ABSTRACT
ABSTRACT Despite improvements in patient survival and quality of life, long-term renal survival has not changed significantly in the recent decades and nephritis relapses affect over 50% of patients with lupus nephritis. Renal fibrosis affecting the tubulointerstitial compartment is a central determinant of the prognosis of any kidney disease. Notwithstanding this evidence, the current 2003 ISN/RPS classification still focuses on glomerular pathology and does not include a mandatory score with clear subcategories of the tubulointerstitial injury in the biopsy. The pathogenesis, and the morphological and molecular characteristics of this process in patients with lupus nephritis will be considered, together with a discussion about the concepts the clinician needs to efficiently address in this injury during daily practice and in future clinical trials. Both tubulointerstitial inflammation and fibrosis are strongly correlated with poor renal outcomes in lupus nephritis, regardless of the extent of glomerular damage. Therefore, it is essential to develop reliable and noninvasive approaches to predict which patients are most likely to develop CKD so that appropriate interventions can be adopted before ESRD is established. Currently, no ideal method for monitoring kidney fibrosis exists, since repeated renal biopsies are invasive. Promising methods for assessing and monitoring fibrosis non-invasively include imaging techniques, such as magnetic resonance imaging or ex vivo confocal microscopy, integrated in computational and digital pathology techniques. Finally, beyond specific immunosuppressive treatment in Lupus Nephritis, identifying and treating cardiovascular risk factors should be a cornerstone of treatment in these patients.
RESUMEN A pesar de las mejoras en la sobrevida de los pacientes y su calidad de vida, la sobrevida renal en el largo plazo no ha cambiado significativamente durante las últimas décadas, y las recidivas nefríticas afectan a más del 50% de los pacientes con nefritis lúpica. La fibrosis renal, que afecta el compartimiento tubulointersticial, es un factor determinante central en el pronóstico de todas las patologías renales. A pesar de la evidencia, la actual clasificación ISN/RPS del 2003 todavía se concentra en la patología glomerular y no incluye un score obligatorio con claras subcategorías de la lesión tubulointersticial en la biopsia. Se hablará de la patogenia y las características morfológicas y moleculares de este proceso en pacientes con nefritis lúpica, así como de los conceptos que el clínico necesita para abordar esta lesión de manera eficiente en su práctica cotidiana y en los estudios clínicos a futuro. Tanto la inflamación tubulointersticial como la fibrosis se relacionan fuertemente con desenlaces renales pobres en la nefritis lúpica, con independencia de la extensión del dañío glomerular. Resulta por lo tanto esencial desarrollar sistemas confiables y no invasivos para predecir cuáles pacientes tendrán mayor probabilidad de desarrollar enfermedad renal crónica, a fin de realizar las intervenciones apropiadas antes de que se establezca la enfermedad renal terminal (ERT). En la actualidad, no existe un método ideal para monitorear la fibrosis renal, dado que las biopsias repetidas son procedimientos invasivos. Algunos de los métodos promisorios para evaluar y monitorear la fibrosis de manera no invasiva son las técnicas de imágenes, tales como la resonancia magnética o la microscopía confocal ex vivo, integradas en técnicas de patología computarizadas y digitales. Finalmente, más allá del tratamiento inmunosupresor específico para la nefritis lúpica, identificar y tratar los factores de riesgo cardiovascular deberá ser uno de los pilares de tratamiento en estos pacientes.
Subject(s)
Humans , Pathological Conditions, Signs and Symptoms , Pathologic Processes , Fibrosis , Lupus Nephritis , Female Urogenital Diseases , VaricoceleABSTRACT
T cell-mediated rejection (TCMR) is one of the main mechanisms of rejection in organ transplantation, which is also the most common type of acute rejection.Based on Banff classification on allograft pathology (Banff classification) in 2019, TCMR can be divided into acute TCMR (aTCMR) and chronic active TCMR (caTCMR) according to the characteristics of immune lesions.In this article, the basic definition of TCMR, the research progress on TCMR pathology according to Banff classification for renal allograft, and the basic pathological changes and diagnostic grading of TCMR were reviewed, aiming to provide evidence for early identification, diagnosis and treatment of TCMR and prevent the progression of TCMR into caTCMR, thereby guarantying the long-term survival of both the renal allograft and recipient.
ABSTRACT
Background: Kidney transplantation is the preferred mode of renal replacement therapy for the endstage renal disease, with dramatic improvements in patient and graft survival over the last 50 years. In the modern era of immunosuppression, 1-year patient survival is close to 98%, and 1-year allograft survival rates have improved to 90% for deceased donor kidney transplants and 95 % for living donor kidney transplants with some inter-center variability. The aim of the study: To elucidate the etiology of graft dysfunction among renal transplant recipients. Materials and methods: A retrospective study was conducted among 155 patients who underwent both cadavers and live donor transplant from October 2009 to March 2011 at a tertiary care center in Chennai, South India. All the transplant recipients were regularly followed with serum urea and creatinine, urine routine, calcineurin inhibitor drug levels in the serum, USG Abdomen, urine culture depending on the graft status. Graft dysfunction defined by a rise in the creatinine more than 25% or 0.3 to 0.5 mg per dl from the baseline. Those who developed graft dysfunction were presented for graft biopsy and managed based on the report accordingly. S. Thirumavalavan, Krishna Kumar, S. A. K. Noor Mohamed, R Vijaya Kumar. Etiology of graft dysfunction in renal transplant recipients. IAIM, 2019; 6(3): 313-318. Page 314 Results: Among the 155 transplant recipient patients, 66 (44%) patients developed graft dysfunction and underwent renal biopsy. The graft dysfunction was due to chronic allograft dysfunction (interstitial fibrosis and tubular atrophy) in 24 (15.4%) patients, acute cellular rejection in 13 (8.4%) patients, acute antibody-mediated rejection in 2 (1.3%) patients, acute tubular necrosis in 9 (5.8%) patients, calcineurin toxicity in 6 (3.9%) patients, thrombotic microangiopathy in 6 (3.9%) patients, IgA nephropathy in 3 (1.9%) patients and transplant renal artery stenosis in 1(0.6%) patient. Conclusion: Among the various causes, acute cellular, acute antibody rejection and chronic allograft nephropathy holds nearly 25% of the incidence of graft dysfunction. It indicates appropriate immunological evaluation, appropriate immunosuppression, use of induction agents in high-risk patients and protocol renal biopsy to identify early rejection in high-risk patient and appropriate early intervention is important to improve long-term term graft and patient survival.