It should be noted some problems in the pathological diagnosis of primary glomerular diseases

In recent years, renal biopsy technology is the rapid spread of the pathological diagnosis of kidney disease, in particular, considerable progress in the diagnosis of glomerular disease. But indeed there are some urgent attention and improvement. The first clear pathological diagnosis of renal biopsy light microscopy, immunopathologic, and electron microscopy diagnosis. Around as soon as possible to create conditions for active collaboration, so that with the necessary conditions of the renal biopsy diagnosis. Some units (including the low quality of some of the conditions of good general hospital) producer, such as optical mirror slice is too thick (should be 2 to 3μm), the lack of special stains (PASM, PAS, Masson, and other necessary special stains, etc.); The renal biopsy specimen of the small number of units without immunofluorescence or immunohistochemistry, namely the pathology report; quite a number of unit power microscope, ultrastructural examination is not into the routine examination in the pathology. Some units lack pathologist familiar with the kidney pathology or kidney disease have a more extensive knowledge of pathology, general practitioners, or both, the lack of close cooperation and discussion. Above, greatly affect the correct pathological diagnosis of renal biopsy, should pay more attention and timely improvement of the Journal of Nephrology. Second edition, Beijing: People's Health Publishing House, 1996.424 ~ 435]. We focus on the pathological diagnosis of primary glomerular diseases in China could easily cause confusion and deserves our attention some of the issues the child proposed for the reference and correction of their fellow
1, minimal change nephropathy (MCD)
Necessary to conscientiously observe the ultrastructural changes of the electron microscope, diffuse foot process fusion and glomerular generally electron dense, even in the vice mesangial small electron dense as an important pathological features of MCD. Immunofluorescence specimens unsatisfactory or no glomerular rely only on observed by light microscopy to be confused with mild lesions with mild mesangial proliferative glomerulonephritis and early membranous nephropathy, can even be mistaken for the normal glomerulus. In the diagnosis of insufficient evidence, temporarily known as the glomerular minor lesion may be more appropriate.
Despite international IgM nephropathy is still controversial or different views, a massive proteinuria or nephrotic syndrome, renal pathology immunofluorescence showed mesangial area clear of IgM deposition under the light microscope can be mild mesangial proliferative , although electron microscopy of glomerular epithelial cell foot suddenly wide range of integration, we should still diagnosis of mesangial IgM nephropathy, and should be further follow-up. Middle-aged patients with minimal change disease, erythrocyte sedimentation rate abnormal increase in the fast should be carefully excluded the possibility of malignancy.
2, focal segmental glomerulosclerosis (FSGS)
Note first of all distinguish the glomerular lesions of focal segmental glomerular sclerosis with focal segmental sclerosis, which may occur in a variety of glomerular diseases, while the former is a specific renal ball disease. In recent years, many scholars abroad to promote the classic FSGS, collapsing glomerulopathy and state-of-the-art glomerular injury in two subtypes should be increased. Collapsing glomerulopathy (collapsing glomerulopathy, CG) has its own pathology and clinical particularity. CG of the pathological features of the glomerular capillary loops showed the limitations of segmental collapse. Sometimes as a global collapse, GBM performance wrinkled, folded, glomerular epithelial cells were significantly swelling, hypertrophy and hyperplasia of epithelial cells was more nuclear, cytoplasm containing a transparent kind of DROP or vacuolization, the vast The majority of patients were nephrotic syndrome, urinary protein> 10g/24h, the efficacy of hormonal and cytotoxic drugs, the majority of patients with renal function deterioration. Therefore, CG is considered to be the poor prognosis of a special kind of pathological changes of FSGS. According to reports, CG is a high incidence among blacks, CG about 5% to 15% of [the Kidney Int FSGS in 1994,45:1416 1424]. State-of-the-art glomerular damage (glomerular tip lesion) means the glomerular sclerosis uttermost parts in the urine of the vascular pole, and is generally believed that this kind of pathological changes in patients on hormonal and cytotoxic treatment response is better, FSGS in prognosis relatively good kind of pathological changes.
Pathological type of FSGS in elderly patients with nephrotic syndrome should be excluded from renal amyloidosis, diabetic nephropathy, light chain nephropathy and multiple myeloma nephropathy may be, can be combined with clinical and Congo red staining, the specific antibody immune staining (such as anti-Kappa or lambda light chain antibodies) and ultrastructure of careful observation to be identified.
Several domestic Kidney Disease Research Center of primary nephrotic syndrome, renal biopsy data analysis showed that the FSGS proportion of large difference can be> 15% or <5%. This variation causes speculation and pathologist to master standard, diagnostic thinking, especially glomerular diseases associated with glomerular lesions of focal segmental sclerosis appropriately diagnosed, yet to be domestic kidney disease academic as soon as possible unified.
3, membranous nephropathy
Atypical membranous nephropathy (ie, addition to the pathology of membranous nephropathy itself, there are varying degrees of mesangial cells and mesangial matrix, immunopathologic, and electron microscopy with membranous nephropathy), consideration should be given to the type Ⅴ lupus nephritis or hepatitis B virus associated glomerulonephritis secondary to glomerular diseases may, clinical, serological, serum HBV antigen detection and kidney slices by immunohistochemical detection of antigen (such as HBV antigen) further confirmed.
In the light microscope, the early membrane lesion (Ⅰ of membranous nephropathy) often lack a clear pathological changes, such as the lack of immunofluorescence specimens glomerular immunofluorescence specimens is not ideal, necessary for careful observation in the electron microscope the GBM epithelial cell side with or without electronic dense material (ED) and (or) using paraffin section immunohistochemistry to observe the distribution and the formation of IgG, C3, should not solely on the basis of the results of light microscopy misdiagnosed as mild disease, minimal change or mild mesangial proliferative nephritis.
Pathologically confirm the diagnosis in patients with membranous nephropathy, particularly ESR abnormal increase in the elderly patients should be the detailed examination to exclude malignancy (such as lymphoma, lung cancer), renal amyloidosis may.
4, mesangial proliferative glomerulonephritis (MsPGN)
China with a high incidence can have a variety of different clinical manifestations, response to treatment and prognosis of variation is great. Generally based on the characteristics of immunofluorescence into IgA and non-IgA mesangial proliferative glomerulonephritis, the former immunofluorescence IgA-based, the latter of IgG or IgM-dominated deposition in the mesangial area. Light microscopy should be based on the mesangial cells and stromal hyperplasia of the degree of glomerular capillary loops open and pressure, divided into light, medium and heavy three. Different response to treatment and prognosis.
For MsPGN patients should be combined with the clinical and the laboratory examination, pay attention to the differentiated kidney damage caused by systemic diseases and allergic purpura, systemic lupus erythematosus and cirrhosis. The primary MsPGN patients should also consider whether the dissipation of the capillary proliferative glomerulonephritis (acute infection glomerulonephritis) of.
Patients with hematuria, renal pathology immunofluorescence negative, thin light microscope, normal or showed mild mesangial proliferative lesions should be carefully investigating the family history of the hematuria, and careful observation of the GBM ultrastructural changes and the relevant checks to exclude basement membrane nephropathy or the possibility of early Alport syndrome.
5, the capillary proliferative glomerulonephritis
Should be noted that the difference of the capillary proliferative glomerulonephritis dissipation of mesangial proliferative glomerulonephritis, electron microscopy former GBM epithelial cells of the "Hump" to dissipate moth-eaten legacy lucent zone to assist in identifying; In addition, the combination of acute nephritic syndrome history, C3 dynamic change, ASO titer, and infection and the onset interval to help both identify all help.
Capillary proliferative glomerulonephritis characteristic pathological types of glomerulonephritis in the acute infection, many cases of domestic IgA nephropathy light microscope, the pathological changes in the endothelial cells, mesangial cell proliferation, capillary loops compression for outstanding performance, it should be based on immune fluorescence and clinical manifestations (serum IgA level, ASO, C3, infection and onset interval, etc.) to distinguish between the two.
Ⅳ lupus nephritis can be expressed endocapillary proliferative nephritis pathological changes, it should be combined with antinuclear antibodies and other immunological tests and other clinical manifestations of carefully identified.
6, membrane proliferative glomerulonephritis (MPGN)
Idiopathic nephritis should be carefully observed in the electron microscope, the distribution of parts according to the electron-dense material, and in combination with other pathological features (if double-track sign, immunofluorescence features) distinguish Ⅰ, Ⅱ, Ⅲ type.
Western developed countries MPGN type Ⅰ the MPGN incidence rate decreased significantly, and may improve related health conditions, air pollution. In the pathological type accounting for primary nephrotic syndrome in 10% to 15% of the vast majority of type MPGN Ⅰ.
Pathological manifestations of MPGN patients, in conjunction with clinical and laboratory tests (including kidney immune pathology examination), carefully exclude the hepatitis B virus associated glomerulonephritis, hepatitis C virus associated glomerulonephritis, cryoglobulinemia kidney damage and lupus nephritis possible.
7, crescentic nephritis
In recent years, anti-neutrophil cytoplasmic antibodies (ANCA) testing is widely used in clinical practice, crescentic nephritis is traditionally divided into Ⅰ, Ⅱ, Ⅲ type of classification is under attack, most scholars recently advocated basis for ANCA and anti- glomerular basement membrane (GBM), results in greater detail is divided into five types [of The kidney 5th ed. Philadephia: WBS Saunders Company, 1996. 1 392 ~ 1 432].
Based solely on light microscopic examination to confirm the diagnosis of crescentic glomerulonephritis is not enough, should be combined with immunofluorescence, serum anti-GBM antibody and ANCA detection and clinical manifestations (such as hemoptysis, etc.), carefully identify the crescentic glomerulonephritis of what kind of type, take reasonable treatment, the prognosis is crucial. Anti-GBM antibody-positive rapidly progressive glomerulonephritis (RPGN) I light microscope and electron microscope in the early lesions often can be observed in a clear and serious GBM rupture, degeneration; ANCA positive RPGN Ⅲ type (Many scholars believe that the small blood vessels inflammation of the kidneys localized) in most patients with renal biopsy specimens can be observed more diffusely distributed segmental capillary loops fibrinoid necrosis, and a small number of patients (20%) can be found in necrotizing renal arteritis. Show the different types of crescentic nephritis their pathological features. Must be pointed out that the RPGN I type renal biopsy specimen by immunofluorescence examination, the early shows IgG and C3 along the GBM was smooth lines, kind of typical distribution, but the course of the disease later, because of the GBM rupture, degeneration and / or anti-GBM and GBM combine to form immune complexes and which led to the generation of the second antibody, some patients with IgG and C3 can be presented to the granular distribution along the GBM, etc., often misdiagnosed as immune complex-mediated type II RPGN. Type III RPGN kidney specimens by immunofluorescence negative or only weak IgM and / or C3 deposition. We believe that the RPGN patients with conventional anti-GBM antibodies and ANCA testing, carefully observe the pathological changes and clinical data for the right to distinguish between different types of RPGN is very important.
8, sclerosis of glomerular nephritis and sclerosing glomerulonephritis
Various types of glomerulonephritis sustainable development, so that part of the (more than 50%) completely destroyed leading to global sclerosis. Glomerulus, the surviving structure can still identify the type of the original glomerular pathology may be said of a certain type of glomerulonephritis caused by proliferative sclerosing glomerulonephritis. If the structure of the remaining glomerulus has been unable to identify the type of primary glomerular lesions, can be collectively referred to as proliferative sclerosing glomerulonephritis. More than 70% of the total number of glomerular glomerular sclerosis, can be called sclerosing glomerulonephritis. Glomerulosclerosis by other systemic diseases such as diabetes, amyloidosis, hypertension, small vessel vasculitis, systemic lupus erythematosus and other systemic diseases caused should be noted that the identification of renal pathology and clinical Changsha: Hunan Science and Technology Press, 1993.41 53.]
In summary, the diagnosis of primary glomerular disease should be closely combined with clinical and related inspections, serious rule out the possibility of systemic or genetic disease, response to light microscopy, immunofluorescence and electron microscopy Ultrastructural pathological changes, careful observation and comprehensive analysis in order to obtain a correct diagnosis of pathological types of primary glomerular diseases.

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