Rapidly progressive nephritis

Introduction to acute nephritis Acute nephritis is an abbreviation for acute rapid progressive glomerulonephritis (APG). It has a rapid onset of disease, and its renal function deteriorates sharply in a few days, weeks or months, and it is more common to have oliguria (nouria) acute renal failure. basic knowledge The proportion of illness: 0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: uremia, nausea and vomiting, hiccups, upper gastrointestinal bleeding, pulmonary edema, pericarditis, cerebral edema, anemia

Cause of acute nephritis

The following diseases cause acute nephritis

(a) primary glomerular disease

1. Primary diffuse crescentic nephritis

(1) Type I: IgG linear deposition (anti-glomerular basement membrane antibody mediated).

(2) Type II: IgG particle-like deposition (immune complex mediated).

(3) Type III: deposition with little or no Ig (lack of immune response).

(4) Anti-neutrophil granule antibody (ANCA) induction (vasculitis).

2. Secondary to other primary glomerulonephritis, membrane proliferative glomerulonephritis (especially type II), membranous glomerulonephritis with additional anti-basal membrane nephritis, IgA nephritis (rare).

(B) associated with acute staphylococcal infection of infectious diseases, glomerulonephritis, acute or subacute infective endocarditis, chronic sepsis caused by visceral suppurative lesions and glomerulonephritis.

Other infections: shunt nephritis, hepatitis B virus nephritis, human immunodeficiency virus infection.

(C) systemic erythematous scars with multiple system diseases, pulmonary hemorrhagic-nephritis syndrome, allergic purpura, diffuse vasculitis such as necrotizing granuloma, allergic vasculitis and other types, mixed cryoglobulinemia Rheumatoid arthritis with vasculitis, malignant tumors and recurrent polychondritis.

(d) Penicillamine, hydralazine, allopurinol and rifampin.

[Pathogenesis]

(1) The traditional view of light microscopy is that there are a large number of parietal and visceral epithelial cells proliferating in the early renal capsule (mainly by parietal epithelial cells), and the proliferating epithelial cells overlap in the cyst to form epithelial cells. The crescentic crescent or ring surrounds the entire renal capsule wall layer, called the ring body. Some people think that there may be crescent formation within a few days after the onset of the disease. Fibrin can be seen between the proliferating epithelial cells, and multinuclear macrophages. Cells, neutrophils and red blood cells, etc., these lesions can be quite extensive, even involving about 80% of glomeruli, in the longer cases, the proliferation of each layer of epithelial cells can be seen between the emergence of new collagen fibers, after The formation of fibrous crescents has gradually been established. It is now recognized that the number and severity of crescent formation are closely related to the prognosis. The principle of crescent formation is not well understood. It is considered to be fibrin through pathological glomerular capillaries. The blood vessel wall exudes into the small cystic cavity and stimulates the reactive proliferation of epithelial cells. However, whether fibrin can cause such a significant degree of dermal cell proliferation is questionable, and there may be other The influencing factors, the role of macrophages have been paid attention to, macrophages promote fibrinogen deposition in the glomerulus, macrophages proliferate on the balloon wall, and transform into epithelioid cells, forming a crescent, new moon The body can disappear on its own.

Focal necrosis can occur in the glomerular capillary plexus with crescent, followed by capillary atrophy and collapse, and adhesion to the crescent is blocked, and finally the entire glomerulus can undergo hyalinization or fibrosis. In addition, proliferative changes are also seen in the glomerular capillary plexus.

In addition to glomerular prominent lesions, the pathological changes may have cell infiltration, edema and fibrosis in the interstitial, and the degree of interstitial lesions also affects the prognosis.

(2) Immunofluorescence examination showed that the immune complexes were granulated and the anti-basement membrane antibody was linearly deposited. The immunofluorescence was linear and most of them were IgG positive, of which about 1/2~2/3 Cases may have C3 deposition, other immunoglobulins are rare, and immunofluorescence changes in the immune complex type are C3, IgG and fibrin (original) in the damaged glomerular capillary sputum, more than 70%. There is fibrin (original) in the case of new moon, which is easy to see in the fresh proliferating crescent, but it is absent in the so-called old crescent in the long time. There is never a variety in the crescent. Immunoglobulin.

(C) It can be seen by electron microscopy that the fresh crescentic epithelial cells are highly swollen and the volume is increased to 32 m. There are fibrin bundles (fibres) and fibrin-like substances between the early proliferating balloon epithelial cells. The latter is more common in very fresh. The crescentic body, especially when it is caused by anti-basement membrane disease; acute inflammatory changes such as glomerular capillary endothelial cells and mesangial cells proliferating and narrowing of the lumen are observed under electron microscope, and some cases are in the basement membrane. There are fibrin and even a few electron dense deposits on the cell side. The glomerular basement membrane may have irregular thickening, thinning, rupture or nail-like protrusion. The basement membrane of the mesangial area may have obvious thickening and immune complex deposition. The site may be in the basement membrane of the basement membrane endothelial cell side, and the epithelial cell side basement membrane may also exhibit hump-like deposition.

Rapid progressive nephritis prevention

1. Pay attention to rest, avoid fatigue, prevent infection, diet with low protein, pay attention to vitamin supplements, and avoid using drugs that damage the kidneys.

2. During the drug treatment, the clinic will be reviewed every 1 to 2 weeks to observe the urine routine, liver and kidney function, and growth and development to guide the completion of the treatment.

3. After the control of active lesions and after the completion of the course of treatment, renal biopsy should be repeated to evaluate the pathological changes of renal tissue and to observe whether there is a chronic tendency, so as to take timely measures.

In short, pay attention to the protection of residual renal function, correct various factors that reduce renal blood flow (such as hypoproteinemia, dehydration, hypotension, etc.) and prevent infection, are important links in prevention.

Acute nephritis complications Complications uremia nausea and vomiting hiccups upper gastrointestinal bleeding pulmonary edema pericarditis cerebral edema anemia

Rapid renal function decline, early oliguria or anuria, patients often develop into uremia within a few weeks to several months and edema, nausea and vomiting, hiccups, upper gastrointestinal bleeding, and pulmonary edema, pericardium Inflammation, cerebral edema, acidosis, hyperkalemia, anemia and other complications.

Rapid progressive symptoms of nephritis Common symptoms Urine osmotic pressure decreased urinary calcium increased urinary anuria proteinuria hematuria

Most cases are based on acute onset, rapid progression of the disease, oliguria or anuria, gross hematuria with a large number of proteinuria and progressive renal dysfunction and other typical clinical manifestations, and combined renal biopsy showed that more than 50% of glomeruli have crescent formation Pathological changes, it is generally not difficult to make a diagnosis, but pay attention to atypical cases.

After clearing the diagnosis of this disease, it should be differentiated from idiopathic or secondary, and it is important to pay attention to the diagnosis of the basic cause of the disease, because the prognosis of acute nephritis caused by various diseases is different, and the treatment methods and effects are different. Most authors It is believed that the prognosis of glomerulonephritis caused by acute streptococcal infection is better than that caused by the peripheral disease. In addition, it is also caused by the disease of the whole body. If early diagnosis, such as purpuric glomerulonephritis, the prognosis may be more arteries. Inflammation or pulmonary hemorrhage-nephritis syndrome is better, but these diseases are often confused in diagnosis, and attention should be paid to identification.

Acute nephritis check

1. Outstanding performance is continuous increase of blood urea nitrogen and creatinine, endogenous heparin clearance rate is significantly reduced, varying degrees of metabolic acidosis and hyperkalemia, blood calcium is generally normal, blood phosphorus is also in the normal range, always mirror Lower hematuria, urine FDP is higher than normal.

2. Serum complement levels are normal, often accompanied by cryoglobulinemia.

3. Blood routine mainly has anemia performance.

4. Blood immunological examination: anti-glomerular basement membrane antibody can be detected in type I patients; type II patients may have immune complexes, cold globulin and rheumatoid factor positive, serum total complement and C3 in type I, II patients Can be reduced; patients with type III have no special changes in the above examinations.

5. Accurate diagnosis depends on renal puncture, that is, more than 50% of glomeruli have obstructive crescent formation to diagnose.

Diagnosis and differentiation of acute nephritis

diagnosis

Diagnosis is based on clinical performance and examination.

Differential diagnosis

(A) Identification with prerenal or post-renal acute renal failure In addition, attention should be paid to pre-renal factors aggravating renal dysfunction in rapidly progressive nephritis.

(B) when there is difficulty in the differential diagnosis of acute interstitial nephritis or acute tubular necrosis, a clear diagnosis of renal biopsy is needed.

(C) glomerulonephritis after severe streptococcal infection This disease is mostly reversible, oliguria and renal dysfunction lasts for a short time, renal function is generally expected to recover after 4 to 8 weeks of disease, renal biopsy or dynamic course observation Help the two identify.

(D) with hemolytic uremic syndrome, rapid hypertension, etc. In addition, legionnaire caused by acute renal failure can be cured, because it is often accompanied by lung lesions, reported misdiagnosed as pulmonary hemorrhage - Cases of nephritic syndrome.

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