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Related Concept Videos

Kidney Transplant I: Introduction01:28

Kidney Transplant I: Introduction

A kidney transplant is a surgical approach that involves replacing a non-functioning kidney with a healthy one from a donor. This procedure is often a treatment option for end-stage renal disease (ESRD) patients. The method requires careful recipient selection, including evaluating various medical and psychosocial factors. These criteria vary between transplant centers but generally include assessments of the patient's overall health, adherence to medical recommendations, and lifestyle...
Kidney Transplant III: Nursing Management01:16

Kidney Transplant III: Nursing Management

Postoperative Nursing Management for Kidney Transplant PatientsPostoperative nursing management care includes monitoring the surgical site, encouraging early movement, and promoting lung health through breathing exercises. Nurses also administer prescribed medications like H2-blockers, such as famotidine, or proton pump inhibitors, like omeprazole, to help prevent gastrointestinal ulcers and bleeding. Fungal infections in the mouth and bladder can result from immunosuppressive and antibiotic...
Kidney Transplant II: Surgical Procedure01:26

Kidney Transplant II: Surgical Procedure

Preoperative ManagementThe primary goals of preoperative management in kidney transplantation are to optimize the patient’s metabolic state and prepare them for surgery through diet adjustments, necessary dialysis, and tailored medical treatment. This phase also involves comprehensive infection screening and patient education about the surgical procedure and postoperative care to improve outcomes and adherence.Medical ManagementA comprehensive evaluation is required for both the living donor...
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...

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Reply to Comment on "Clazakizumab in the treatment of chronic active antibody-mediated kidney transplant rejection: Results from the IMAGINE phase 3, randomized, double-blind, placebo-controlled study".

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Related Experiment Video

Updated: May 9, 2026

Mouse Kidney Transplantation: Models of Allograft Rejection
16:15

Mouse Kidney Transplantation: Models of Allograft Rejection

Published on: October 11, 2014

Microvascular Inflammation in Kidney Transplantation.

Emmett Tsz Yeung Wong1,2,3, Robert Balshaw4, Ian W Gibson5,6

  • 1Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.

Journal of the American Society of Nephrology : JASN
|May 7, 2026
PubMed
Summary
This summary is machine-generated.

Microvascular inflammation in kidney transplants, defined by glomerulitis and peritubular capillaritis scores, does not independently predict graft loss when adjusted for T-cell-mediated rejection and de novo donor-specific antibodies.

Keywords:
kidney transplantationrejectionrenal transplantationtransplant pathology

Related Experiment Videos

Last Updated: May 9, 2026

Mouse Kidney Transplantation: Models of Allograft Rejection
16:15

Mouse Kidney Transplantation: Models of Allograft Rejection

Published on: October 11, 2014

Area of Science:

  • Nephrology
  • Transplantation Immunology
  • Pathology

Background:

  • Microvascular inflammation (g+ptc≥2) is common in kidney transplants, often occurring with T-cell-mediated rejection (TCMR) or de novo donor-specific antibodies (dnDSA).
  • The independent prognostic value of microvascular inflammation without DSA is not well understood.

Purpose of the Study:

  • To determine the independent impact of microvascular inflammation (g+ptc≥2), TCMR, and dnDSA on death-censored allograft loss.
  • To analyze these factors in a modern kidney transplant cohort using time-dependent analyses.

Main Methods:

  • A single-center cohort of 689 kidney transplant recipients (2004-2021) was analyzed.
  • Cox models with time-dependent covariates were used to assess the impact of g+ptc≥2, TCMR, and dnDSA on graft survival.
  • Events were analyzed individually and in a combined model.

Main Results:

  • Microvascular inflammation (g+ptc≥2) occurred in 15% of recipients, with 88% having concurrent or sequential TCMR and/or dnDSA.
  • Individually, g+ptc≥2, TCMR, and dnDSA were associated with graft loss.
  • In a combined model, only TCMR and dnDSA remained independently associated with death-censored allograft loss.

Conclusions:

  • In contemporary kidney transplant recipients on tacrolimus, microvascular inflammation (g+ptc≥2) without DSA does not independently predict graft loss.
  • TCMR and dnDSA are the primary drivers of graft loss in this context.