1. Why does lupus erythematosus damage the kidneys?
SLE is a complex autoimmune disease characterized by the presence of multiple autoantibodies. There are 3 mechanisms involved in the occurrence of nephritis, one is the immune reaction of antibody binding with glomerular antigens, such as autoantibodies and multiple components in the kidney, such as acetyl heparin sulfate, phospholipids, Ⅳ collagen, thylakoid and endothelial cell antigens; one is the implantation of circulating antigens into the glomerulus and then binding with autoantigens to initiate the immune reaction; the third is the deposition of circulating immune complexes in the glomerulus to initiate the immune response.
After the immune response is initiated, the complement system is activated, causing a series of immune damage reactions, such as increased capillary permeability, infiltration of inflammatory cells such as neutrophil monocytes, etc. These cells release a large amount of lytic enzymes or proteases, a large amount of inflammatory factors such as IL-2, IL-6, TGF-α, TNF-β, etc. and complement activation products, which lead to kidney tissue damage.
2. Do all patients with lupus develop nephritis?
Almost all SLE have histological, immunopathological or ultrastructural changes of renal tissue damage, only to different degrees. Simply put, all have nephritis. Those with minor damage may have no clinical or urinalysis abnormalities, but have impaired histology.
3.What tests are needed to confirm the diagnosis of nephritis, and can the presence of urine protein be diagnosed?
Patients with SLE should have their urine routinely reviewed. If there is persistent proteinuria or hematuria, lupus nephritis is highly suspected. Patients with lupus nephritis have a variety of clinical manifestations, with varying degrees of severity. In the early stages, patients may present with simple hematuria or simple proteinuria, and if this condition persists, nephritis should be suspected. Sometimes it is important to note that proteinuria or hematuria can have false positives, such as urine contamination or urinary tract infection, and only after these conditions are ruled out can nephritis be diagnosed.
4.Does the patient have to have a kidney biopsy?
The role of kidney biopsy is to clarify the pathological type of nephritis in order to guide the treatment and judge the prognosis. In mild lupus nephritis (24h proteinuria less than 0.5-1g), those who are in rapid remission after conventional treatment may not have a kidney biopsy, but when there is obvious proteinuria and hematuria, abnormal kidney function and poor treatment effect, it is better to have a kidney biopsy if conditions allow (normal coagulation function, etc.).
5.What are the types of lupus nephritis? Is there any difference in medication for each type?
Currently, the types of lupus nephritis are mainly typed by pathological type (see below). The medication for each type should be used according to the actual situation of the patient with a light or heavy treatment plan. In general, type I and some type II patients do not require special therapeutic measures for lupus nephritis and only need to receive immunosuppressants or glucocorticoids according to the principles of systemic treatment for SLE, but for those with significant urinalysis abnormalities, they need to receive a treatment regimen for lupus nephritis.
Type I: lupus nephritis in the thylakoid micropathic zone Glomeruli are normal under light microscopy, but deposits of immune complexes can be seen in the thylakoid zone under immunofluorescence.
Type II: thylakoid proliferative lupus nephritis On light microscopy, only varying degrees of thylakoid cell hyperplasia or increased thylakoid stroma are seen, accompanied by deposition of immune complexes in the thylakoid region. Electron microscopy or immunofluorescence examination may show very small, isolated deposits of immune complexes on the epithelial side or subendothelium in addition to deposits in the thylakoid region.
Type III: focal lupus nephritis The lesions involve 50% of the glomeruli (focal). Lesions may present as active Class III (A) or inactive Class III (C), segmental (S) or spherical (G), intra- or extra-capillary proliferation, usually with localized deposits of immune complexes under the segmental endothelium. It may or may not be accompanied by changes in the tegmental area.
Type IV: diffuse lupus glomerulonephritis The lesions involve 50% of the glomeruli. Lesions may appear as active Class IV-S (A) or inactive Class IV-S (C), segmental (S) or spherical (G), intra- or extra-capillary proliferation, usually with localized deposits of immune complexes under the diffuse endothelium. It may or may not be accompanied by changes in the thylakoid region. Glomerular lesions are classified as segmental (S)-meaning that the lesion does not exceed 50% of a single glomerulus; globular-meaning that the lesion exceeds 50% of a single glomerulus.
Type V: membranous lupus nephritis Diffuse or segmental subepithelial immune complex deposits with or without alterations in the thylakoid region are found by light microscopy, immunofluorescence, or electron microscopy. Type V lupus can often coexist with type III or type IV, when both diagnoses are required.
Type VI: sclerosing lupus nephritis Sclerosis occurs in 90% of glomeruli. No active lesions.
6. How likely is lupus nephritis to develop into uremic syndrome?
There are many factors affecting the prognosis of lupus nephritis. In general, patients with type I and II, unless pathologically transformed, generally have a better prognosis. Type III with proliferative lesions involving only a few glomeruli has a 5-year incidence of end-stage renal failure of less than 5%; type III with glomerular necrotic lesions or crescent formation has a prognosis similar to that of IV(A). Most believe that type IV lupus nephritis has a worse prognosis.
Type V has slow renal decompensation, with 5-year and 10-year renal viability rates of 96.1% and 92.7%, respectively. However, it is important that the prognosis must also take into account therapeutic factors, whether to adhere to treatment or to choose the most appropriate treatment plan, and the 5-year renal survival rate of type IV patients has now increased to 82%.