International braz j urol : official journal of the Brazilian Society of UrologyMarcos Tobias-Machado, Ricardo C Brianson, John Eder Gamarra Bravo, Alcedir Raiser, Eliney Faria
INTRODUCTION: Horseshoe kidney is an uncommon congenital fusion anomaly that can make renal tumor surgery especially challenging because of altered rotation, limited mobility, variable vascular supply, and an unpredictable collecting system (1-7). This video presents a robot-assisted partial nephrectomy for a high-complexity renal tumor in this setting. CASE PRESENTATION: A 33-year-old man, with ECOG 0 and no relevant comorbidities, was diagnosed with a 7.5-cm solid renal mass in the central posterior portion of the left moiety of a horseshoe kidney. The lesion had a RENAL score of 10p. Contrast-enhanced computed tomography and three-dimensional reconstruction were used to understand the relationship between the tumor, aberrant vessels, renal hilum, and collecting system, supporting the decision to attempt nephron-sparing surgery (5, 8). Surgical technique and results: The procedure was performed through a transperitoneal robotic approach with the patient in right lateral decubitus using the Da Vinci Si platform. Port placement followed a standard renal robotic configuration, with a paramedian supraumbilical camera port, three robotic working ports along a craniocaudal lateral axis, a caudal fourth-arm port, and two medial assistant ports for suction, exposure, and support during renorrhaphy. After exposure of the horseshoe kidney and left hilar dissection, two arterial branches and one renal vein were identified. Tumor excision was performed under vascular control, with 20 minutes of warm ischemia and no collecting system opening, followed by two-layer absorbable renorrhaphy with adjunctive hemostatic agents. The operative time was 150 minutes. No transfusion, conversion, drain placement, or relevant immediate complication occurred. The urinary catheter was removed after 24 hours, and the patient was discharged 72 hours after surgery. Pathology showed clear cell renal cell carcinoma, Fuhrman grade 3, pT2N0M0, with negative surgical margins. During 12 months of oncologic follow-up, renal function remained stable and semiannual imaging showed no evidence of recurrence. Contemporary video reports have also emphasized the feasibility of advanced robotic renal surgery and complex partial nephrectomy strategies in selected patients (9, 10). CONCLUSION: In a carefully selected patient, robot-assisted partial nephrectomy supported by three-dimensional planning was feasible for a complex renal tumor in a horseshoe kidney, with negative surgical margins, preserved renal function, and no recurrence during 12 months of follow-up.
Journal of renal careAmir Faravan, Mansour Ghafourifard, Akram Ghahramanian, Azad Rahmani, Hossein Namdar Areshtanab, Mostafa Ghasempour
BACKGROUND: Patient-to-patient peer support has been identified as a promising approach for the management of chronic kidney disease and has been associated with improved clinical and psychosocial outcomes. Multiple factors may influence the implementation and effectiveness of peer support programs across different healthcare settings. OBJECTIVES: This qualitative meta-synthesis aimed to identify the key facilitators influencing peer support among patients with chronic kidney disease. METHODS: A systematic review and qualitative meta-synthesis were conducted. The electronic databases Web of Science, PubMed and Scopus were systematically searched to identify relevant studies. Thomas and Harden's three-stage thematic synthesis approach was used to synthesize the findings of the included qualitative studies. The methodological quality of the selected studies was assessed using the Critical Appraisal Skills Programme (CASP) tool. RESULTS: A total of 15 studies were included in the meta-synthesis. The analysis identified three main themes related to facilitators of peer support: (a) Cultivating a supportive culture through the healthcare system, (b) Weaving deep connections and good rapport and (c) Engaged and motivated peer supporters and recipients. CONCLUSIONS: This qualitative meta-synthesis demonstrates that successful implementation of peer support programs for people living with CKD depends on the interaction of organizational support, meaningful peer relationships and active participant engagement. These findings provide a conceptual framework that can inform the design, integration and strengthening of peer support programs within routine kidney care.
BACKGROUND: Toxic acute renal failure (ARF) involves severe oxidative stress. The Nrf2 pathway is a key antioxidant defense mechanism. OBJECTIVES: To investigate whether naloxone combined with hemoperfusion alleviates oxidative injury via Nrf2 activation in toxic ARF. METHODS: In this single-center retrospective cohort study at Qiqihar Medical University Hospital, 67 patients were enrolled through medical record screening. The control group (n=39) received hemoperfusion alone; the observation group (n=28) received additional intravenous naloxone (0.8 mg bolus + 2.0 mg/24 h infusion for 7 days). Renal function and oxidative markers were assessed before treatment, at 24 h and day 7. Multivariate regression analysis was used to adjust for confounding factors. Separately, 30 rats were randomized into control, model and treatment groups (n=10 each). The treatment group received intraperitoneal naloxone (1.0 mg/kg) plus simulated hemoperfusion. RESULTS: After adjusting for baseline imbalances, combined therapy was independently associated with significant reductions in Scr and BUN in patients (adjusted β = -8.52, 95% CI: -12.37 to -4.67, P < 0.001) and with significant improvements in renal function and histopathology in rats. Combined therapy decreased tubular injury markers (β2-MG, KIM-1, NGAL, L-FABP) in rats. Mechanistically, it was associated with activation of the Nrf2/HO-1/NQO1 pathway, enhanced SOD activity and reduced MDA levels. Improvements were time-dependent (24 h to day 7). CONCLUSIONS: Naloxone combined with hemoperfusion activates the Nrf2 pathway, attenuates oxidative stress and improves renal function in toxic acute renal failure.
Pakistan journal of pharmaceutical sciencesJiebo Huang, Yuan Fu, Lin Chen, Yan Liang, Nie Wu
BACKGROUND: Secondary hyperparathyroidism (SHPT) is a common complication in uremic hemodialysis patients, associated with disordered calcium (Ca) and phosphorus (P) metabolism. The long-term efficacy of cinacalcet (Cin) versus calcitriol (Cal) in achieving composite control of parathyroid hormone (iPTH) and Ca × P product remains unclear. OBJECTIVES: To compare the 12-month efficacy and safety of Cin versus Cal in treating SHPT and to explore correlations between treatment outcomes and changes in iPTH, Ca and P. METHODS: This retrospective cohort study included SHPT patients on maintenance hemodialysis from June 2023 to June 2025. After propensity score matching (1:1), 75 patients were assigned to each Cin or Cal group. The primary endpoint was the composite response rate (iPTH ≤ 300 pg/mL and Ca × P < 55 mg²/dL²) at 12 months. Correlation analyses assessed associations between achieving the composite endpoint and changes in biochemical parameters. RESULTS: At 12 months, the composite response rate was significantly higher in the Cin group than in the Cal group (42.67% vs. 16.00%, P < 0.001). Cin produced greater reductions in iPTH and P and lower Ca and Ca × P levels (all P < 0.05). Achieving the composite endpoint correlated positively with greater reductions in iPTH (r = 0.453) and Ca (r = 0.463). ΔiPTH was moderately correlated with ΔP (r = 0.604, P < 0.001). Hypocalcemia was more frequent with Cin (16.00% vs. 4.00%, P=0.014), but no serious adverse events led to treatment discontinuation. CONCLUSION: Cin is more effective than Cal in helping uremic hemodialysis patients achieve composite control of iPTH and Ca × P. Therapeutic success correlates with reductions in iPTH and Ca and iPTH decline is closely linked to improved P levels, highlighting the importance of integrated management of SHPT.
BACKGROUND: Chronic kidney disease (CKD) associated osteoporosis leads to an increased risk of bone fracture in patients with CKD. Evidence on the efficacy and safety of anti-osteoporotic medications is limited for this group. This systematic review aimed to examine the efficacy and safety of anabolic parathyroid hormone (PTH) treatment in patients with CKD Stages 4-5D. METHODS: MEDLINE, EMBASE and ClinicalTrials.gov were searched systematically for randomized controlled trials (RCTs) investigating teriparatide, natpara, or abaloparatide in adult patients with CKD Stages 4-5D, including kidney transplant recipients. The primary outcome was the change in bone mineral density (BMD) during follow-up measured at the lumbar spine (LS), femoral neck (FN) and total hip (TH). The secondary outcomes included bone turnover markers, fractures, histomorphometric results from bone biopsies and adverse events (AEs). RESULTS: Two RCTs were included. A subgroup analysis of patients with CKD Stage 4 (n = 5) showed that teriparatide improved BMD at the LS and FN. Another trial (n = 61) in CKD Stage 5D showed significant BMD improvement at the TH compared to the control group. AEs were observed with higher frequency in the teriparatide-treated group. CONCLUSION: Treatment with teriparatide seems to improve BMD in patients with CKD Stages 4-5D, but evidence on efficacy and safety is limited. TRIAL REGISTRATION: PROSPERO: CRD42024527086.
Pakistan journal of pharmaceutical sciencesHan Yang, Xin Wang, Jin-Ying Chen, Bo Liu, Hao-Tian Qi, Xiao-Xia Kang, Wei-Chen Nie, Rui Chen, Tao Ding
BACKGROUND: DKD is a leading cause of end-stage renal disease with limited therapeutic options. OBJECTIVES: This study evaluated the effects of Xiaoshen Formula (XSF) on glucose/lipid metabolism and renal injury in a DKD model of mice and preliminarily explored its mechanisms involving the JAK/STAT pathway and PPARγ. METHODS: Diabetes and early-stage DKD were established in KK-Ay mice. Successfully modeled mice were randomly assigned to preventive or therapeutic administration groups; C57BL/6J mice served as blank controls. Biochemical parameters, kidney index and renal histopathology (hematoxylin-eosin staining and transmission electron microscopy) were assessed. Renal protein expression was determined by Western blot. RESULTS: Compared with blank controls, model mice exhibited increased body weight, polydipsia, polyphagia, disrupted glucose/lipid metabolism and renal injury, confirming successful modeling. Irbesartan reduced fasting blood glucose, kidney weight, organ index and renal injury. XSF-H significantly improved glucose/lipid metabolism, reduced food/water intake and kidney weight/organ index and alleviated renal injury, with overall efficacy ranking: high-dose > therapeutic > low-dose. Western blot showed lower levels of JAK2, p-STAT-6, TGF-β1, and FN, and higher levels of PPARγ in the Irbesartan and XSF groups compared with the model group. CONCLUSION: This study provides experimental evidence that XSF may delay early DKD progression. XSF ameliorates fasting blood glucose, stabilizes body weight, improves glucose/lipid metabolism and attenuates renal injury and no obvious hepatorenal toxicity under limited conditions. Findings suggest that XSF delays DKD progression may be associated with modulation of the JAK/STAT signaling pathway and inhibition of renal fibrosis.
Renal failureYu Liu, Xinni Zhang, Jie Song, Tingwei Cheng, Lan-Gen Zhuang, Xiao-Yan Pei, Guo-Xi Jin
Diabetic kidney disease (DKD) progression is driven by residual inflammation, potentially exacerbated by volatile organic compounds (VOCs). However, the impact of xylene exposure on the DKD immune microenvironment remains unclear. We evaluated the association between urinary VOC metabolites and DKD prevalence using NHANES data. Network toxicology and bulk transcriptomics (GSE142025) were integrated to identify core targets and profile immune infiltration. Single-cell RNA sequencing (GSE209781) validated macrophage heterogeneity and hub gene dynamics, and molecular docking assessed xylene-receptor binding affinities. Elevated urinary xylene metabolite (DPMA) correlated with increased DKD odds (OR = 4.03, 95% CI: 1.80-9.00). Multi-omics identified ITGAM, CSF1R, and CTSS as primary hub genes enriched in immune pathways. Both bulk and single-cell RNA sequencing analyses revealed that DKD tissues exhibited M2-like macrophage enrichment and an expansion of fibrotic SPP1+ subsets. This altered microenvironment positively correlated with hub gene upregulation along the macrophage developmental trajectory. Molecular docking suggested potential binding between xylene isomers and these receptors (binding free energies: -4.7 to -5.9 kcal/mol). Environmental xylene exposure is independently associated with higher DKD odds. These findings generate the hypothesis that xylene may interact with specific macrophage receptors (ITGAM, CSF1R, CTSS), potentially promoting M2-like macrophage polarization and fibrotic remodeling. This putative environmental-immunological axis warrants further experimental validation.
Renal failureLiyu Lin, Yiqi Su, Bing Yu, Ziyan Shen, Ying Huang, Caifeng Li, Jie Teng
IgA nephropathy (IgAN) has a heterogeneous clinical course. We retrospectively studied 180 patients with biopsy-proven IgAN and at least 3 years of clinical follow-up. Patient-specific eGFR slopes were estimated from available measurements at biopsy and the 6-, 12-, 18-, 24-, 30-, and 36-month follow-up points. We built a post hoc multivariable model guided by clinical relevance. Oxford T was treated as categorical, with T0 as reference. The median eGFR slope was -1.12 mL/min/1.73 m2/year, and 35 patients (19.4%) met the operational rapid-progression threshold of < -5 mL/min/1.73 m2/year. In the primary model, higher ln(UACR + 1) predicted a steeper decline (β= -0.612, 95%CI -1.073 to -0.150). T2 lesions predicted a 3.87 mL/min/1.73 m2/year faster loss than T0 (β= -3.870, 95%CI -7.087 to -0.654), whereas T1 did not differ from T0. The model R2 was 0.159 (adjusted R2=0.130). UACR and T2 estimates remained negative under HC3 inference and after excluding influential observations, although T2 was less stable in some restricted analyses. Baseline albuminuria was the most consistent adverse marker of eGFR slope. T2 lesions were linked to faster decline as well, but this estimate derived from only 16 patients (8.9%) and lost statistical significance when analysis was restricted to ≥5 measurements, making the finding tentative and strictly hypothesis-generating.
BACKGROUND: Diagnostic performance varies across glomerular disease (GD) subtypes, and whether artificial intelligence (AI) outperforms pathologists with different experience levels remains uncertain. OBJECTIVE: To evaluate pathology-based AI models for GD classification and compare their performance with pathologists. METHODS: PubMed, Embase, Web of Science, and Cochrane Library were searched through 15 July 2026. Studies using pathology images and pathology diagnosis as the reference standard were included. Random-effects models pooled sensitivity, precision, accuracy, F1 score and area under the curve (AUC). RESULTS: Fifteen studies comprising 39,536 validation sample units, not necessarily unique patients, were included. For subtypes with at least 10 validation datasets, AI achieved high performance for membranous nephropathy (MN; sensitivity 0.96, precision 0.94, accuracy 0.96, F1 score 0.95, AUC 0.98), IgA nephropathy (IgAN; sensitivity 0.92, precision 0.91, accuracy 0.94, F1 score 0.90, AUC 0.96), and minimal change disease (MCD; sensitivity 0.92, precision 0.87, accuracy 0.96, F1 score 0.89, AUC 1.00). AI also showed higher accuracy than senior pathologists for IgAN, MN, and MCD; however, comparator evidence was sparse and should be interpreted cautiously. Most included studies were retrospective, and substantial heterogeneity was observed across datasets, imaging modalities, model architectures, and validation strategies. CONCLUSIONS: Pathology-based AI shows strong potential for GD classification, but current head-to-head evidence is insufficient to establish superiority over pathologists, particularly senior pathologists. Prospective multicenter studies integrating multimodal clinical data and standardized external validation are needed.
Renal failureLei Chen, Ye Zhu, Shiying Xie, Xiangshen Liu, Xia Gao, Yongjie Jin, Shunliang Yang, Dong Wang
Diabetic kidney disease (DKD) is a major cause of chronic kidney diseases. Panoptosis has emerged as a key contributor to renal injury. However, the specific panoptosis-related genes (PRGs) that drive diabetic tubular injury remain unknown. TNFSF10, a known regulator of apoptosis and inflammation, has been linked to podocyte injury in DKD, but its role in diabetic tubular injury remains unknown. To address this, we integrated weighted gene co-expression network analysis, machine learning algorithms, and clinical data from the Nephroseq database to identify PRGs associated with DKD. The biological function of the identified hub gene was further characterized by integrating single-cell and single-nucleus RNA sequencing data with analytical frameworks for cellular communication, trajectory inference, and regulatory network. In this study, we identified TNFSF10 as a conserved and robust hub PRG for DKD. TNFSF10 expression was significantly upregulated in DKD kidneys and inversely correlated with glomerular filtration rate. TNFSF10high kidneys exhibited elevated fibrosis and inflammation scores. scRNA/snRNA analysis revealed its predominant expression in injured proximal tubular cells. Importantly, TNFSF10+ proximal tubular cells showed transcriptomic signatures consistent with panoptosis activation and inflammatory signaling, along with enhanced ligand-receptor interactions with fibroblasts and immune cells. Consistently, TNFSF10 treatment induced cell death and increased the expression of multiple inflammatory genes in vitro. Collectively, our results suggest that TNFSF10 is associated with tubular injury and kidney fibroinflammation in DKD. These exploratory findings suggest it may represent a promising candidate for DKD, and further in vivo functional validation is required to confirm its diagnostic and therapeutic potential.
BACKGROUND: Older adults represent a rapidly growing segment of the hemodialysis (HD) patient population. However, the specific clinical variations and dialysis management strategies employed for geriatric patients in Thailand remain poorly characterized. METHODS: We analyzed baseline data from 839 hemodialysis patients enrolled in the Thai-HDcohort, a prospective multicenter study across 13 clinical sites in Thailand. Patients were stratified into a geriatric group (≥ 65 years of age, n = 412) and a younger control cohort (< 65 years of age, n = 427). Demographics, vascular access modalities, baseline laboratory markers, pharmacotherapy, and dialysis prescriptions were compared between the two groups. RESULTS: Geriatric patients were more frequently treated in hospital-based facilities (75.0% vs. 67.4%, p = .002). The geriatric group exhibited lower body weight (57.7 vs. 63.0 kg, p < .001) and lower serum albumin (hypoalbuminemia prevalence: 11.6% vs. 5.1%, p = .001). Regarding practice patterns, geriatric patients relied more heavily on tunneled cuffed catheters at enrollment (38.1% vs. 27.7%, p = .005) and were likely to initiate HD using a catheter (41.0% vs. 27.1%, p < .001). Geriatric prescriptions also favored a higher utilization of a 3.0 mmol/L dialysate potassium bath (40.0% vs. 23.7%, p < .001), and a higher dialysate calcium bath of 3.0 mmol/L (19.9% vs. 12.9%, p = .011). CONCLUSIONS: In this cross-sectional study, geriatric hemodialysis patients showed distinct variations in prescriptions and vascular access. Longitudinal follow- up is essential to determine whether these conservative, individualized strategies improve clinical and survival outcomes.
Peritoneal dialysis (PD)-associated peritonitis is a leading cause of technique failure. We aimed to develop and internally validate a Cox regression‑based nomogram for predicting peritonitis‑free survival in incident PD patients. This single-center retrospective cohort study included 372 patients who underwent peritoneal dialysis between June 2018 and December 2024, with follow-up through December 2025. LASSO‑Cox regression was used to select predictors from 23 candidate variables. A nomogram was constructed to predict 6‑, 12‑, and 24‑month peritonitis‑free survival. Model performance was assessed by concordance index (C‑index), time‑dependent ROC, calibration curves, and decision curve analysis. Over a median follow‑up of 26.3 months, 92 (35.4%) and 34 (30.4%) peritonitis events occurred in the training and validation cohorts, respectively. Nine predictors (education, start age, BMI, hemoglobin, potassium, sodium, albumin, calcium, phosphorus) were retained. Independent predictors were lower education (≤9 vs >9 years: HR 1.93, 95% CI 1.03-3.64), lower hemoglobin (HR 0.99, 0.97-1.00), lower albumin (HR 0.92, 0.87-0.97), and lower phosphorus (HR 0.53, 0.29-0.99). The C‑index was 0.707 (95% CI 0.650-0.765). Time‑dependent ROCs in the training cohort were 75.8%, 77.5%, and 69.7% at 6, 12, and 24 months; in the validation cohort, they were 77.7%, 63.8%, and 58.4%, respectively. Calibration was satisfactory at 6 and 12 months (Brier scores 6.0%-11.1%), with wider clinical net benefit at 12-24 months. This nomogram using nine routinely available variables demonstrated moderate discrimination and satisfactory calibration for predicting peritonitis‑free survival in PD patients. While promising, the model requires external validation in larger, multicenter cohorts to confirm its generalizability before routine clinical use.
Renal failureYibo Zhuang, Chenlu Fu, Zheng Guo, Yan Xu, Jun Zhou, Huiping Ni, Aihua Zhang
This study demonstrates that gamma-aminobutyric acid (GABA) ameliorates diabetic kidney disease (DKD) by modulating macrophage-driven inflammation and podocyte injury through the JAML/FPR2 signaling axis. In streptozotocin (STZ)-induced DKD mice, GABA administration significantly improved renal function by reducing serum creatinine, urea nitrogen, 24-hour urine protein, attenuated glomerular hypertrophy/mesangial expansion, and suppressed pro-inflammatory cytokine production (TNF-α, IL-1β, iNOS) in renal tissue and serum. GABA inhibited glomerular macrophage infiltration (CD68+ cells) and M1 polarization while mitigating renal apoptosis and podocyte injury by restoring nephrin and podocin. In a high glucose (HG)-stimulated macrophage-podocyte co-culture model, GABA reduced HG-induced podocyte apoptosis in a macrophage ratio-dependent manner by reversing M1 polarization and inflammatory cytokine overproduction. Mechanistically, GABA normalized DKD-elevated JAML expression in renal tissues and podocytes, while JAML overexpression abolished GABA's renoprotective effects by reactivating inflammation, macrophage recruitment, and podocyte apoptosis. Co-IP confirmed JAML interacted with receptor formyl peptide receptor 2 (FPR2), which mediated DKD-driven macrophage infiltration, as FPR2 knockdown abrogated JAML-induced CD68+ cell accumulation. Collectively, GABA alleviated DKD progression by disrupting the JAML/FPR2 axis to suppress macrophage-mediated inflammation and podocyte injury, highlighting its therapeutic potential for diabetic kidney disease.
Roxadustat, a hypoxia-inducible factor prolyl hydroxylase (HIF-PH) inhibitor, is effective for treating renal anemia, with efficacy noninferior to erythropoiesis-stimulating agents. However, data on its adverse effects remain scarce. In medical practice, roxadustat administration reportedly leads to central hypothyroidism; however, the frequency of its occurrence remains unclear. We investigated thyroid function in patients undergoing dialysis who received roxadustat at Saiseikai Yokohamashi Tobu Hospital, with particular focus on the timing of the decrease in serum thyroid-stimulating hormone (TSH) levels after roxadustat initiation and the subsequent course of thyroid function. HIF-PH inhibitors were administered to 43 chronic kidney disease patients including dialysis. After 2 weeks of roxadustat administration, we extracted the data of 16 hemodialysis patients who exhibited absence of residual urine and were able to undergo blood tests. All patients revealed decreased serum TSH levels. In contrast, changes in serum free triiodothyronine and free thyroxine levels were minor. None of the patients reported fatigue, bradycardia, or constipation, which are common symptoms of hypothyroidism. Our findings revealed that roxadustat may cause TSH reduction after 2 weeks of administration, though some patients showed subclinical hypothyroidism with high TSH levels. In a few cases, TSH levels decreased to one-tenth of the normal values. Despite these rapid changes, none of the patients exhibited clinical symptoms. Hence, regular thyroid hormone level monitoring is necessary with roxadustat administration, regardless of patients' history of thyroid function.
Pakistan journal of pharmaceutical sciencesDaoman Xia, Jiana Zang
BACKGROUND: Adolescent diabetic kidney disease (DKD) represents an early-onset microvascular complication characterized by prolonged metabolic exposure and accelerated renal decline. Elevated serum creatinine and blood urea nitrogen (BUN) are key biochemical indicators of impaired renal function. OBJECTIVES: This scoping review aims to systematically map and evaluate pharmacological strategies for slowing the rise of creatinine and BUN in adolescents (aged 10-19 years) with DKD, with emphasis on renoprotective mechanisms, therapeutic sequencing and the potential applicability of these therapies to adolescent populations. METHODS: A scoping review was conducted in accordance with PRISMA-ScR guidelines. A comprehensive literature search was performed using PubMed, Scopus and Google Scholar for studies published between 2020 and 2025. Eligible studies included clinical trials, observational studies, clinical guidelines and relevant reviews focusing on pharmacological interventions in adolescents (10-19 years) with diabetic kidney disease. Study selection was based on predefined inclusion and exclusion criteria. RESULTS: A total of 35 studies and guideline-based references were included in the final synthesis. Intensive glycemic control (insulin for type 1 diabetes; metformin ± insulin for type 2 diabetes) was associated with improved metabolic control and favorable renal outcomes. Renin-angiotensin system blockers consistently reduced albuminuria and induced an acute hemodynamic reduction but stabilized the long-term decline in estimated glomerular filtration rate (eGFR). Sodium-glucose cotransporter-2 (SGLT2) inhibitors demonstrated additional renoprotective effects in type 2 diabetes; risks (euglycemic DKA) limit use in type 1. In adult studies, finerenone attenuated inflammatory and fibrotic pathways; no adolescent data exist. Glucagon-like peptide-1 receptor agonists improved metabolic control and reduced obesity-associated renal stress. However, pediatric-specific evidence remains limited, and much of the available evidence is derived from adult studies. CONCLUSION: Adult data suggest potential benefits of early multi-target pharmacotherapy, but adolescent-specific evidence is needed to confirm a critical role in delaying renal deterioration. Whether integration of conventional and novel agents improves long-term renal outcomes in adolescents requires direct investigation. Further pediatric-focused research is required to establish safety, efficacy and optimal therapeutic strategies.
Renal failureJoel Shah, William Wells-Gatnik, Biff F Palmer, Deborah J Clegg
IgA nephropathy (IgAN) is the most common glomerulonephritis worldwide, characterized by a 4-hit pathogenesis primarily driven by mucosal immune dysregulation in the gut-associated lymphoid tissue (GALT). However, the specific environmental triggers initiating this cascade remain elusive. We propose a novel hypothesis that chronic exposure to ubiquitous micro- and nano-plastics (MNPs) serves as a primary environmental catalyst for IgAN. Through a proposed 5-step cascade, we outline how ingested MNPs directly degrade intestinal tight junctions, precipitating a 'leaky gut' that permits the synergistic influx of plastics and commensal bacterial antigens into the GALT. Acting as a 'Trojan horse,' MNP-corona complexes evade immune detection but trigger chronic inflammation and B-cell dysregulation upon internalization by phagocytes. This persistent immune stimulation drives the aberrant production of galactose-deficient IgA1. Furthermore, we hypothesize that circulating MNPs co-deposit in the renal mesangium alongside immune complexes, acting as a dual generator of both systemic immune complexes and direct structural kidney injury. This potential gene-environment interaction is supported by the intersecting high prevalence of environmental MNPs and IgAN in Asia. Finally, we delineate future in vivo, observational, and epidemiological investigations required to establish this pathophysiological link.
INTRODUCTION: Long-term renal function is an important follow-up after radical nephrectomy for renal carcinoma. Predictive models can help identify patients at risk for chronic kidney disease (CKD) progression and enable early intervention. METHODS: We retrospectively analyzed 649 patients who underwent radical nephrectomy at eight medical centers. The primary cohort from the Affiliated Hospital of Qingdao University comprised 329 patients, randomly divided into training sets (n = 229) and internal validation sets (n = 100) at a 7:3 ratio. An additional 320 patients from seven other centers constituted a multicenter external evaluation cohort. Five machine learning models were developed, including Logistic Regression (LR), Support Vector Machine (SVM), Random Forest (RF), Extreme Gradient Boosting (XGBoost), and Light Gradient Boosting Machine (LightGBM). Model performance was evaluated using the area under the receiver operating characteristic curve (AUC), confusion matrices, and calibration curves. RESULTS: 224 (34.51%) patients experienced postoperative CKD stage progression within three years. LightGBM achieved the highest discriminative performance among the five evaluated algorithms, with an AUC of 0.7508 (95% CI, 0.6399-0.8617) and an accuracy of 0.7200 in the internal validation set, and an AUC of 0.7549 (95% CI, 0.7022-0.8076) and an accuracy of 0.6813 in the external evaluation set. SHAP analysis identified preoperative eGFR, tumor size, post-to-preoperative serum creatinine ratio, preoperative serum creatinine, and age as the five most influential predictors. CONCLUSIONS: We developed and externally evaluated machine-learning models for predicting CKD stage progression after radical nephrectomy. Long-term decline in renal function is an important complication that requires urologists' attention and early prevention during follow-up.
Renal failureXiaorong Wang, Yongmei Hao, Huaying Pei, Lin Yang, Zhe Yan, Lin Mu, Xian Chen, Xi Zhao, Lingling Xing
AIMS: Renal vascular lesions are common in diabetic nephropathy (DN), but their association with echocardiographic indices related to diastolic function remains unclear. This study investigated the relationship between renal vascular lesion severity and echocardiographic indices in biopsy-confirmed DN. METHODS: This biopsy-based cross-sectional study included 360 patients with biopsy-confirmed DN and available echocardiographic data. Renal vascular lesions were evaluated using a composite score of arteriolar hyalinosis and arteriosclerosis, and patients were categorized into three severity groups (scores 0-1, 2-3, and 4). Echocardiographic indices included E/e', e', and left atrial diameter (LA). Multivariable linear regression models were used to assess the associations between renal vascular lesion severity and echocardiographic parameters. Sensitivity analyses were performed using continuous vascular lesion scores and additional covariate adjustment. RESULTS: Among 360 patients, 53, 253, and 54 were classified into the 0-1, 2-3, and 4 score groups, respectively. Compared with the 0-1 group, moderate and severe vascular lesions were associated with higher E/e' (β = 1.814 and 2.910, respectively) and larger LA (β = 1.722 and 2.917, respectively) after multivariable adjustment. Continuous score analysis showed that each 1-point increase in vascular lesion score was associated with higher E/e', larger LA, and lower e'. Associations with E/e' and LA were generally consistent across sensitivity analyses, whereas the association with e' was less stable. CONCLUSIONS: In patients with biopsy-confirmed DN, greater renal vascular lesion severity was associated with higher E/e' and larger LA, highlighting a potential link between renal vascular pathology and echocardiographic indices related to diastolic function.
Renal failureLijun Sun, Mengna Ruan, Ziyu Liu, Xiaojing Tang, Lin Li, Senyan Liu
Automated peritoneal dialysis (APD) is a widely used dialysis modality for patients with end-stage kidney disease (ESKD). However, controversy remains regarding the rate of residual kidney function (RKF) decline between patients treated with APD and continuous ambulatory peritoneal dialysis (CAPD). This study aimed to investigate the effect of peritoneal dialysis modality on the rate of RKF decline in Chinese patients with new-onset ESKD. We conducted a single-center retrospective study to explore the association between PD modalities and RKF decline. A total of 53 patients with new-onset ESKD were enrolled. Of these, 19 patients started with APD and 34 with CAPD. The rates of RKF decline were compared between two groups. Multivariate linear regression was performed to identify risk factors for rapid decline of RKF. Baseline RKF and urine output were comparable between the APD and CAPD groups. At 6 months after PD initiation, RKF was 1.9 ± 1.6 mL/min/1.73 m2 in the APD group, significantly lower than 3.0 ± 1.7 mL/min/1.73 m2 in the CAPD group (p = 0.043). The APD group had a significantly faster mean rate of RKF decline (-6.6 ± 2.5 vs. -4.3 ± 2.3 mL/min/1.73 m2/year, p = 0.002). In multivariate linear regression adjusted for established risk factors, APD use (vs. CAPD) (β = 0.93; p = 0.004) and baseline RKF (β = 0.38; p < 0.001) were significantly associated with accelerated RKF decline. Our findings indicate that Chinese patients initiating dialysis with APD experience faster RKF decline within the first 6 months compared with those starting PD with CAPD. Furthermore, high baseline RKF is associated with rapid RKF decline.
Lactate is frequently measured in patients with acute kidney injury (AKI), but its interpretation remains challenging because circulating lactate reflects systemic metabolic stress rather than kidney injury. Although elevated lactate levels are associated with adverse outcomes in critically ill patients with AKI, its biological and clinical significance varies according to disease context, timing, and the clinical question being addressed. This structured expert narrative review integrates mechanistic insights and clinical evidence to establish a context-dependent framework for interpreting lactate in AKI. We summarize the role of the kidney in lactate metabolism and discuss how impaired renal function, altered perfusion, mitochondrial dysfunction, and immune-metabolic remodeling contribute to lactate accumulation. We further evaluate clinical evidence regarding lactate in AKI risk assessment, severity evaluation, organ-support requirement, and mortality prediction, while emphasizing limitations related to confounding factors and clinical heterogeneity. Emerging clinical contexts, including extracorporeal membrane oxygenation-supported patients, are also considered. Overall, this framework supports a more precise interpretation of lactate as a context-dependent risk marker and metabolic signal rather than a kidney-specific biomarker.
Acute kidney injury (AKI) after liver transplantation (LT) is a frequent complication associated with adverse outcomes, yet practical early postoperative prediction tools remain limited. This retrospective study developed and internally validated an interpretable model for AKI after LT using perioperative variables available by the time of the first urgent postoperative blood test, generally obtained within 1 h after surgery. Adult LT recipients treated from June 2023 to January 2026 were screened. AKI was defined according to Kidney Disease: Improving Global Outcomes criteria. Among 146 screened recipients, 127 were included and randomly divided into training and validation cohorts at a 3:1 ratio. Least absolute shrinkage and selection operator regression selected estimated glomerular filtration rate calculated using the CKD-EPI equation, anhepatic phase time, postoperative natural logarithm-transformed D-dimer, and postoperative alanine aminotransferase. Multivariable logistic regression showed that lower estimated glomerular filtration rate and longer anhepatic phase time were independently associated with AKI. The nomogram achieved area under the receiver operating characteristic curve values of 0.861 in the training cohort and 0.761 in the validation cohort. Five-fold cross-validation and bootstrap internal validation were performed to assess model stability and optimism. Among five evaluated models, support vector machine showed the numerically highest validation AUC of 0.846. Shapley additive explanations identified estimated glomerular filtration rate as the dominant predictor. This early postoperative model may help identify high-risk recipients for intensified renal monitoring and individualized management. External multicenter validation is required before routine clinical implementation.
Ultrasound quarterlyLaura E Garton, Melanie P Caserta, Shweta Bhatt, Mary J Clingan
Renal cell carcinoma (RCC) comprises approximately 90% of malignancy in the kidney. Early stage RCC is often asymptomatic. The majority of RCC are incidentally found on imaging ordered for unrelated medical indications. When diagnosed at an early stage, the survival or even cure rate is high. With more progressive stages, the outcome is less favorable. Tumor-induced angiogenesis affects blood flow in tumors such that patterns of perfusion can be utilized for diagnosis. Contrast-enhanced ultrasound (CEUS) takes advantage of the vascular architecture and provides a real-time assessment of vascularity, helping differentiate between solid and cystic masses. CEUS is a favorable tool for evaluation of indeterminate renal lesions due to its specificity for solid enhancing components, safety profile, and relatively low cost when compared with other imaging modalities including computed tomography (CT) or magnetic resonance imaging (MRI). This case highlights the sensitivity of contrast-enhanced ultrasound for detecting blood flow in a patient with papillary RCC.
Obesity is a major independent risk factor for chronic kidney disease (CKD). Population-level evidence linking immune dysregulation to CKD in obese individuals remains limited. In this cross-sectional study, we analyzed data from community-dwelling adults aged 65-85 years in Shanghai, China. The immune-inflammatory markers were compared between obese and non-obese groups. The associations between routinely measured immune-inflammatory markers (neutrophils, lymphocytes, platelet-to-lymphocyte ratio [PLR]) and CKD prevalence were evaluated using multivariable logistic regression, restricted cubic splines (RCSs). Obese individuals had higher neutrophil, monocyte, and lymphocyte counts and lower PLR than the non-obese group. Among participants with obese, elevated neutrophil and lymphocyte counts were independently associated with greater odds of CKD (adjusted odds ratio [aOR] for highest tertile: 1.42, 95% confidence interval [CI] 1.07-1.90; and 1.53, 95% CI 1.16-2.01, respectively), whereas higher PLR was associated with reduced odds (aOR 0.70, 95% CI 0.53-0.92). Adjusted RCS plots revealed nonlinear associations. Elevated neutrophils and monocytes together with lower PLR emerged as key immunoinflammatory markers that might be associated with obesity-associated CKD. These findings highlight the clinical potential of routine immune-inflammatory biomarkers for early and precise risk stratification of obesity-related CKD.
Renal failureSiyuan Gong, Yonghong Xiong, Wenyuan Li, Yan Leng, Xinqi Deng, Bihan Wang, Baichuan Yang, Yuhang Yang, Wei Li
Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury and is associated with mitochondrial dysfunction, excessive reactive oxygen species (ROS) production, and tubular cell apoptosis. Sigma-1 receptor (Sigma1R), an intracellular chaperone, helps maintain mitochondrial homeostasis and cell survival. Here, Sigma1R expression was significantly downregulated in renal IRI. Fluvoxamine treatment ameliorated renal dysfunction and reduced apoptosis in vivo, whereas Sigma1R overexpression preserved mitochondrial membrane potential and attenuated ROS accumulation in HK-2 cells subjected to hypoxia/reoxygenation. The findings support the functional involvement of Rac1 in Sigma1R-mediated enhancement of PINK1/Parkin-mediated mitophagy, which may facilitate the clearance of damaged mitochondria and restore mitochondrial quality control. Overall, Rac1 is involved in Sigma1R-mediated mitophagy and mitochondrial protection, highlighting Sigma1R as a potential therapeutic target for renal IRI.
Renal failureWei-Bo Le, Jing-Song Shi, Feng Liu, Zhen Cheng
BACKGROUND: Although cigarette smoking is an exposure associated with chronic kidney disease, its role in the progression of IgA nephropathy (IgAN) remains not well defined. We investigated the association between smoking exposure and adverse kidney outcomes in a large Chinese cohort of patients with IgAN. METHODS: This retrospective cohort study included 9,560 adults with biopsy-proven IgAN at Jinling Hospital between 2007 and 2016. Cox proportional hazards models were used to assess kidney failure and a 50% decline in estimated glomerular filtration rate (eGFR). Because only 24 women reported smoking, the primary analysis was restricted to men and adjusted for age (using a restricted cubic spline), eGFR, log-transformed proteinuria, hypertension, diabetes, uric acid, and albumin. RESULTS: Among 9,560 patients, 1,441 (15.1%) were current or former smokers, of whom 1,417 were men. In the 4,494 men, unadjusted hazard ratios (HRs) were 1.31 (95% confidence interval [CI], 1.13-1.51) for kidney failure and 1.26 (95% CI, 1.12-1.42) for a 50% decline in eGFR (both p < 0.001). After adjustment (n = 4,487), the corresponding HRs were 1.27 (95% CI, 1.09-1.48; p = 0.002) and 1.20 (95% CI, 1.07-1.36; p = 0.003). Estimates from the sex-adjusted full-cohort analysis were similar. No significant heterogeneity was observed across prespecified male subgroups defined by age, hypertension, eGFR, or proteinuria (all p for interaction > 0.05). CONCLUSIONS: Baseline current or former smoking was associated with adverse kidney outcomes among men with IgAN. Interpretation is limited by potential residual confounding and the small number of women with smoking exposure.
European journal of pharmacologyLan Luo, Jia Liu, Na Zhang, Wen Meng, Yu Liu
BACKGROUND: Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) with significant clinical impact. Gentiopicroside (GPS), a natural secoiridoid glycoside isolated from traditional medicinal plants, has been reported to exert anti-inflammatory and cytoprotective activities, yet its potential role in renal IRI has not been fully explored. METHODS: Mice underwent bilateral renal ischemia with oral GPS pretreatment. Renal function, histological injury, apoptosis, and inflammation were evaluated. Primary mouse renal tubular epithelial cells (mRTECs) and BUMPT cells were subjected to oxygen-glucose deprivation/reperfusion (OGD/R). Network pharmacology, molecular docking and cellular thermal shift assay (CETSA) were performed to identify potential GPS-associated pathways and targets. JNK signaling was further examined using JNK1-specific siRNA and anisomycin. RESULTS: GPS improved renal function, reduced tubular injury, apoptosis, and inflammation in IRI mice, and increased viability while reducing apoptosis in OGD/R-treated mRTECs and BUMPT cells. Network pharmacology highlighted MAPK signaling, and docking identified MAPK8 (JNK1) as a candidate GPS target. CETSA showed increased JNK1 thermal stability after GPS treatment. JNK1 silencing phenocopied the anti-apoptotic effects of GPS, with no significant additional reduction in JNK phosphorylation or caspase-3 cleavage after GPS treatment. Conversely, anisomycin partially reversed GPS-mediated protection. GPS also attenuated oxidative stress and modulated ferroptosis- and autophagy-associated molecular changes during OGD/R injury. CONCLUSION: GPS protects against renal IRI and OGD/R-induced tubular injury, with JNK/MAPK signaling serving as an important, but not exclusive, mediator of its anti-apoptotic effects. These findings support further investigation of oral GPS as a potential therapy for AKI.
Hemorrhagic fever with renal syndrome (HFRS) is frequently complicated by acute kidney injury (AKI). Although most patients recover from AKI with supportive care, some progress to chronic kidney disease (CKD). The incidence and determinants of CKD progression in patients with HFRS-AKI remain uncertain. Here, 99 patients with HFRS-AKI treated at Jinling Hospital were analyzed retrospectively to determine the rate of CKD progression and identify associated risk factors. Patients were divided into complete recovery (CR) and incomplete recovery (ICR) groups according to CKD progression. Baseline clinical and laboratory data were collected and analyzed. Overall, 27.3% of patients with HFRS-AKI progressed to CKD despite receiving supportive care. Facial flushing was more frequent in the ICR group than in the CR group (40.7% vs. 18.1%, p = 0.033). Multivariate analysis revealed that treatment with Cordyceps sinensis preparations during the AKI phase was an independent protective factor against incomplete kidney recovery (OR: 0.323, 95% CI: 0.114-0.916, p = 0.034). Inverse probability weighting analysis further demonstrated that the use of Cordyceps sinensis preparations was inversely associated with incomplete kidney recovery (β: -1.184, 95% CI: -2.224 - -0.144, p = 0.026). Survival analysis confirmed that Cordyceps sinensis preparation therapy was associated with improved kidney outcomes (log-rank test, p = 0.004). This study provides the first clinical evidence that adjunctive therapy with Cordyceps sinensis preparations during HFRS-AKI is associated with improved kidney outcomes, suggesting that Cordyceps sinensis preparations represents a promising therapeutic approach for viral-induced AKI.
BACKGROUND: Sepsis-associated acute kidney injury (SA-AKI) is associated with poor outcomes. Evidence regarding the relationship between early systolic blood pressure (BP) and clinical outcomes in non-critically ill patients with SA-AKI remains limited. This study aimed to investigate the association between mean systolic BP during the first 48 h after admission and one-year clinical outcomes in this population. METHODS: We conducted a single-center retrospective cohort study of non-critically ill adults with SA-AKI admitted between 2011 and 2020. SA-AKI was defined by a sequential organ failure assessment (SOFA) score increase ≥2 and AKI occurring within 48 h of admission. The exposure was mean systolic BP over the first 48 h (seven measurements at baseline and every 8 h), categorized as ≤100, 101-120, 121-140, and >140 mmHg. Patients were followed for one year. The primary outcome was a composite of ≥25% decline in estimated glomerular filtration rate, long-term dialysis, and one-year mortality. RESULTS: Of 2,920 screened patients, 476 were included. Mean age was 68.4 ± 14.5 years, and 55% were male. AKI stages I, II, and III occurred in 55%, 21%, and 24%, respectively. The primary composite outcome was most frequent in the ≤100 mmHg group (80%) compared with 101-120 (51%), 121-140 (50%), and >140 mmHg (46%) (p < 0.001). In adjusted analyses, mean systolic BP ≤100 mmHg was associated with higher composite outcome (HR 1.84, 95% CI 1.15-2.93; p = 0.010). One-year mortality was highest in systolic BP ≤100 mmHg group (73% vs. 32% in 121-140 mmHg; p < 0.001), with increased adjusted hazards for one-year mortality (HR 2.89, 95% CI 1.68-4.99) and 30-day mortality (HR 2.79, 95% CI 1.12-6.96). CONCLUSION: In non-critically ill patients with SA-AKI, early mean systolic BP ≤100 mmHg within 48 h was associated with worse one-year outcomes, driven largely by higher mortality. Early systolic BP may serve as a prognostic marker for high-risk patients.
Medical education systems vary widely across countries, yet the structure of medical and postgraduate training in China remains relatively unfamiliar to international readers. China has developed a relatively comprehensive pathway spanning undergraduate education, postgraduate programs, standardized residency training, and standardized specialty training, thereby shaping an evolving framework that aims to integrate clinical practice with scientific research. Within this framework, postgraduate nephrology education highlights both clinical training and research development. In recent years, Critical Care Nephrology has demonstrated notable strengths in the management of critical illness, blood purification, and multidisciplinary collaboration. This review provides an overview of the development, current status, and future trends in medical and postgraduate nephrology education in China, with a particular focus on the emerging role of Critical Care Nephrology.
BACKGROUND: A refractory catheter-related infection in patients receiving peritoneal dialysis (PD) represents a major challenge that may require catheter removal and reinsertion. We assessed the effect of a tunnel reconstruction operation on refractory infection in a single center. METHODS: We retrospectively collected data from 10 PD patients who, after inadequate responses to treatment with culture-based antibiotic therapy, underwent a tunnel reconstruction operation designed to resolve a refractory catheter-related infection without requiring transition to hemodialysis. The patients were followed for 3-41 months, and outcomes at months 3 and 12 were analyzed. RESULTS: Tunnel reconstruction surgery was performed in 10 patients, including 7 with exit-site infection and 3 with tunnel infection. No patients developed catheter-related infection, catheter dysfunction, or postoperative complications after 3 months of postoperative follow-up. During the 12-month postoperative follow-up period, there were no catheter-related infections among 7 patients (3 patients were not followed for 12 months). However, 2 patients developed an exit-site infection episode at 33 and 41 months after tunnel reconstruction surgery, respectively. No incidents of PD connector hypersensitivity or catheter leakage occurred during the follow-up period. CONCLUSION: Tunnel reconstruction operation may be a promising salvage option that requires prospective validation in PD patients with refractory catheter-related infections.
Renal fibrosis represents a central pathological driver of chronic kidney disease (CKD), yet the epigenetic mechanisms remain incompletely understood. This study identifies a critical role for the Ubiquitin-like with PHD and RING Finger domains 1 (UHRF1)/G9a axis in this process. We demonstrated that both UHRF1 and the histone methyltransferase G9a are significantly upregulated in fibrotic kidneys from CKD patients and relevant murine models by means of multiple experimental approaches, as well as in activated renal fibroblasts. Fibroblast-specific knockout of UHRF1 markedly attenuated renal fibrosis and concurrently suppressed the expression and enzymatic activity of G9a. Mechanistically, we revealed the pathological mechanism that the UHRF1/G9a axis is associated with the deposition of repressive histone H3 lysine 9 mono-/di-methylation (H3K9me1/me2) marks at the promoter of the anti-fibrotic gene Krüppel-like factor 15 (KLF15), as supported by chromatin immunoprecipitation-quantitative polymerase chain reaction (ChIP-qPCR) and cleavage under targets and tagmentation (CUT&Tag) assays, leading to KLF15 transcriptional silencing. Restoration of KLF15 protein expression upon inhibition of this axis contributed to the amelioration of fibrosis. Collectively, our findings indicate the UHRF1/G9a epigenetic complex as a key regulator of renal fibrosis and highlight its potential as a novel target for alleviating renal fibrosis.
Renal failureJunyi Yang, Baokang Wang, Yang Xun, Xiao Yu
Nephrolithiasis incidence has risen with frequent recurrence, and injury to renal tubular epithelial cells is central to its pathology. Ferroptosis, an iron-dependent form of regulated cell death, has been implicated in kidney diseases, but its role in nephrolithiasis remains unclear. In this study, we investigated whether CD74 is associated with ferroptosis-related tubular injury during nephrolithiasis and explored the potential involvement of NF-κB signaling. A glyoxylate-induced mouse model showed prominent calcium oxalate deposition, impaired renal function, altered expression of ACSL4 and GPX4, and increased oxidative stress. Integrating bulk transcriptomics, protein-protein interaction networks, bioinformatics, and a public single-cell RNA-sequencing dataset, we identified CD74 as a candidate ferroptosis-associated gene showing increased expression during nephrolithiasis progression. In vitro, oxalate exposure in human HK-2 cells induced CD74 upregulation together with ferroptosis-associated molecular and biochemical changes. CD74 knockdown improved cell viability and redox homeostasis and attenuated ferroptosis-associated marker changes, whereas CD74 overexpression aggravated oxidative injury and ferroptosis. Mechanistically, CD74 modulation was associated with changes in NF-κB signaling activity, and pharmacological modulation of NF-κB partially reversed the corresponding cellular phenotypes. Together, these findings support a potential role of CD74-associated NF-κB signaling in ferroptosis-related tubular injury during nephrolithiasis. These findings suggest that the CD74/NF-κB axis may represent a potential therapeutic direction and provide mechanistic insight for future studies.
Renal failureDoaa Al Qaoud, Anas Haifawi, Walla Al-Qaoud, Ala'a Al-Ma'aiteh, Tamara Kufoof, Mohamad Rasoul Alrashaideh, Abedulrhman S Abdelfattah, Mariam Al-Husari, Abdel R…
INTRODUCTION: Urgent-start peritoneal dialysis (USPD) provides kidney replacement therapy (KRT) for children with acute kidney injury (AKI) or stage 5 chronic kidney disease (CKD) requiring dialysis. Pediatric data from resource-limited settings remain limited. METHODS: We retrospectively described 18 children who underwent USPD at a tertiary center in Jordan between January 2022 and December 2024. USPD was defined as initiation of peritoneal dialysis (PD) within 14 days of catheter insertion. Early complications occurred within 14 days of the first PD exchange, and late complications thereafter. RESULTS: Sixteen children had AKI, and two had stage 5 CKD. Etiologies were hemolytic uremic syndrome (6/18, 33.3%) and acute tubular necrosis (4/18, 22.2%). Thirteen (72.2%) initiated PD within 24 h: five at 4-12 h and eight at 24 h. Six developed early complications: a leak on 4/18 (22.2%) and an exit-site infection on 2/18 (11.1%), without overlap. Five developed late complications. Peritonitis affected 4/18 (22.2%) and accounted for five episodes; other late events included a leak in two children, an exit-site complication in one, and catheter obstruction in one, with overlapping categories. At one year, 9/16 children with AKI (56.3%) were no longer receiving dialysis, 3/16 (18.8%) remained on PD, and 4/16 (25.0%) had died. Of the two children with stage 5 CKD, one remained on hemodialysis, and one was dialysis-free after transplantation. CONCLUSIONS: This descriptive, single-center experience on USPD delivery, complications, and one-year outcomes. The small sample, absence of a comparator group, and heterogeneity preclude conclusions about safety, timing effects, or predictors.
Renal failureZongchen Jiang, Linjie Zhong, Jungang Fang, Chang Liu, Ran Ji, Yange Hu, Xin Zhao, Wensheng Qi
Despite advancements in solute clearance technologies, cardiovascular mortality in maintenance intermittent hemodialysis (IHD) patients remains disproportionately high. The traditional clearance-based paradigm fails to fully explain this survival gap. Here, we propose conceptualizing IHD as a repetitive iatrogenic stressor and introduce the framework of Repetitive Dialytic Stress Syndrome (RDSS). We postulate that rapid fluctuations in intravascular volume and osmolarity impose a cyclical hemodynamic burden, inducing subclinical microcirculatory shock. Current evidence demonstrates how this recurrent perfusion deficit triggers systemic ischemia-reperfusion injury. This cascade manifests as synchronous organ stunning, driving myocardial fibrosis, cerebral white matter injury, gut endotoxemia, and residual kidney function loss. By redefining dialysis adequacy to include hemodynamic stability, we highlight how therapeutic strategies optimizing physiological stability can mitigate RDSS and improve long-term outcomes.
Cognitive impairment is common in maintenance hemodialysis, but practical risk-assessment tools remain limited. We evaluated the association between baseline serum brain-derived neurotrophic factor (BDNF) and 1-year screening-defined incident cognitive impairment and examined whether BDNF added predictive information beyond routine clinical, laboratory, and baseline cognitive variables. This single-center prospective cohort included 130 maintenance hemodialysis patients with baseline Montreal Cognitive Assessment (MoCA) scores ≥26. The primary outcome was screening-defined incident cognitive impairment, defined as follow-up MoCA <26. Serum BDNF was measured by enzyme-linked immunosorbent assay. Five models were assessed using repeated 5-fold cross-validation; repeated nested cross-validation was added as a sensitivity analysis. During follow-up, 70 patients (53.8%) met the screening-defined outcome. Each 1-SD higher BDNF level was associated with lower odds of the outcome [adjusted OR, 0.52 (95% CI, 0.34-0.80); p = 0.003]. In the primary analysis, random forest and extreme gradient boosting (XGBoost) had AUCs of 0.798 and 0.797, respectively. Adding BDNF to the XGBoost base model changed AUC from 0.770 to 0.797 (DeLong p = 0.236), PR-AUC from 0.746 to 0.779, and Brier score from 0.190 to 0.181. In nested validation, XGBoost AUC was 0.782 (SD 0.019), while paired Base and Base + BDNF AUCs were 0.761 and 0.782, respectively. Lower BDNF was associated with the screening-defined outcome, but its added predictive value was small and statistically uncertain. Serum BDNF may therefore have value as an adjunctive marker for refining risk estimates rather than as a stand-alone predictor; independent multicenter external validation is required before clinical use.
This cross-sectional study investigated the association between central thyroid hormone resistance and chronic kidney disease (CKD) in patients with type 2 diabetes mellitus (T2DM) who have normal peripheral thyroid hormones. The study included 2,759 T2DM patients with normal serum free triiodothyronine (FT3) and free thyroxine (FT4) levels. Central thyroid sensitivity was quantified using the Thyroid Feedback Quantile-based Index (TFQI), thyrotrophic thyroxine resistance index (TT4RI), TSH Index (TSHI), and FT3/FT4 ratio. Utilizing multivariable logistic regression and restricted cubic splines (RCS), we found that elevated TSH levels and increased central thyroid hormone resistance (indicated by higher TFQI, TT4RI, and TSHI) were independently associated with an increased risk of CKD. Notably, RCS analysis revealed a significant non-linear relationship (p < 0.001). Participants in the highest TSH quartile exhibited a 1.5-fold increased risk of CKD in multivariable regression (OR 1.50, 95% CI 1.08-2.07). Crucially, this association remained robust after propensity score-matched analyses (n = 684 pairs, OR 1.66, 95% CI 1.21-2.27). In conclusion, for T2DM patients with normal peripheral thyroid hormones, elevated TSH and reduced central thyroid hormone sensitivity are independently associated with a heightened risk of eGFR-defined CKD. These easily calculated indices may serve as valuable clinical biomarkers for early renal risk stratification.
International journal of oncologyZhifei Che, Dongwen Huang, Jiaming Lin, Xincen Wang, Rongjin Feng, Xianping Che, Yubin Wang
Renal cell carcinoma (RCC) is the main pathological type of kidney cancer, which accounts for approximately 85‑95% of all cases of kidney cancer. Despite the emergence of targeted therapies and immunotherapies, however, the development of resistance remains common. Eomesodermin (Eomes) is a member of the T‑box transcription factor family that links both developmental biology and immune regulation with tumor‑associated programs. In RCC, its function appears to be context‑dependent. In tumor‑infiltrating leukocytes, Eomes has been shown to support mature natural killer cell and memory CD8+ T‑cell function, whereas persistent or dysregulated Eomes is associated with exhausted CD8+ T cells and Eomes‑positive type 1 regulatory T‑like immunosuppressive cells. In both intrinsic RCC tumor cells and stromal/endothelial compartments, current knowledge remains relatively limited, and what evidence there is has often been derived from indirect RCC pathway research, other tumor types or developmental models. The present review summarizes Eomes‑associated mechanisms in RCC through distinguishing among infiltrating leukocytes, tumor cells and stromal/endothelial compartments, and also through separating direct RCC evidence from indirectly derived mechanistic inferences. Epigenetic regulation, PI3K/Akt/mTOR signaling, Wnt/β‑catenin signaling, angiogenesis and therapeutic resistance are also discussed according to the strength of the available evidence. Current data support that Eomes stands as an exploratory biomarker and hypothesis‑generating therapeutic node, rather than as an established clinical target. Further research should be performed, however, to validate the cell‑type‑specific functions of Eomes in RCC tissues, single‑cell and spatial datasets, in addition to experimental RCC models.
Gut microbesKenan Wang, Weiwei Fan, Qizhen Tang, Quanxin Su
Kidney stones represent a globally prevalent disease with a rising incidence associated with multiple factors, including obesity and metabolic syndrome. While traditional research has primarily focused on dietary nutrition and metabolic abnormalities, recent years have seen growing recognition of the gut microbiota as a key novel regulator in stone formation. Accumulating cross-sectional evidence suggests that kidney stone patients are often associated with alterations in gut microbiota composition and function compared with healthy individuals. The gut microbiota may influence kidney stone formation risk through multiple potential mechanisms, including affecting oxalate metabolism, calcium-phosphorus absorption, short-chain fatty acid and bile acid pathways, and regulating systemic inflammatory and immune states. More importantly, this "gut-kidney axis" function of the gut microbiota holds clinical translational potential, suggesting that targeted microbial interventions may emerge as novel strategies for preventing and treating kidney stones. This review explores the association between gut microbiota and kidney stones, discussing clinical evidence, underlying mechanisms, and intervention strategies while analyzing current challenges and outlining future research directions.
Renal failureMatias Hilska, Tomi Toukola, Jan-Ola Wistbacka, Simo-Pekka Koivisto, Tomi Sarkkinen, Aapo Pikkujämsä
INTRODUCTION: Cardiac surgery-associated acute kidney injury (CSA-AKI) is associated with increased post-operative complication rate and decreased survival. There is limited knowledge regarding the long-term risk of progressing to end-stage renal disease (ESRD) following cardiac surgery. METHODS: We analyzed the association of CSA-AKI and the cumulative incidence of progression to ESRD in a cohort of consecutive non-emergent cardiac surgical patients operated between 2000 and 2016. Peri-operative data were collected prospectively, while survival and ESRD data were collected retrospectively. We compared the risk of progression to ESRD in patients who experienced mild or moderate-to-severe CSA-AKI to those who did not. Secondarily, we analyzed survival in these respective groups of patients. RESULTS: The median survival time was 13.7 years (95% confidence interval [CI] 13.3,14.1), over a median follow-up time of 11.9 years (interquartile range 7.8,16.6) among the 3753 patients included in the study. Mild AKI occurred in 383 (10.2%) patients, and moderate-to-severe AKI in 129 (3.4%) patients. Altogether, 63 patients developed ESRD during follow-up, and the 20-year cumulative incidence of ESRD was 1.8% (CI 1.4%, 2.4%). When compared to patients without AKI, the hazard ratio of progression to ESRD was 2.62 (CI 1.36, 5.06) in patients with mild AKI and 8.56 (CI 4.33, 16.9) in patients with moderate-to-severe AKI. Peri-operative AKI was also associated with worse long-term survival and with more frequent post-operative complications. CONCLUSION: A clinically significant proportion of patients progress to ESRD during a long-term follow-up after cardiac surgery. CSA-AKI is associated with an increased risk of progressing to ESRD.
Regional citrate anticoagulation (RCA) has been increasingly adopted as a preferred anticoagulation strategy in continuous renal replacement therapy (CRRT). However, Citrate accumulation during RCA-CRRT represents a major clinical challenge. This review provides an overview of the mechanisms underlying citrate accumulation, its diagnostic criteria, and the primary factors contributing to citrate accumulation, including excessive citrate infusion dose, insufficient citrate loss across the filter, impairment of citrate metabolism. In addition, the clinical consequences of citrate accumulation and current management strategies are summarized, aiming to provide insights for optimizing the safety and efficacy of RCA-CRRT.