Background. Therapeutic donors (TDs) are individuals who undergo organ removal for medical treatment with no replacement organ, and the organ is then transplanted into another person. Transplant centers in the United States have started using TDs for kidney transplantation (KT). TD-KT recipient outcomes may be inferior to those of non-TD-living-donor (non-TD-LD)-KT or deceased-donor (DD)-KT because of the conditions that led to nephrectomy; however, these outcomes have not been sufficiently evaluated. Methods. This was a retrospective cohort study using Organ Procurement and Transplantation Network data. Via optimal matching methods, we created 1:4 fivesomes with highly similar characteristics for TD-KT and non-TD-LD-KT recipients and then separately for TD-KT and DD-KT recipients. We compared a 6-mo estimated glomerular filtration rate (eGFR) between groups (primary endpoint) and a composite of death, graft loss, or eGFR <30 mL/min/1.73 m² at 6 mo (secondary). Results. We identified 36 TD-KT recipients with 6-mo eGFR. There was also 1 death and 2 graft losses within 6 mo. Mean ± SD 6-mo eGFR was not significantly different between TD-KT, non-TD-LD-KT, and DD-KT recipients (59.9 ± 20.7, 63.3 ± 17.9, and 59.9 ± 23.0 mL/min/1.73 m², respectively; P > 0.05). However, the 6-mo composite outcome occurred more frequently with TD-KT than with non-TD-LD-KT and DD-KT (18%, 2% [P < 0.001], and 8% [P = 0.053], respectively). Conclusions. Early graft function was no different between well-matched groups, but TD-KT demonstrated a higher risk of otherwise poor 6-mo outcomes compared with non-TD-LD-KT and DD-KT. Our results support selective utilization of TD kidneys; however, additional studies are needed with more detailed TD kidney information to understand how to best utilize these kidneys. Export

Chronic Kidney Disease (CKD) affects approximately 14% of adults globally and is a progressive, multifactorial disorder of the kidney characterized by structural or functional nephron impairment. CKD has been linked with several other comorbidities, including diabetes, hypertension, obesity, and aging, which increase the complexity of the disease. Because early-stage CKD is frequently asymptomatic, diagnosis is frequently delayed, resulting in increased risk of progression to End-Stage Kidney Disease (ESKD). Diagnostic tools such as estimated glomerular filtration rate (eGFR) and albuminuria remain limited for early diagnosis, making the condition more threatening. Recent molecular biology research has identified chronic inflammation, oxidative stress, mitochondrial dysfunction, fibrosis, and regulated cell death as central mechanisms driving CKD progression. Novel biomarkers, including kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and cystatin C, along with multi-omics technologies, have created opportunities for earlier diagnosis, risk stratification, and precision-based therapies, although most remain investigational rather than established for routine clinical use. Current treatment approaches, such as renin–angiotensin–aldosterone system inhibitors and sodium-glucose cotransporter-2 inhibitors, can slow but not halt disease progression. This review describes CKD epidemiology, molecular mechanisms, current and experimental diagnostics, advances in therapeutic strategies, and future directions. It emphasizes the role of molecular biomarkers and precision medicine in optimizing patient care and outcomes.