, about half Eosin red deposits can be seen in the glomeruli of patients, limited to the mesangial area, occasionally in the glomerular basement membrane and arteriolar wall with similar eosin deposits and "transparent-like" changes, mesangial cells and matrix Not found in the peripheral capillary wall, the findings in immunofluorescence are quite diverse, and IgA-based, IgA nephropathy, is not discussed in this section.

Common manifestations of IgG or IgM are granular diffuse distribution, which may be associated with C3 deposition in the mesangial area, or with a small amount of deposition of IgM or IgG and IgA. This is the pathogenesis of IgM deposition and The clinical significance is still unclear, and some mesangial proliferative nephritis can be free of immunoglobulin and complement deposition. Whether it can be classified as a small lesion nephropathy with obvious mesangial hyperplasia is also controversial. Occasionally, only C3 deposition can be used. Immunoglobulin deposition, electron microscopy, is typically characterized by fine-grained or uniform electron-dense deposits in the mesangial area. It is believed that IgA nephropathy and systemic disease renal damage should be excluded when large granular electron dense deposits are involved. In addition, epithelial cells may have swelling and disappearance of the foot, and the basement membrane may also be slightly altered.

Diagnosis and differentiation of non-IgA mesangial proliferative nephritis

It needs to be differentiated from systemic lupus erythematosus, allergic purpura, rheumatoid arthritis, hereditary nephritis, pulmonary hemorrhagic-nephritis syndrome, kidney damage caused by Kimura disease and D-penicillamine, and vasculitic kidney damage.

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.