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IgA nephropathy is the most common primary glomerulonephritis worldwide and a leading cause of chronic kidney disease and kidney failure, with geographic and ancestral variation and a course ranging from asymptomatic urinary abnormalities to progressive loss of kidney function. This narrative review links the multi-hit model to risk stratification, biomarkers, current management, and emerging therapies, and highlights implementation gaps. Risk assessment is longitudinal, prioritizing proteinuria and estimated glomerular filtration rate trajectories and integrating Oxford MEST-C, prediction tools, and biomarker and multi-omics approaches, while recognizing limitations in histologic reproducibility and model calibration. Current management is anchored in optimized supportive care aimed at sustained proteinuria reduction and kidney protection, including intensive blood pressure control with maximal tolerated renin–angiotensin system blockade, dietary sodium restriction and lifestyle measures, and sodium–glucose co-transporter 2 inhibitors for eligible patients. For selected higher-risk patients with persistent proteinuria despite optimized supportive care, immunomodulatory strategies are discussed, including systemic corticosteroids and targeted-release budesonide (Nefecon), emphasizing structured toxicity risk mitigation and cautioning against assuming interchangeability among alternative oral budesonide formulations. Emerging therapies are organized around mechanism-aligned targets across the BAFF/APRIL axis, complement pathways, and endothelin-based approaches, with growing interest in sequencing and combination regimens layered on supportive care. Key gaps include reliance on surrogate endpoints, limited long-term durability and safety data, and uneven evidence for special populations. Full article

Diabetic nephropathy and diabetic atherosclerosis often develop together and share similar metabolic disturbances. Lipid abnormalities are common in diabetes, yet their roles in kidney and vascular injury are not fully understood. In diabetic kidney disease, altered lipid uptake, reduced fatty acid oxidation, and accumulation of harmful lipid species contribute to cellular stress, mitochondrial injury, inflammation, and fibrosis. In parallel, disordered lipid handling in the vasculature promotes endothelial dysfunction and atherosclerotic plaque development. However, not all lipid accumulation appears to be detrimental, and some findings suggest adaptive or context-dependent effects, leading to inconsistent results across studies. In this review, we summarize current evidence on lipid metabolism in diabetic nephropathy and atherosclerosis, compare shared and distinct features, and discuss ongoing controversies. We also briefly address the therapeutic relevance of targeting lipid pathways and highlight areas that require further investigation. Compared with prior reviews that mainly discussed fatty kidney as an emerging concept in chronic kidney disease research, this review specifically focuses on diabetic kidney disease and integrates kidney-specific lipid trafficking, kidney–vessel crosstalk, conflicting evidence, and mechanism-based therapeutic implications. Full article

Hypertensive nephropathy (HN) is a leading cause of chronic kidney disease and end-stage renal disease worldwide and results from the long-term effects of hypertension on renal structure and function. The pathogenesis of HN is complex and involves haemodynamic disturbances, renal vascular injury, oxidative stress, chronic inflammation, and progressive interstitial fibrosis. In recent years, increasing attention has focused on the role of non-coding RNAs (ncRNAs)—including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs)—as key regulators of gene expression involved in these processes. This review summarises the current understanding of the molecular mechanisms underlying HN, with particular emphasis on the roles of oxidative stress, activation of the renin–angiotensin–aldosterone system, transforming growth factor beta signalling, and inflammatory and fibrogenic pathways. The contribution of dysregulated ncRNAs to endothelial dysfunction, inflammatory responses, apoptosis, angiogenesis, and renal remodelling and fibrosis is also discussed. Particular attention is given to miRNAs and lncRNAs as mediators of disease progression and potential biomarkers, as well as to the emerging role of circRNAs in hypertensive kidney injury, including their involvement in the regulation of redox balance and intercellular communication. Collectively, available evidence indicates that ncRNAs represent a critical link between haemodynamic stimuli and persistent molecular alterations in renal tissue, highlighting their potential as diagnostic markers and therapeutic targets in HN. Full article

Background: Ectopic fat deposition has been demonstrated to play a critical role in the onset and progression of renal dysfunction. However, research on renal parenchymal fat deposition and its association with renal dysfunction in type 2 diabetes mellitus (T2DM) remains limited, particularly regarding its association with early kidney injury. The present study aimed to further investigate the relationship between renal fat fraction (FF) and biomarkers of kidney injury, thereby providing new evidence for the potential link between intrarenal fat accumulation and early renal impairment in T2DM. Methods: This cross-sectional study enrolled 60 patients with T2DM. Renal FF was quantitatively assessed using magnetic resonance imaging (MRI). Clinical characteristics, body composition parameters, and biochemical indices were collected. Levels of kidney injury biomarkers, including tumor necrosis factor receptors 1 (TNF-R1), tumor necrosis factor receptors 2 (TNF-R2), chitinase-3-like protein 1 (YKL-40), and kidney injury molecule-1 (KIM-1), were measured using enzyme-linked immunosorbent assay (ELISA). To evaluate the correlations between fat distribution and inflammatory biomarkers, Pearson correlation analysis was performed. Furthermore, linear regression analysis was conducted to explore the associations between renal FF and kidney injury biomarkers with adjustments for potential confounders such as smoking status, diabetes duration, and visceral fat. Lasso regression was used to screen variables. Results: The results demonstrated that renal FF was significantly positively correlated with serum YKL-40 (r = 0.3, p = 0.021), TNF-R1 (r = 0.246, p = 0.042), and urinary KIM-1 (r = 0.396, p = 0.004), indicating a close association between renal fat accumulation and early kidney injury biomarkers. In regression analyses adjusted for age, sex, and duration of diabetes, the associations between renal FF and these biomarkers remained significant. After further adjustment for potential confounders, including smoking history, alcohol consumption, hypertension, renin-angiotensin-aldosterone system (RAAS) inhibitors, sodium-dependent glucose transporters 2 (SGLT2) inhibitors, glucagon-Like Peptide-1 (GLP-1) receptor agonists, and lipid-lowering drugs, renal FF remained significantly associated with TNF-R1 (β = 0.327, p = 0.015), KIM-1 (β = 0.352, p = 0.021), and YKL-40 (β = 0.275, p = 0.025). Moreover, even after additional adjustment for visceral fat, the associations of renal FF with TNF-R1 and KIM-1 persisted. After using the Benjamini–Hochberg procedure for false discovery rate, the relationship between renal FF and KIM-1 had a significant difference. Variables of age and gender were excluded to build the parsimonious modeling using Lasso regression. It suggested that renal fat accumulation may contribute to kidney injury independently of visceral adiposity. Conclusions: The study systematically demonstrates a significant association between renal FF and early biomarkers of kidney injury in T2DM, which may suggest the potential role of renal fat accumulation in the pathogenesis of diabetic nephropathy. These findings provide clinical data support for the development of a fat-targeted intervention study. Future research should further elucidate the long-term mechanistic role of renal FF in diabetic nephropathy, as well as its potential value in early diagnosis and therapeutic applications. Full article

The complement system is the primary defense mechanism against pathogens, acting through opsonization, the membrane attack complex, and classical, lectin, or alternative pathways. These pathways result in the production of key complement components, including C3a (complement component), C5a, and C3b, which recruit inflammatory cells. Complement dysregulation leads to renal disease through the overproduction of anaphylatoxins or inappropriate formation of the membrane attack complex. The levels of complement components have been shown to be useful as predictive markers in acute kidney injury, especially in conditions of alternative pathway activation, and in diseases of immune complex pathology such as lupus nephritis and IgA nephropathy. Genetic defects in complement regulatory proteins result in diseases such as C3 glomerulopathy or atypical hemolytic uremic syndrome, in which uncontrolled C3 convertase activity results in renal failure. Therapeutic interventions targeting complement components, including eculizumab or pegcetacoplan, improve patient outcomes in atypical hemolytic uremic syndrome and C3 glomerulopathy, respectively, while other interventions improve renal function in IgA nephropathy. These findings underscore the dual role of the complement system, which is not only implicated in the progression of renal diseases but also provides the potential for the development of therapeutic interventions for the treatment of various forms of nephropathy. Full article

Background/Objectives: Light-chain cast nephropathy remains a major cause of morbidity in newly diagnosed multiple myeloma (MM), and rapidly reducing circulating free light chains (FLCs) is considered essential for renal recovery and survival. Methods: We conducted a single-center retrospective study evaluating high- and medium-cut-off hemodialysis (HCO/MCO HD) in newly diagnosed MM patients presenting with acute kidney injury (AKI). Consecutive patients treated at the University Medical Center Ljubljana between 1 January 2020 and 31 December 2023 were included. As per institutional protocols, HCO/MCO HD- and myeloma-directed therapy were initiated on the day of diagnosis. Primary endpoints were the magnitude of FLC reduction, renal and hematologic responses at three months, and overall survival. Results: The median FLC concentration at presentation was 9630 mg/L. FLC levels declined rapidly after HCO/MCO HD initiation, reaching 2400 mg/L by day 7, 1083 mg/L by day 14, and 370 mg/L by day 30. MCO HD achieved kapa FLC clearance comparable to HCO HD for the lambda isotype. Despite a median of only four HCO/MCO-HD sessions, the reduction in FLC was rapid, with an additional decline observed over time, while the median FLC concentration fell below 500 mg/L. At three months, the overall hematologic response was 87%, including very good partial response or better in 35% of patients, and renal response in 79% of patients. Achieving a ≥70% FLC reduction by day 7 was associated with superior outcomes, including markedly longer median overall survival (82.5 vs. 23.2 months). Conclusions: Our data show that HCO/MCO-HD treatment alongside anti-myeloma therapy achieves sustained FLC reduction in newly diagnosed MM with AKI and early FLC reduction is highlighted as a key determinant of survival. Full article

Background: Growth differentiation factor-15 (GDF-15) is a stress-responsive cytokine associated with inflammation, metabolic dysfunction, and cardiovascular disease. Its role as a biomarker of microvascular complications in type 2 diabetes (T2D) remains incompletely defined. Objective: To evaluate circulating GDF-15 levels and their association with microvascular complications in patients with T2D. Methods: This cross-sectional study included 160 participants divided into three groups: T2D (n = 93), obesity without carbohydrate disorders (n = 36), and healthy controls (n = 31). Microvascular complications (neuropathy, nephropathy, retinopathy) were assessed. Multivariable logistic regression and receiver operating characteristic (ROC) analysis were performed. Results: GDF-15 levels were significantly higher in T2D compared with non-diabetic individuals (267.5 ± 168.9 vs. 118.3 ± 55.5 pg/mL, p < 0.001). Higher GDF-15 was associated with neuropathy (odds ratio (OR) 1.985; 95% confidence interval (CI) 1.431–2.753) and nephropathy (OR 1.673; 95% CI 1.243–2.254) in unadjusted models. After adjustment, only nephropathy remained independently associated (OR 1.405; 95% CI 1.026–1.923). ROC analysis showed moderate discriminative ability for nephropathy (area under the curve (AUC) = 0.763). Conclusions: Circulating GDF-15 levels are significantly elevated in patients with T2D and are associated with microvascular complications, with the strongest independent association observed for diabetic nephropathy. These findings suggest that GDF-15 may represent a promising biomarker reflecting metabolic stress and risk of diabetic complications. Full article

Background: The endothelial activation and stress index (EASIX), derived from the serum lactate dehydrogenase, creatinine, and platelet counts, is a composite biomarker for endothelial dysfunction and systemic stress. It has been developed to predict clinical outcomes in hematologic malignancies. This study aimed to investigate the EASIX’s predictive role in contrast-induced nephropathy (CIN) and in-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Methods: A total of 1552 patients with STEMI who underwent primary PCI were retrospectively included. The patients were divided into two groups: CIN (+) and CIN (−). Baseline demographic, laboratory, clinic, and procedural variables were compared between the two groups. Logistic regression analysis was performed to identify independent predictors of CIN and in-hospital mortality, while receiver operating characteristic (ROC) curves were used to determine the optimal EASIX cut-off values. Results: CIN developed in 7.6% (n = 118) of the study population, and these patients had significantly increased EASIX scores. Those with CIN were older and exhibited higher rates of diabetes mellitus, chronic kidney disease (CKD), and decreased left ventricular ejection fraction (LVEF) (all p < 0.001). In multivariable analysis, age (OR 1.053), CKD (OR 1.338), reduced LVEF (OR 0.965), and EASIX (OR 2.467) independently predicted CIN. EASIX > 0.93 demonstrated strong discriminatory ability (AUC 0.785; sensitivity 72% and specificity 72%). EASIX also independently predicted in-hospital mortality (OR 3.592), with an optimal cut-off > 0.88 (AUC 0.774). Conclusions: By integrating markers of renal function, endothelial activation, and systemic stress, EASIX may serve as a useful and reliable indicator for predicting CIN development and in-hospital mortality in STEMI patients undergoing primary PCI. Full article

Objectives: To investigate the effects of Roxadustat and recombinant human erythropoietin (rHuEPO) on glycemic control and glycated hemoglobin (HbA1c) in non-dialysis type 2 diabetic kidney disease (DKD) patients with anemia. Methods: This retrospective study enrolled 449 patients, who were divided into three groups—the rHuEPO group (n = 252), the Roxadustat group (n = 102), and the switch group (n = 95)—in which patients were converted from rHuEPO to Roxadustat. All treatments lasted for more than three months. Changes in HbA1c and other indicators within groups as well as differences among groups were evaluated. Results: In the rHuEPO group, HbA1c levels decreased from 7.08 ± 1.19 to 6.41 ± 0.60 (p < 0.001), and they returned to baseline levels by 6–12 months (p > 0.05). In the Roxadustat group, HbA1c fluctuated but none of the differences reached statistical significance (p > 0.05). In the switch group, HbA1c decreased during rHuEPO treatment (p < 0.05) and returned to baseline after switching to Roxadustat (p > 0.05). No significant changes in blood glucose levels were observed in any group after treatment (p > 0.05). Multivariate linear regression analysis showed that changes in iron metabolism parameters, erythrocyte parameters, inflammatory markers, and glucose-lowering or lipid-lowering regimens had no significant effect on the change in HbA1c in the Roxadustat group (F = 0.834, p = 0.620), while the multivariate model of rHuEPO group also lacked statistical significance (F = 1.142, p = 0.170). After treatment, all three groups showed improvements in anemia, iron metabolism, renal function, inflammatory markers, and lipid profiles compared with baseline (p < 0.05). Additionally, further improvements in these parameters were observed after the transition from rHuEPO to Roxadustat (p < 0.05). Compared with rHuEPO group, the Roxadustat group exhibited significantly greater increases in hemoglobin, red blood cell count, total iron-binding capacity, transferrin, and serum iron (p < 0.05). Conclusions: In non-dialysis DKD patients with anemia, rHuEPO can significantly decrease HbA1c values, while Roxadustat does not. Roxadustat offers advantages over rHuEPO in terms of efficacy and assessment of glycemic control. Full article

Background: Diabetic nephropathy (DN), also referred to as diabetic kidney disease, represents one of the most common microvascular complications of type 2 diabetes mellitus (T2DM) and remains a leading cause of end-stage renal disease worldwide. Conventional clinical markers, including albuminuria and estimated glomerular filtration rate (eGFR), are widely used for diagnosis and staging but may have limited sensitivity for detecting early renal injury and predicting disease progression. In recent years, circulating microRNAs (miRNAs) have emerged as promising non-invasive biomarkers that reflect underlying molecular mechanisms of diabetic nephropathy and may complement traditional clinical indicators. Objective: The present study aimed to evaluate serum and urinary levels of hsa-miRNA-770-5p across different stages of diabetic nephropathy and to assess its potential diagnostic value in relation to established indicators of renal function. Methods: A total of 257 participants were included and divided into four groups: healthy controls, patients with T2DM without nephropathy, patients with T2DM and DN in CKD stages I–II, and patients with DN undergoing maintenance hemodialysis (MHD). Serum and urinary levels of miRNA-770-5p were measured using quantitative real-time polymerase chain reaction (qPCR) and analyzed using the 2^−ΔΔCt method. Statistical analyses included comparisons between groups using ANOVA, correlation analyses with renal function parameters such as eGFR and proteinuria/albuminuria, and receiver operating characteristic (ROC) curve analysis to evaluate diagnostic performance. Results: Serum levels of miRNA-770-5p were significantly elevated in patients with DN and in patients undergoing maintenance hemodialysis compared with healthy controls and patients with T2DM without nephropathy. In contrast, urinary levels of miRNA-770-5p were markedly reduced in patients with DN. Serum levels in patients with T2DM without nephropathy were slightly lower than those observed in healthy controls. Significant correlations were identified between miRNA-770-5p levels and renal function parameters, including eGFR and proteinuria/albuminuria, supporting the biological relevance of this microRNA in renal injury. ROC curve analysis demonstrated good discriminatory ability for differentiating DN from T2DM without nephropathy (serum AUC = 0.82; urine AUC = 0.79). Conclusions: hsa-miRNA-770-5p demonstrates distinct and opposite patterns in serum and urine that correlate with the severity of diabetic nephropathy. The complementary changes observed in circulating and urinary levels support the potential of miRNA-770-5p as a non-invasive biomarker that may complement conventional clinical markers and provide additional insight into the molecular mechanisms involved in the development and progression of diabetic nephropathy. Full article

Background: BK polyomavirus (BKPyV) infection is of notable concern in kidney transplant recipients, as it can cause BKPyV-associated nephropathy (BKPyVAN). Currently, there is no effective treatment for BKPyV infection, underscoring the need for preventive strategies. There is emerging evidence that donor-derived BKPyV plays a role in the development of BKPyV DNAemia. To further explore this hypothesis, we conducted a retrospective, multi-center cohort study to evaluate the risk of developing BKPyV DNAemia in kidney recipient pairs sharing the same donor. Methods: At the Leiden University Medical Center (LUMC), deceased donor kidney transplant recipients (2011–2021) were identified and classified according to the occurrence of BKPyV DNAemia within the first year post-transplantation. For each recipient, the contralateral kidney recipient from the same donor was identified through national transplant registries. Cox regression was used to assess whether BKPyV DNAemia in the LUMC recipient was associated with an increased risk of BKPyV DNAemia in the contralateral recipient. Results: Among 117 recipient pairs, BKPyV DNAemia was more frequent when the contralateral recipient was affected (28.8% [15/52]), compared with pairs in which the contralateral recipient remained unaffected (10.8% [7/65], p = 0.013). Multivariable Cox regression analysis confirmed this increased risk (HR 4.9, 95% CI: 1.8–13.6; p = 0.002). Conclusions: This study shows a significantly increased risk of BKPyV DNAemia in recipients of deceased donor kidneys when the contralateral kidney recipient develops BKPyV DNAemia. These findings highlight the influence of donor-derived factors in BKPyV transmission in kidney transplantation. Full article

Background and Objectives: Renal transplantation is the optimal treatment for end-stage renal disease, yet long-term allograft survival remains threatened by immune-mediated injury and chronic nephropathy. Conventional monitoring using serum creatinine and protocol biopsy suffers from limited sensitivity for early, subclinical injury. Liquid biopsy-based biomarkers offer a non-invasive alternative. Materials and Methods: We conducted a systematic narrative review of studies published between January 2010 and December 2024, identified through PubMed, Scopus, and Web of Science. Results: Extracellular vesicles carry injury-specific molecular cargo reflecting the biological state of tubular, glomerular, and endothelial cells; urinary EV CXCL9 protein and exosomal CD3ε mRNA have demonstrated AUC values of 0.81–0.88 for the detection of T-cell-mediated rejection. Donor-derived cell-free DNA quantifies global graft cell death; the FDA-cleared AlloSure assay achieves an AUC of 0.74 and NPV of 84% at the validated ≥1.0% threshold established in the DART trial. Donor-specific antibodies—particularly complement-fixing C1q-positive DSAs—confer markedly inferior 5-year graft survival compared with DSA-negative recipients (54% versus 93%). Multi-biomarker panels integrating all three modalities yield AUCs of 0.88–0.94 and NPVs of 91–95%. Conclusions: The integration of EV, ddcfDNA, and DSA monitoring into a unified surveillance framework offers a clinically meaningful advance over creatinine-based monitoring. Prospective randomized trials confirming improvement in long-term allograft survival will be the critical next step. Full article

Acute kidney injury (AKI) is a major complication of lupus nephritis and kidney transplantation, inevitably causing ischemia–reperfusion (I/R) injury. We previously confirmed that high-dose voclosporin induces drug nephropathy through aberrant peroxisome accumulation. The latter induces increased renal indole-3-aceticT acid (IAA) production due to the decreased expression of the IAA-degrading enzyme indolethylamine N-methyltransferase (INMT). Conversely, INMT overexpression prevents this nephropathy, suggesting that high-dose voclosporin could enable a novel therapeutic approach. This prompted us to test whether INMT overexpression with high-dose voclosporin could avert nephrotoxicity and protect against I/R injury. Inmt-overexpressing mice treated with high-dose voclosporin exhibited absence of peroxisomal abnormalities and resistance to I/R injury. RNA sequencing revealed the downregulation of tubular injury markers NGAL (Lcn2) and KIM-1 (Havcr1) concurrent with significant cytokine suppression. Mechanistic analysis revealed the robust induction of Regnase-2, an mRNA decay factor, which directly targeted stem–loop structures within the 3′ untranslated region of Lcn2 and Havcr1, thereby promoting their degradation in proximal tubular cells. Importantly, Regnase-2 knockdown mice showed Lcn2 upregulation, mitochondrial dysfunction, and peroxisomal abnormalities culminating in AKI, underscoring its renal protective effects. High-dose voclosporin under Inmt overexpression promoted Regnase-2-mediated mRNA decay to suppress tubular injury. This protective effect extended beyond I/R to rhabdomyolysis- and lipopolysaccharide-induced AKI to prevent nephropathy. Our findings demonstrate the potential transformative therapeutic approach of administering high-dose voclosporin to promote the prophylactic effect of Regnase-2 augmentation against AKI in both native and transplanted human kidneys. Full article

Objective: To assess the safety and diagnostic outcomes of image-guided, non-target renal biopsies performed in cancer patients. Materials and Methods: We retrospectively identified patients who underwent percutaneous, image-guided, non-target renal biopsy between January 2017 and December 2020 in our institution. We recorded demographics, clinical, procedural, and pathologic details. Univariate and multivariable logistic regression models were used to assess the association between various variables and diagnostic yield or development of adverse events. Results: A total of 318 biopsies were performed in 318 patients (178 male, 140 female) with a median BMI of 28.4 kg/m². Median systolic and diastolic BP at the time of biopsy were 133 mmHg and 74 mmHg, respectively. Tissue was obtained using 18-gauge needles (99%). Adverse events were documented in 57 cases (18%), with 12 cases (3.8%) classified as grade 2 or higher per SIR classification. Diagnosis was achieved in 310 biopsies (97%). The median number of the glomeruli identified by light microscopy, immunofluorescence, and electron microscopy was 25, 8, and 3, respectively, and a higher number of identified glomeruli was associated with diagnostic yield in univariate analysis, although not in multivariable analysis. Diastolic BP higher than 80 mmHg and CT imaging guidance were associated with the development of adverse events in univariate analysis, and CT use remained so in the final multivariable analysis (p < 0.001). No other variables, including pre-biopsy anticancer or immunotherapy medications, were associated with increased risk of adverse events. Conclusions: Percutaneous, image-guided, non-target renal biopsy in cancer patients using an 18-gauge needle has a high diagnostic yield and safety profile. Full article

Background: The primary aim of pancreas transplantation in type 1 diabetic kidney transplant recipients is to reduce mortality caused by complications of progressing cardiovascular diseases and to protect kidney graft from the recurrence of diabetic nephropathy. The aim of this study was to analyze the results of the first deceased donor kidney transplantation (KTx) in patients with end-stage kidney disease caused by long-lasting type 1 diabetes (T1D), performed alone or simultaneously with the pancreas (SPK), in a long-term follow-up period. Methods: Groups of 101 consecutive T1D patients after KTx and 93 patients after SPK performed in two transplant centers with a minimal follow-up period of 5 years were included in the analysis. Results: Recipient, kidney graft, and death-censored kidney graft survival in a follow-up period of up to 20 years did not differ between KTx and SPK groups. In the entire observation period, total diabetes duration was shorter in the SPK group compared to KTx (28.1 ± 7.4 vs. 34.9 ± 11.0 years), and myocardial infarction (21 vs. 7%), limb amputation (12 vs. 3%), and proteinuria (40 vs. 18%) were more common in the KTx group than in SPK. The estimated glomerular filtration rate was lower in KTx recipients compared to SPK. Recipient survival was affected by the recipient’s age and the duration of dialysis vintage, and kidney graft survival was affected by the duration of dialysis vintage, episodes of acute rejection, and high pretransplant sensitization in patients. Conclusions: Despite reduced diabetes duration, a decreased frequency of cardiovascular disease complications and better kidney graft function, a simultaneously transplanted pancreas does not improve patient or kidney graft survival in T1D kidney recipients. Full article