Search Results (1,438)

Background: Primary glomerular diseases (PGDs) are a leading cause of end-stage kidney disease (ESKD). While sex differences in chronic kidney disease progression have been reported, their role in PGDs remains unclear. Methods: We analyzed 2081 patients with biopsy-proven PGDs from the Turkish Society of Nephrology Glomerular Diseases Working Group (TSN-GOLD) registry. Baseline demographic, clinical, biochemical, and histopathological characteristics were compared between women and men. Outcomes were assessed as a composite of ESKD or death. Logistic and Cox regression models were applied to identify independent risk factors. Kaplan–Meier analyses evaluated survival differences. Results: At baseline, women and men had similar rates of hypertension (36.8% vs. 34.7%, p = 0.322). Women more frequently presented with leukocyturia (31.7% vs. 17.2%, p < 0.001) and hematuria (57.8% vs. 52.3%, p = 0.016), whereas men had higher proteinuria (5011 ± 4925 vs. 4388 ± 4529 mg/day, p = 0.003) and were more likely to be active smokers (20.7% vs. 7.4%, p < 0.001). Serum albumin (3.3 ± 0.8 vs. 3.2 ± 0.9 g/dL) and eGFR (79.7 ± 44.3 vs. 78.7 ± 45.5 mL/min/1.73 m²) were comparable between sexes (both NS). During a median follow-up of 24 months (IQR 7-60), 431 patients (20.7%) reached the composite outcome of ESKD or death (137 deaths [6.6%], 294 ESKD [14.1%]). In the multivariable Cox regression model, lower baseline eGFR (HR 0.98, 95% CI 0.98–0.98, p < 0.001), lower serum albumin (HR 0.65, 95% CI 0.55–0.77, p < 0.001), higher proteinuria (HR 1.03, 95% CI 1.00–1.05, p = 0.043), and biopsy diagnosis of RPGN (HR 3.78, 95% CI 1.37–10.45, p = 0.010) were independent predictors of poor prognosis. Sex was not an independent predictor of outcome (p = 0.48). Kaplan–Meier analysis demonstrated no significant survival difference between women and men (log-rank p = 0.052). Conclusions: In this nationwide PGD cohort, women and men differed significantly in baseline biochemical and clinical parameters, yet sex was not independently associated with progression to ESKD or death. Instead, disease severity at baseline and histopathological features were the main drivers of prognosis. Full article

Chronic kidney disease (CKD) affects more than 10% of the world’s population, increasing the risk of cardiovascular disease and mortality. Background: Nephroprotective interventions can reduce the risk of end-stage renal disease, delay the time to dialysis, and prolong life. However, there is ongoing debate about the effectiveness of combining amino acid ketoanalogues (KAA) with a low-protein diet (LPD) to slow CKD progression. This study aimed to retrospectively analyze kidney function outcomes after a 6-month KAA+LPD regimen in patients with CKD. Methods: The analysis included results from 38 non-dialyzed patients (12 F, 26 M; age 64.0 ± 13.6 years) with stable CKD in stages G4 to G5, who followed LPD with KAA (Ketosteril, Fresenius Kabi) treatment as part of the Polish National Health Fund Ketosteril Drug Program. Results: No significant change in estimated glomerular filtration rate (eGFR) was observed during 6 months of KAA+LPD therapy. However, eGFR increased or decreased in half of the patients (p < 0.001), and this change was associated only with initial protein intake and urinary phosphate excretion. Initial high phosphate excretion was independently associated with an increase in eGFR, and initial phosphaturia > 0.5 g/24 h identified eGFR improvement (sensitivity 84.2%; specificity 57.9%; AUC 0.712; p = 0.018) in CKD patients who started KAA+LPD treatment. Conclusions: Six-month treatment with KAA+LPD may be associated with stabilization of kidney function in patients with CKD stages G4-G5. The individual effect of KAA+LPD on renal function may be related to the initial protein intake level and urinary phosphate excretion. Further studies are needed to validate these findings across larger patient populations with a broader spectrum of symptoms. Full article

Chronic kidney disease–mineral and bone disorder (CKD-MBD) is a major complication of end-stage renal disease and is associated with increased morbidity and mortality. Sclerostin, an osteocyte-derived glycoprotein that inhibits the Wnt/β-catenin signaling pathway, has been implicated in the dysregulation of bone metabolism in dialysis patients. However, comparative data on sclerostin levels and their clinical determinants between hemodialysis (HD) and peritoneal dialysis (PD) patients remain limited, particularly in Southeast Asian populations. This cross-sectional study was conducted at Hue Central Hospital, Vietnam, between June 2023 and January 2026. A total of 89 end-stage renal disease patients were consecutively enrolled (HD: n = 51; PD: n = 38). Median serum sclerostin levels were 584.21 (IQR: 301.18–1479.50) pg/mL in the HD group and 684.21 (IQR: 407.48–940.35) pg/mL in the PD group, with no significant difference between groups (p = 0.839). Serum sclerostin was inversely correlated with PTH in both HD (r = −0.444, p = 0.001) and PD patients (r = −0.341, p = 0.036). In the HD group, total femur BMD showed a significant inverse correlation with sclerostin (r = −0.304, p = 0.030). In multivariable analysis, Log_PTH remained an independent predictor of sclerostin across all three sequential models in the HD group (Model 1: B = −0.340, p = 0.001; Model 2: B = −0.270, p = 0.035; Model 3: B = −0.268, p = 0.039; adjusted R² range: 0.197–0.217) and in the combined HD + PD cohort (Model 1: B = −0.271, p < 0.001; Model 2: B = −0.263, p < 0.001; Model 3: B = −0.249, p = 0.003; adjusted R² range: 0.141–0.158). In the PD subgroup, Log_PTH was significant in Models 1 and 2 but not in Model 3; none of the models reached overall statistical significance (all p ≥ 0.081), and findings should be considered exploratory given the limited sample size. Serum sclerostin levels did not differ significantly between HD and PD patients. PTH was the most consistent independent predictor of sclerostin across dialysis modalities and analytical models, underscoring its central role in CKD-MBD pathophysiology. Larger prospective multicenter studies are warranted to validate these findings and further clarify the clinical utility of sclerostin in dialysis populations. Full article

Schistosomiasis (bilharzia) is a parasitic infection caused by trematodes of the Schistosoma genus and remains a significant health burden in endemic regions. Granulomatous host responses to deposited Schistosoma eggs in small veins and tissues result in progressive changes and characteristic imaging findings. This diagnostic radiological review synthesizes the published literature and highlights key and robust imaging findings that facilitate the diagnosis of Schistosoma mansoni and Schistosoma haematobium, with emphasis on modality-specific patterns and disease staging. Schistosoma mansoni primarily affects the liver, causing periportal fibrosis visible as “pipe-stem” echogenic thickening upon ultrasonography, which may progress to portal hypertension and chronic liver disease. Liver cirrhosis is the end-stage disease manifested as an irregular liver contour with surface nodularity and lobar redistribution as right lobe atrophy with left and/or caudate lobe hypertrophy. Schistosoma haematobium predominantly affects the genitourinary system, causing urinary bladder wall thickening and calcification. Early disease, within three months of infection, may present with fine calcification, firstly in the bladder base and then extending to the whole bladder and even to the ureters. Calcification appears as a line or two parallel lines on radiography and as a circle in axial computed tomography (CT) images, which is pathognomonic for early-stage Schistosomiasis. In contrast studies, including conventional urography and CT urography, Schistosoma eggs appear as bubble-like filling defects in the ureter, kidney, and bladder, manifested as ureteritis, pyelitis, and cystitis cystica. Late stages appear as coarse calcification, fibrosis, strictures, and reduced bladder capacity and are associated with an increased risk of bladder squamous cell carcinoma. Moreover, Schistosomiasis calcification can present in genital organs, especially in the seminal vesicles; in the prostate in males; and in the vulva, cervix, and perineum in females. Ultimately, Schistosoma mansoni and haematobium eggs can reach the spinal cord, leading to acute myelopathy with paraparesis, urinary retention, or paraplegia. Recognition of characteristic imaging patterns of Schistosomiasis is essential for early diagnosis, accurate staging, and prevention of long-term complications. Full article

Annually, there are more than two million deaths from liver disease. This is driven by organ inflammation and scarring, leading to a decline in function and regeneration. Frequently, this can develop into decompensated liver disease, resulting in the loss of physiological balance and toxin build-up within the body, with an increased risk of patient mortality. Currently, there are no approved medicines for the long-term treatment of liver cirrhosis. The only successful treatment option for end-stage liver disease patients is donor organ transplantation. However, patient requirement outstrips the number of donated organs. To address this bottleneck, researchers around the world have developed cell-based prototype systems to restore failing liver function, with some in clinical trials. Although significant progress has been made, no mainstream commercial liver assist products are available for routine clinical use. In this study we developed a stem cell-derived vascularized liver tissue implant prototype from pluripotent cells. The liver tissue was produced from a stem cell line that is banked at clinical grade, and displayed stable and mature liver function over a 6-week period in vitro. This included decreasing levels of the fetal marker, alpha-fetoprotein, when the serum albumin increased. This was further supported by stable alpha-1-antitrypsin secretion and cytochrome P450 function. Following the establishment of stable liver tissue, it was delivered as a cell product or attached to an electrospun polycaprolactone scaffold, to form a tissue implant. Next, cellular material was quality-controlled, and subsequently shipped to a contract research organization for external in vivo validation. The transplanted liver tissue functioned when implanted into the kidney capsule and subcutaneously, remaining functional for up to two weeks in vivo. Full article

Background: Finerenone and sodium–glucose cotransporter-2 inhibitors provide cardiovascular and renal benefits in patients with chronic kidney disease (CKD) and heart failure (HF), but real-world comparative evidence is limited. Methods: This retrospective study used the TriNetX database. Adults ≥ 40 years with CKD stages 1–5 and HF [LVEF > 40%; excluding end-stage renal disease (ESRD) or dialysis] receiving finerenone were compared with those on SGLT2 inhibitors. Propensity score matching (1:1) yielded 333 patients per cohort. Kaplan–Meier and Cox models estimated hazard ratios (HRs) with 95% confidence intervals. Results: After matching, baseline characteristics were reasonably balanced, with some residual imbalance remaining. All-cause mortality was similar between finerenone and SGLT2 inhibitors at 6 months (HR 0.98; 95% CI 0.50–1.90) and 1 year (HR 0.93; 95% CI 0.53–1.66). All-cause hospitalization or ER visits were also comparable at 6 months (HR 1.07; 95% CI 0.84–1.36) and 1 year (HR 1.04; 95% CI 0.83–1.29). Finerenone was associated with a modest, borderline reduction in HF hospitalization at 1 year, without consistent effects across timepoints or a mortality benefit; thus, this finding is hypothesis-generating (HR 0.81; 95% CI 0.66–0.99). Safety outcomes were similar between groups. Conclusions: In this real-world analysis, finerenone was associated with similar all-cause mortality, overall hospitalization, and renal safety outcomes compared with SGLT2 inhibitors, with a modest reduction in HF hospitalization at 1 year that should be interpreted cautiously given the exploratory nature of the study. These findings are hypothesis-generating and underscore the need for prospective head-to-head trials to better define optimal therapy sequencing in patients with HFpEF and CKD. Full article

Background: Certain metabolites of the tryptophan-kynurenine (Trp-KYN) pathway, which are primarily cleared via tubular transport, have been linked to end-stage kidney disease (ESKD). Uromodulin—a protein expressed exclusively in the kidneys—is a key regulator of renal structure and function, as well as a direct marker of tubular health. This preliminary study explores the hypothesis that serum uromodulin correlates with Trp-KYN metabolites, potentially revealing new pathophysiological pathways in patients undergoing kidney replacement therapy (KRT). Given the link between serum uromodulin, Trp-KYN metabolites, and tubular function, we examined their correlation in KRT patients. Furthermore, we assessed how various clinical and dialysis parameters influence serum uromodulin levels. Methods: A total of 64 stable patients from a single dialysis center receiving hemodialysis (HD) or hemodiafiltration (HDF) were enrolled. Pre- and post-dialysis concentrations of uromodulin, Trp, KYN, kynurenic acid (KYNA), 3-hydroxykynurenine (3-OHKYN), and their reduction ratios (RRs) were established. High-performance liquid chromatography (HPLC) was used to estimate the KYN pathway metabolite levels, whereas uromodulin concentration was measured using an immunoenzymatic assay. Results: Detectable serum uromodulin was found in only 30 patients. This group was predominantly male (p < 0.001) and characterized by shorter dialysis vintage (p < 0.001), a higher prevalence of residual kidney function (RKF) (p = 0.001) and diabetes mellitus (p = 0.028), higher pre-dialysis serum phosphorus levels (p = 0.015), and more frequent use of loop diuretics (p = 0.004). Furthermore, univariate analysis revealed significantly higher pre-dialysis (p = 0.004) and post-dialysis (p = 0.025) serum Trp concentrations in the uromodulin-positive group. Pre-dialysis serum uromodulin concentration correlated positively with pre-dialysis Trp level (p < 0.001) and negatively with the pre-dialysis KYN/Trp ratio (p = 0.008), but not with other metabolites that are also subject to tubular transport mechanisms. Post-dialysis uromodulin levels correlated positively only with post-dialysis Trp level (p = 0.005). Patients treated with HDF had significantly higher RR for uromodulin than those treated with HD (p = 0.01). Conclusions: The presented data indicate that serum uromodulin levels are correlated with RKF. Additionally, the presence of detectable serum uromodulin may indicate reduced immunological activation, leading to diminished activity within the Trp-KYN pathway. Full article

Background: Chronic kidney disease-associated pruritus (CKD-aP) is characterised as pruritus in individuals with advanced chronic kidney disease (CKD) without a discernible alternative etiology. This study assessed the prevalence, severity, and effects of CKD-aP on sleep and health-related quality of life (HRQoL) among end-stage kidney disease patients (ESKD) undergoing maintenance hemodialysis (MHD) in an Indian cohort. Methods: This cross-sectional, single-centre study included adults with renal failure undergoing MHD for ≥3 months. The primary outcome was CKD-aP prevalence and its relationship with demographic, clinical, and laboratory variables. Secondary outcomes included CKD-aP severity, characteristics, HRQoL, and sleep quality scores. Statistical analysis was conducted using SPSS v21, with a significance level of p < 0.05. Results: The 12-item Pruritus Severity Scale found mild CKD-aP to be the most common (37% of patients). The 5-D Itch Scale found that patients with moderate-to-severe CKD-aP had longer daily itching (52.9%) with a nonsignificant change over time (p = 0.18), and the back (77.9%) was the most affected site. The Dermatology Life Quality Index revealed that 75.5% of patients had HRQoL impairment. The Skindex-16 found that moderate-to-severe CKD-aP was linked to a greater symptom burden and emotional distress. The Pittsburgh Sleep Quality Index found poorer sleep quality as CKD-aP worsened. Conclusions: CKD-aP is common in patients undergoing hemodialysis and negatively impacts quality of life, emphasizing the need for routine assessment and targeted management. Full article

Diabetic kidney disease (DKD) is a primary cause of end-stage renal disease (ESRD), and while ferroptosis is known to contribute to DKD pathogenesis, the regulatory role of the NLRP3 inflammasome in this process remains elusive. To address this research gap, we explored whether NLRP3 inhibition alleviates DKD by suppressing ferroptosis using streptozotocin-induced diabetic wild-type and NLRP3-knockout C57BL/6 mice, alongside high-glucose-cultured (30 mM) human renal tubular epithelial (HK-2) cells with or without siNLRP3 transfection. Inflammatory cytokines (IL-6, TNF-α, and IL-1β) were measured using an ELISA; oxidative stress markers (CSSG, MDA, GSH, and ROS) and the iron ion content via colorimetric assays; mitochondrial morphology by transmission electron microscopy (TEM); and ferroptosis-related proteins (ACSL4, COX2, and GPX4) through Western blotting. Our findings demonstrate that NLRP3-knockout diabetic mice displayed markedly reduced urinary albumin excretion and serum creatinine levels (p < 0.01) compared with wild-type diabetic controls, concurrent with suppressed renal iron overload and ferroptosis, diminished inflammatory cytokine levels, and attenuated oxidative stress. Pathological assessments further revealed ameliorated renal fibrosis and preserved mitochondrial ultrastructure in NLRP3-deficient mice. In vitro, siNLRP3 transfection abrogated high-glucose-induced inflammation, oxidative stress, and ferroptosis in HK-2 cells, effects that were reversed by the ferroptosis inducer erastin (p < 0.01). Mechanistically, NLRP3 deficiency was associated with upregulated GPX4 expression and downregulated ACSL4 and COX2 expression. Collectively, these results indicate that inhibition of the NLRP3 inflammasome mitigates DKD progression by suppressing ferroptosis, underscoring its translational potential as a therapeutic target for this condition. Full article

Background: Hospitalized patients with chronic kidney disease (CKD) are at high risk for acute kidney injury (AKI), dialysis, and mortality, yet CKD is often treated as a clinically homogeneous condition. Whether distinct cardiometabolic comorbidity patterns define meaningful inpatient CKD subgroups with differential outcome risks remains unclear. Methods: We conducted a retrospective cross-sectional study of adult hospitalizations for CKD using the 2022 Healthcare Cost and Utilization Project National Inpatient Sample. Hospitalizations were classified into five mutually exclusive CKD phenotypes using a rule-based framework based on diabetes mellitus, heart failure, hypertension, and vascular disease: isolated, hypertensive/vascular, metabolic, cardiorenal, and multimorbid cardiometabolic. Outcomes included AKI, dialysis during hospitalization, and in-hospital mortality. Survey-weighted multivariable logistic regression models were used to estimate adjusted odds ratios (aORs). Sensitivity analyses excluded end-stage kidney disease and dialysis dependence and restricted this study to non-transfer hospitalizations. The effect modification by age was assessed for dialysis. Results: Among 1,062,813 CKD hospitalizations, the unadjusted outcome rates varied substantially across phenotypes. After adjustment, cardiorenal CKD was associated with higher odds of acute kidney injury (aOR 1.16, 95% CI 1.12–1.19) and in-hospital mortality (aOR 1.54, 95% CI 1.50–1.58), whereas multimorbid cardiometabolic CKD demonstrated the strongest association with dialysis during hospitalization (aOR 2.34, 95% CI 2.25–2.43). Hypertensive/vascular CKD was not associated with a difference in mortality risk, while metabolic CKD was associated with a lower adjusted mortality rate compared to isolated CKD. Integrated analyses revealed distinct phenotype-specific risk profiles rather than a single severity gradient. Our findings were robust across the sensitivity analyses, and age significantly modified phenotype–dialysis associations. Conclusions: Hospitalized CKD populations exhibit marked phenotype-specific heterogeneity in AKI, dialysis, and mortality risk. A simple, clinically interpretable phenotype framework identifies distinct inpatient failure patterns and may inform future studies evaluating phenotype-specific risk stratification and management strategies. Full article

Oxidative stress (OS) is elevated in patients with end-stage kidney disease undergoing maintenance dialysis and contributes to increased cardiovascular risk. While kidney dysfunction and dialysis can generate OS, the acute effects of a single dialysis session remain unclear due to variability in study design and the biomarkers used. In this observational study, blood samples from 68 hemodialysis patients were collected before and after a single session. Plasma levels of the reactive oxygen species marker superoxide (O₂^•−) and OS-damage marker lipid hydroperoxides (LOOHs), protein-bound malondialdehyde (PrMDA), protein-bound thiobarbituric acid reactive substances (PrTBARSs), and protein carbonyls (PrCOs) were measured. LOOHs increased significantly by 50% post-dialysis, whereas PrMDA and PrTBARSs decreased modestly by ~10%. No significant changes were observed in O₂^•− or PrCOs. Dialysis vintage correlated positively with LOOHs, PrMDA, and PrTBARSs, but not with O₂^•− or PrCOs. No significant associations were found between OS markers and comorbidities, medication or sex. The post-dialysis rise in LOOHs, an early-formed and least accumulating lipid peroxidation marker, may reflect acute changes in OS during a single HD session. The rising association of PrMDA and PrTBARSs with dialysis vintage may suggest cumulative OS over time. Full article

The American Heart Association (AHA) recently formalized cardiovascular–kidney–metabolic (CKM) syndrome to characterize the systemic interplay among cardiovascular failure, chronic kidney disease (CKD), and metabolic disturbances. Despite evolving clinical management, identifying a unifying cellular driver of this multi-organ deterioration remains a critical priority. This review explores the hypothesis that mitochondrial dysfunction serves as the fundamental pathological nexus of CKM syndrome, driving the progression from early-stage metabolic risk to end-stage organ failure. We synthesize evidence demonstrating how nutrient overload and lipotoxicity precipitate a vicious cycle of bioenergetic failure. In the cardiovascular system, ATP deficiency and impaired mitophagy lead to the structural remodeling observed in both heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF). In the kidney, the high mitochondrial density of proximal tubules renders them uniquely susceptible to oxidative stress and mitochondrial DNA (mtDNA) leakage, which subsequently triggers systemic inflammation. Furthermore, we analyze how established therapies—including sodium–glucose co-transporter 2 (SGLT2) inhibitors, Glucagon-like peptide-1 (GLP-1) receptor agonists, and non-steroidal mineralocorticoid receptor antagonists (MRAs)—exert organ-protective effects via mitochondrial mechanisms, promoting metabolic efficiency, reducing reactive oxygen species generation, stabilizing mitochondrial integrity, and promoting mitochondrial quality control processes. Finally, we review emerging mitochondrial-targeted strategies, such as mitoquinol, elamipretide and NAD+ boosters, which aim to restore the SIRT1-PGC-1 α signaling axis. Mitochondria function as the central engines of the CKM axis. A shift toward a mitocentric clinical model may enable earlier intervention and more precise targeting of the mechanisms driving organ crosstalk. Future success depends on multidisciplinary collaboration and the validation of mitochondrial biomarkers to advance precision medicine in CKM syndrome. Full article

Diabetic kidney disease (DKD) remains a primary driver of end-stage kidney disease and cardiovascular morbidity despite the optimized use of renin–angiotensin system (RAS) inhibitors and sodium-glucose cotransporter-2 (SGLT2) inhibitors. Recent evidence identifies the overactivation of the mineralocorticoid receptor (MR) as a critical, independent pathway leading to persistent renal inflammation and fibrosis. In the diabetic milieu, MR overactivation—driven by both aldosterone and ligand-independent factors such as Rac1 GTPase and oxidative stress—triggers pro-inflammatory and pro-fibrotic gene networks. Unlike traditional steroidal mineralocorticoid receptor antagonists (MRAs), the novel non-steroidal MRA finerenone exhibits a distinct binding mode that more effectively blocks the recruitment of transcriptional co-activators, thereby silencing detrimental downstream signaling in podocytes, fibroblasts, and myeloid cells. Preclinical models have demonstrated that MR blockade significantly reduces albuminuria and preserves podocyte integrity independent of systemic blood pressure. These findings translated into landmark clinical trials; the FIDELIO-DKD and FIGARO-DKD trials established that finerenone significantly reduces the risk of kidney disease progression and cardiovascular events across a broad spectrum of chronic kidney disease stages in type 2 diabetes. Furthermore, recent data from the FINEARTS-HF and CONFIDENCE trials suggest a synergetic benefit when combined with SGLT2 inhibitors, offering more robust cardiorenal protection with a manageable risk of hyperkalemia. This review synthesizes the current understanding of MR pathophysiology and clinical evidence, providing a comprehensive framework for the integration of MRAs into the evolving standard of care for patients with diabetic kidney disease. Full article

Background: Emerging evidence highlights the importance of the MIF–sCD74 axis in health and disease, including its role in regulating cell death. While studies in routine cardiac surgery suggest perioperative relevance, its role in end-stage heart failure (ESFH) patients undergoing left ventricular assist device (LVAD) implantation remains unexplored. Moreover, although MIF and sCD74 induce necroptosis in neonatal cardiac myofibroblasts, the effects of MIF, its paralog D-DT, and sCD74 on adult cardiac myofibroblasts (CMFs) are unknown. Methods: Plasma concentrations of sCD74, MIF and D-DT were measured perioperatively in a small cohort of patients with ESHF undergoing LVAD implantation (n = 20). As a preclinical model of ESHF, primary adult CMFs were treated with recombinant MIF, D-DT and sCD74 to evaluate their effects on cellular viability and health. Results: In LVAD patients, sCD74 and D-DT levels were significantly increased 24 h postoperatively, whereas MIF levels were reduced compared to baseline. ROC curve analysis demonstrated a good discriminatory power of 24 h post-OP sCD74 (AUC = 0.83), sCD74/MIF ratio (AUC = 0.82), and D-DT levels (AUC = 0.88) for acute kidney injury, composite outcome, and right heart failure (RHF), respectively. In adult CMFs, MIF and sCD74 synergistically reduced viable cell counts (p = 0.0083), whereas D-DT reduced cell counts in an sCD74-independent manner (p = 0.0004). Yet, measures of metabolism, proliferation, apoptosis and necrosis along with inflammatory gene expression remained unchanged. Conclusions: Our findings indicate that the balance of MIF, D-DT, and sCD74 during LVAD implantation may be clinically relevant. In particular, an imbalance characterized by elevated sCD74 or D-DT and reduced MIF levels 24 h post-surgery was associated with unfavorable clinical outcomes. Yet, the current findings are exploratory and hypothesis-generating because of a small sample size. Thus, the prognostic value of plasma levels for postoperative complications after LVAD implantation, and the effects of MIF/D-DT/sCD74 imbalance on cardiac myofibroblasts, need to be validated in larger cohorts and in advanced human experimental models. Full article

Autosomal dominant polycystic kidney disease (ADPKD), with a prevalence of approximately 1 in 1000, is the most common inherited cause of end-stage renal disease (ESRD). It is primarily caused by mutations in the PKD1 or PKD2 genes. Multiple studies have demonstrated that deficiency of polycystin proteins, dysregulation of signaling pathways, and activation of inflammatory factors contribute to the progression of ADPKD. The cAMP-targeting drug tolvaptan is currently the only approved therapy for ADPKD; however, its side effects and high cost have limited its widespread use. Meanwhile, mTOR inhibitors, AMPK-targeting agents, anti-inflammatory agents, and dietary interventions have shown promising results in treating ADPKD. Furthermore, the emergence of novel targets such as Notch3 and AURKA offers new directions for ADPKD therapy. This article aims to review the pathogenesis of ADPKD and current treatment advances, while exploring potential new targets for future research, hoping to provide a scientific theoretical foundation for disease management. Full article