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The Hidden Threat of Antibodies: How Do HLA Antibodies Cause Tubular Disease in Transplanted Kidneys?
Kidney transplantation has become one of the important methods for the treatment of end-stage renal disease, but with the development of technology, subsequent problems cannot be ignored. Among them, transplant tubulopathy (TG) is one of the important problems affecting kidney function. TG can lead to decreased kidney function and is closely related to the presence of various antibodies. Therefore, understanding how HLA antibodies trigger TG has become an important focus of current clinical and research.
What is transplant tubulopathy?
Transplant tubulopathy is a morphological lesion that occurs after kidney transplantation. Its main feature is the duplication and multi-layering of the renal tubular basement membrane. Typical manifestations of TG include proteinuria, hypertension, and progressive decline in renal function. Studies show that TG develops in approximately 5–10% of cases within five years of kidney transplantation, and in some cases, TG may be discovered asymptomatically during routine biopsies.
Causes and mechanisms of TG
It is currently believed that TG is mainly a morphological manifestation of chronic antibody-mediated rejection, especially closely related to the accumulation of donor-specific antibodies against HLA class II antigens. However, TG is not limited to chronic antibody-mediated rejection. In 1/3 to 1/4 of cases, other conditions such as microvascular thrombosis (TMA), HCV infection, or T cell-mediated rejection (TCMR) may also be present. pathological factors.
In addition to donor-specific antibodies, non-HLA antibodies may also play an important role in renal tubular injury caused by transplanted renal tubulopathy.
Diagnosis of TG
The diagnosis of transplanted renal tubule lesions usually relies on pathological examination, especially the double contour of the renal tubular basement membrane as the main indicator. In the early stages, TG appears as a localized lesion that may only affect a few renal tubules, so sufficient renal tissue sampling is required for evaluation. As the disease progresses, the damage may become more widespread, accompanied by tubular fibrosis and further decline in renal function.
Treatment strategies for TG
Management of patients with TG usually includes the use of ranidone-aldosterone system (RAAS) inhibitors to reduce intratubular pressure and active control of comorbid conditions such as hypertension and diabetes. In addition, appropriate weight management and lifestyle modifications are also incorporated into the treatment strategy.
Conclusion
With in-depth research on TG and its causes, medical professionals have become increasingly aware of the important role of HLA antibodies in this process. However, as new research continues to emerge, many unanswered questions remain. Faced with such complex immune responses and renal tubular lesions, how should we more effectively manage and prevent complications after kidney transplantation in the future?
