Kashiv P, Saxena K, Balwani MR, Kute VB. Reply: Chronic kidney disease after liver transplantation: Accurate measurement, early acute kidney injury, and renal-protective strategies. World J Transplant 2026; 16(3): 124182 [DOI: 10.5500/wjt.124182]
Corresponding Author of This Article
Vivek B Kute, MD, Department of Treasury, Indian Society of Organ Transplantation (ISOT), Saraswati Kidney Care Center, 13, New Sneh Nagar, Nagpur 440015, Maharashtra, India. drvivekkute@rediffmail.com
Research Domain of This Article
Transplantation
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letter
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World J Transplant. Sep 18, 2026; 16(3): 124182 Published online Sep 18, 2026. doi: 10.5500/wjt.124182
Reply: Chronic kidney disease after liver transplantation: Accurate measurement, early acute kidney injury, and renal-protective strategies
Pranjal Kashiv, Khushboo Saxena, Manish Ramesh Balwani, Vivek B Kute
Pranjal Kashiv, Department of Nephrology, All India Institute of Medical Sciences, Nagpur 441108, Mahārāshtra, India
Khushboo Saxena, Nephrology, IKDRC, Ahmedabad 380016, Gujarāt, India
Manish Ramesh Balwani, Department of Nephrology, Saraswati Kidney Care Center, Nagpur 440015, Maharashtra, India
Vivek B Kute, Department of Treasury, Indian Society of Organ Transplantation (ISOT), Nagpur 440015, Maharashtra, India
Author contributions: Kashiv P was responsible for study design, literature review, data curation, interpretation of evidence, drafting of the manuscript, and coordination of all stages of manuscript preparation and revision; Balwani MR contributed to the conception and design of the study, provided senior oversight, supervised the work, and critically revised the manuscript for important intellectual content; Saxena K contributed to data curation, literature review, and critical review of the manuscript; Kute VB contributed to conception, senior supervision, overall project administration, and critical revision of the manuscript for important intellectual content.
AI contribution statement: No artificial intelligence tools were used in the generation of the manuscript. ChatGPT was used solely for minor grammatical corrections and language refinement, without influencing the scientific content, interpretation, or conclusions of the work.
Conflict-of-interest statement: On behalf of all the authors, the corresponding author confirms that there are no conflicts of interest related to this manuscript.
Corresponding author: Vivek B Kute, MD, Department of Treasury, Indian Society of Organ Transplantation (ISOT), Saraswati Kidney Care Center, 13, New Sneh Nagar, Nagpur 440015, Maharashtra, India. drvivekkute@rediffmail.com
Received: July 3, 2026 Revised: July 13, 2026 Accepted: July 15, 2026 Published online: September 18, 2026 Processing time: 83 Days and 14 Hours
Abstract
In this article, we comment on the article by Sessa et al published in the recent issue of the World Journal of Transplantation, who revisit the three-decade single centre cohort of Muñoz-Serrano et al and conclude that chronic kidney disease (CKD) after liver transplantation (LT) is a modifiable determinant of long-term survival rather than an unavoidable consequence of calcineurin inhibitor exposure. We share their central position and welcome the weight they give to perioperative acute kidney injury (AKI), to calcineurin inhibitor minimisation through basiliximab induction and mycophenolate, and to the disciplined control of hypertension and metabolic disease. Our intention is to carry the argument one step further, because three problems lie beneath the literature they assemble and constrain what any inventory of risk factors can deliver. The first is metrological. Almost every reported association, including the signal attached to female sex, and the reported incidence itself, which varies according to the definition of CKD applied, the time point of ascertainment and whether creatinine-based or measured filtration is used, derive from creatinine-based estimates of glomerular filtration, a measure the same authors concede performs poorly in patients who are sarcopenic, oedematous and metabolically deranged. The second concerns timing, since the most powerful and most modifiable determinant of chronic injury is the passage from early AKI to fixed nephropathy, a transition that draws surveillance away from isolated tacrolimus trough concentrations, which did not predict one year disease in the index cohort, towards intrapatient variability and time within the therapeutic range. The third is therapeutic, because the prevailing synthesis omits the sodium glucose cotransporter 2 inhibitors, agents with established renal benefit in non-transplant CKD populations that deserve formal evaluation after LT. Measured accurately, protected early and evaluated pharmacologically, the kidney of the liver transplant recipient is more defensible than current practice assumes.
Core Tip: Sessa et al recast chronic kidney disease after liver transplantation as a preventable threat to survival. We press their case further. The creatinine-based estimates that underpin every reported risk factor, the female sex signal included, should give way to cystatin C, measured glomerular filtration and the albuminuria axis. Surveillance should follow intrapatient tacrolimus variability rather than isolated troughs that fail to predict chronic disease. And nephroprotective pharmacotherapy, sodium glucose cotransporter 2 inhibitors foremost among them, deserves formal trial in this population rather than continued neglect.
