INTRODUCTION:Phospholipase A2 receptor (PLA2R) is the major autoantigen in membranous nephropathy (MN); however, the trajectories of anti-PLA2R antibodies and their prognostic implications remain unclear. METHODS:In this retrospective cohort study, we analyzed 1,528 patients with PLA2R-associated MN (2011-2022), each with at least three serial measurements of anti-PLA2R antibody levels. Group-based trajectory modeling was applied to identify distinct longitudinal patterns of antibody change. Associations between antibody trajectories and clinical outcomes were assessed using multivariable Cox proportional hazards and logistic regression models, complemented by Kaplan-Meier analysis. RESULTS:Four distinct serum anti-PLA2R antibody trajectories were identified: rising (5.3%), low-stable (74.8%), declining (14.9%), and high-stable (5.0%). The low-stable group had the lowest rates of renal function decline (15.3%), clinical non-remission (18.8%), and relapse (31.6%). Compared to this group, the risks of renal function decline were significantly higher in the rising (adjusted hazard ratio [aHR] = 3.69; 95% confidence interval [CI]: 2.57-5.30), declining (aHR = 1.66; 95% CI: 1.24-2.21), and high-stable (aHR = 4.18; 95% CI: 2.91-6.00) groups. Similarly, the rates of clinical remission were significantly lower (aHR = 0.38 for rising; aHR = 0.61 for declining; aHR = 0.28 for high-stable), while the odds of relapse were higher (adjusted odds ratio 3.13, 2.35, and 3.17, respectively) in these three groups. These associations remained consistent across sex and age subgroups. CONCLUSION:Serum anti-PLA2R antibody trajectories represent a robust prognosis biomarker in MN, useful for risk stratification and clinical decision-making. Patients with high-stable or rising antibody trajectories require heightened clinical attention due to significantly increased risks of renal function decline, clinical non-remission, and relapse.

Background:Lupus nephritis (LN) treatment response remains heterogeneous. We investigated associations between peripheral/renal T-cell profiles and treatment response, and explored renal T-cell infiltration as a mediator. Methods:This retrospective cohort study analyzed data from 424 LN patients. Peripheral CD4+/CD8+ T-cell counts were measured via flow cytometry, and renal interstitial infiltrations were assessed immunohistochemically. Associations with treatment response were evaluated using generalized linear and logistic regression models, adjusting for clinicopathological factors. Mediation analysis examined renal T-cell infiltration in connecting peripheral immunity and treatment outcomes. Results:The study cohort consisted of 424 patients with biopsy-confirmed LN, predominantly female (84.67%), with a mean age of 30.37 ± 11.18 years. Responders, comprising 68.4% of the cohort, exhibited significantly higher peripheral CD4+ T-cell counts (median 310 vs. 265 cells/μl, P = .002) and CD4/CD8 ratios (0.94 vs. 0.73, P < .01), with adjusted OR of 1.002 (95% CI 1.001-1.003) and 2.462 (95% CI 1.414-4.288), respectively. These associations remained significant after Bonferroni correction. Nonresponders showed increased renal interstitial CD8+ T-cell infiltration (148 vs. 80 cells/mm2, P < .001), while higher renal interstitial CD4/CD8 ratios predicted remission (OR = 8.312, 95% CI 2.593-26.645). The peripheral CD4/CD8 ratio provided incremental predictive value over standard clinical-pathological indices (AUC improvement: 0.711 vs. 0.678, P = .022). Mediation analysis revealed that the renal interstitial CD4/CD8 ratio mediated 11.97% of the total effect of the peripheral CD4/CD8 ratio on treatment response (indirect effect β = 0.011, P = .016). Conclusion:Peripheral and renal interstitial T-cell profiles, particularly CD4/CD8 ratios, are significantly associated with treatment response in LN. Renal interstitial T-cells partially mediate the impact of peripheral immune status on clinical outcomes.

Abstract Background The disease spectrum of intratubular light chain amyloidosis (AL) remains unkown. Methods Patients with intratubular AL from a single center were retrospectively analyzed and stratified into 3 groups: Group 1, complicated by extra-tubular amyloidosis; Group 2, complicated by light chain cast nephropathy (LCCN); and Group 3, isolated intratubular AL. Clinical features, pathological findings, treatment regimens, and renal prognosis were compared across the groups. Results The cohort (126 patients) was predominantly male (65.1%), with a mean age of 57 years and a high prevalence of the λ-light chain (78.6%). Group 1 was characterized by the lowest serum creatinine (Scr) and albumin, but the highest urinary protein and prevalence of systemic amyloidosis (all P < 0.05). Group 2 presented with higher Scr, prevalence of anemia and multiple myeloma (MM), elevated involved-to-uninvolved light chain ratio, and increased density of amyloid casts compared with Group 1 (all P < 0.05). Group 3 displayed similar hematological parameters and amyloid cast density as Group 1, with 1 patient displaying extrarenal amyloidosis. Overall, the hematological response rate was 54.3% and the renal remission rate was 26.4%. One patient in Group 3 progressed to MM. Group 2 had the highest incidence of end-stage renal disease (P < 0.05). Multivariate analysis identified Scr at biopsy as an independent predictor of renal prognosis. Conclusion Intratubular AL is frequently identified in patients with renal AL and LCCN, presenting with characteristics associated with these two disorders. Isolated intratubular AL could progress to MM or systemic amyloidosis, thereby necessitating vigilant clinical monitoring.

[This corrects the article DOI: 10.1016/j.ekir.2026.103791.].

Introduction: IgA nephropathy with minimal change disease (MCD-IgAN) is a rare subtype of IgAN with a high rate of response to corticosteroids but a poor prognosis in steroid-dependent (SD) patients. Case Presentation: A young male patient with SD-MCD-IgAN, who was treated sequentially with rituximab (RTX) and later with obinutuzumab (OBZ) over a 10-year follow-up period, initially presented with nephrotic syndrome and achieved rapid complete remission (CR) with full-dose corticosteroids. However, during the first 2 years, the patient experienced four relapses despite the addition of various immunosuppressants. These relapses were accompanied by complications such as skin infections, acute kidney injury, and serosal effusions. The initial renal biopsy revealed MCD-IgAN, while a repeat biopsy 8 months later revealed IgAN with focal segmental glomerulosclerosis. RTX (375 mg/m2) was introduced after remission was achieved with full-dose corticosteroids. The patient remained in CR with RTX administered based on CD19+ B-cell counts for an initial period of 3 years. Following discontinuation of medication for the subsequent 3 years, the patient experienced a relapse but achieved CR again with low-dose corticosteroids and a single dose of RTX (1.0 g). However, the patient experienced a further relapse after another 3 years of medication cessation. Subsequently, OBZ (1.0 g) was administered along with low-dose corticosteroids, leading to rapid CR and long-term medication-free status. Conclusion: In SD-MCD-IgAN, anti-CD20 maintenance therapy during CR reduces relapse and enables long-term steroid-free remission. If relapse occurs later, it can be controlled with low-dose steroids and resumed anti-CD20 therapy, re-establishing sustained remission.

AIMS:Monoclonal gammopathy-associated kidney lesions typically present with a single pathological pattern, but the coexistence of multiple patterns in the same patient is rare and poorly characterized. This study aimed to delineate the clinicopathological spectrum and outcomes of these complex cases. METHODS AND RESULTS:Twenty-three patients with coexistent pathological patterns were identified from native kidney biopsies. The most frequent combinations were light chain cast nephropathy (LCCN) with light chain deposition disease (LCDD) (34.8%), followed by LCCN with light chain amyloidosis (AL) (21.7%) and LCCN with light chain proximal tubulopathy (LCPT) (21.7%). Multiple myeloma was the predominant underlying haematological disorder (87.0%). Compared with isolated AL, the LCCN+AL group showed more severe acute tubular injury and chronic tubulointerstitial damage (both P < 0.05). The LCCN+LCDD group exhibited more severe acute injury but milder chronic fibrosis than isolated LCDD (P < 0.05). The LCCN+LCPT group had the most favourable prognosis, whereas the LCCN+AL group had the worst, with a median survival of only 32 months and significantly higher mortality than isolated LCCN, isolated AL and LCCN+LCPT groups (all P < 0.05). CONCLUSIONS:Monoclonal gammopathy-associated kidney lesions with coexistent pathological patterns represent a highly heterogeneous entity with distinct features and varied prognoses. The combination of LCCN with AL identifies a particularly high-risk group. Kidney biopsy is crucial for precise classification and prognosis assessment.

Introduction:Pauci-immune endocapillary proliferative glomerulonephritis (GN) (Pauci-I-EPGN) is a rare glomerular disease with a heterogeneous and poorly understood etiology. Here we describe the clinicopathological features, immune cell infiltration patterns, and treatment outcomes of Pauci-I-EPGN. Methods:Fifteen patients with biopsy-proven Pauci-I-EPGN, diagnosed between January 2012 and June 2025, were studied retrospectively. Results:Fifteen patients (7 males and 8 females) aged 50.1 ±13.0 years at renal biopsy were included. The median 24 hour urine protein was 2.00 g/d (0.30-7.77 g/d), with a median serum creatinine level of 1.14 mg/dL (0.54-5.36 mg/dL). Seven cases had prodromal infection. Light microscopy (LM) showed endocapillary proliferative lesions in glomeruli. Immunofluorescence (IF) staining was negative for IgG, IgA, IgM, component C3, component C1q, and light chains. Electron microscopy (EM) revealed no electron-dense deposits. Immunohistochemical staining showed that inflammatory cells in glomeruli were mainly cluster of differentiation CD68+ cells and a small number of CD3+ cells. Multiplex IF staining demonstrated that CD68+ CD163+ cells were the predominant infiltrating cell type in glomeruli. Extensive transforming growth factor-beta (TGF-β) expression was observed within glomeruli. Besides, urinary soluble CD163 levels normalized to urinary creatinine (u-Cr) were elevated in 12 patients and correlated with the number of glomerular CD68+ CD163+ macrophages. Among 11 patients with a median follow-up period of 16.4 months (0.6-80.5 months), 5 achieved complete remission, 2 achieved partial remission, 1 showed stable kidney function, and 3 had progressive renal disease (1 progressed to end-stage renal disease [ESRD]). Conclusion:Pauci-I-EPGN is a rare distinct entity characterized by abnormal activation of intraglomerular M2 macrophages and CD8+ T cell infiltration, with inflammation-fibrosis imbalance driven by TGF-β overexpression. Corticosteroids may offer a potential therapeutic benefit for this type of disease. The overall outcomes in this cohort were generally favorable.

Kidney tubulointerstitial disease culminates in renal fibrosis, which is a key determinant of subsequent end-stage renal disease. Krüppel-like factor 4 (KLF4), one of the Yamanaka transcription factors, controls various essential cellular functions, and has been implicated in kidney diseases. However, evidence regarding the role of KLF4 in renal fibrosis specifically within tubular epithelial cells and fibroblasts remains limited. In our study, we observed significant induction of KLF4 protein in tubular and interstitial myofibroblasts from mouse and human fibrotic kidneys. Mice with epithelium or fibroblast-specific deletion of KLF4 showed reduced extracellular matrix (ECM) deposition and downregulation of Hippo signaling components in both fibrotic models. Gain- and loss-of-function experiments supported that KLF4 signaling was responsible for TGF-β1-induced ECM production in both tubular cells and fibroblasts. Mechanistically, KLF4 protein can interact with YAP protein, promote YAP activation and drive the expression of downstream signaling proteins, whereas inhibition of the Hippo signaling suppresses KLF4-mediated ECM deposition in both epithelial cells and fibroblasts. Interestingly, KLF4's action in tubular cells may play a more significant role in fibrogenesis compared to its role in fibroblasts. Finally, inhibition of KLF4 signaling with Kenpaullone dramatically improved ECM deposition in fibrotic nephropathy models. Inhibiting KLF4/YAP signaling dramatically improve kidney fibrogenesis, suggesting that targeting this signaling pathway may shine light on therapeutic strategies to mitigate kidney fibrosis in patients with chronic kidney diseases.

Background. This study aims to investigate the spectrum and prognosis of membranous nephropathy (MN) in patients with Sj & ouml;gren's syndrome (SS). Methods. SS patients with biopsy-proven kidney involvement who were diagnosed at our center between April 2007 and February 2024 were retrospectively reviewed and analyzed. Results. A total of 290 SS patients with kidney involvement were enrolled. The frequency of MN increased from 16.28% during the 2007-2010 period to 44.05% during the 2021-2024 period. After 2016, MN became the most common renal pathologic type, surpassing tubulointerstitial nephritis. PLA2R antibody or antigen was detected in 74 SS-MN patients, in whom 37 (50%) showed a negative result. Within the PLA2R-negative group, five out of 15 showed positivity for EXT1/EXT2 antigen and one out of eight for THSD7A antigen. Sixty-one SS patients with MN were followed up for >6 months, and 44 (72.13%) of them achieved renal complete remission (CR). Compared with PLA2R-negative patients, PLA2R-positive patients spent a longer time to achieve CR (1.46 +/- 1.16 vs. 0.74 +/- 0.47 years, P = .015) and had a higher rate of progression to the renal endpoint (8/32 vs. 1/29, P = .028). After adjusting for age, proteinuria, and eGFR, Cox regression analysis showed that PLA2R positivity remained a risk factor for CR [HR = 0.511, 95% CI (0.262 to 0.998), P = .049]. Conclusions. MN has become the predominant renal pathologic type in SS. PLA2R-positivity testing followed by EXT1/EXT2 and THSD7A testing is recommended for SS-MN patients. Although most patients can achieve renal CR, the prognosis is usually poor in PLA2R-positive SS-MN patients.

Immunoglobulin light chain (AL) amyloidosis is a rare clonal plasma cell disorder with high rate of missed diagnosis, misdiagnosis and mortality. Conventional assays, such as serum immunofixation electrophoresis (IFE) and serum free light chain (FLC) assay, are unable to accurately detect low concentrations of monoclonal protein (M protein), especially as a patient's renal function deteriorates. The heavy/light chain (HLC) assay, a relatively new method, can quantify intact immunoglobulins in serum and has proven to be valuable in the diagnosis and monitoring of multiple myeloma (MM). However, there is limited research on its application in AL amyloidosis. In this study, we evaluate the value of HLC assay in AL amyloidosis patients at different disease stages, and compare it to the performance of IFE and FLC assay. Among 40 untreated patients, 34 (85%) were positive for IFE, 34 (85%) had an abnormal free light chain ratio (FLCr), and 31 (78%) had an abnormal heavy light chain ratio (HLCr). Among 67 serum samples obtained from 44 treated patients, 57 (85%) were positive for IFE, 9 (13%) had abnormal FLCr, and 45 (67%) had abnormal HLCr. There were 1 (14%) of 7 patients in complete response (CR), 17 (68%) of 25 patients in very good partial response (VGPR), 9 (82%) of 11 patients in partial response (PR) and 6 (75%) of 8 patients in no response (NR) showed an abnormal HLCr. Our findings identified the potential value of the HLC assay in the detection of M proteins and response and serologic residual disease monitoring.

OBJECTIVES:This study aimed to analyze the clinical and prognostic differences in immune-mediated membranous nephropathy (MN) concurrent with other forms of glomerulonephritis. MATERIALS AND METHODS:A retrospective cohort study at Jinling Hospital from 2015 to 2023 included patients with PLA2R antibody levels ≥ 14RU/mL who underwent renal biopsy. Those with immune-mediated MN and concurrent glomerulonephritides were compared to a control group with isolated MN diagnosed in 2015. RESULTS:Concurrent glomerulonephritis was found in 5.53% of the MN cohort, including 61 patients with IgA nephropathy (IgAN-MN), 49 with diabetic nephropathy (DN-MN), and 131 with focal segmental glomerulosclerosis (FSGS-MN). Compared to the control group, those with IgAN-MN showed increased severity of glomerular injury yet had a reduced degree of interstitial fibrosis. The DN-MN group exhibited intensified glomerular damage; however, no significant difference was observed in the extent of tubulointerstitial damage. Additionally, the FSGS-MN group displayed more severe damage to both glomerular and tubulointerstitial structures. Both the DN-MN group and the FSGS-MN group exhibited a significantly lower complete remission rate compared to the control group. The renal endpoint event rates were 29.51% for IgAN-MN, 46.94% for DN-MN, and 33.59% for FSGS-MN, which were all significantly higher than the 18.99% rate in the control group. CONCLUSION:Patients with MN who test positive for serum Anti-PLA2R antibodies may present with other forms of glomerulonephritis. The prognostic outcomes of MN in the presence of concurrent IgAN, DN, or FSGS are notably poorer than those of isolated MN. Renal biopsy is valuable for definitive diagnosis and prognostic evaluation.

Clinically, acute kidney injury (AKI) stems from a diverse array of causes including ischemia, exposure to nephrotoxic agents, or sepsis. Renal tubular cells are particularly vulnerable and often sustain the most significant damage during AKI. This raises the question of whether there exists a common pathophysiological mechanism or pathway in renal tubular cells that underlies the development of AKI. We observed that tubular Galectin-3 is significantly up-regulated in four AKI mouse models and its tissue expression shows a positive correlation with tubular injury in human kidneys affected by AKI. The urinary Galectin-3 levels were markedly elevated in a cohort of patients with AKI and these levels correlated with the severity of kidney dysfunction. Based on predictions from bioinformatic analysis and JASPAR database, ChIP-PCR and luciferase-reporter assays demonstrated the direct binding of the transcription factor KLF4 to a specific sequence in the Galectin-3 gene promoter. Furthermore, mice with proximal tubular-specific deletion of KLF4 exhibited reduced kidney injury and inflammation, along with lower Galectin-3 expression in both cisplatin and ischemia-reperfusion-induced AKI. Targeting the KLF4/Galectin-3 axis with Kenpaullone and GB1107 confirmed protective effects against cisplatin-induced cell death and acute kidney injury, respectively. Our study highlights the KLF4/Galectin-3 pathway as a key mediator in the pathogenesis of AKI. Disrupting this signaling pathway may provide a promising therapeutic approach for the treatment of AKI.

Diabetic kidney disease (DKD) is a prevalent and severe complication of diabetes and plays a pivotal role in the pathogenesis and progression of DKD. However, the current clinical application of the treatment methods does not yield effective results. Tacrolimus has been utilized in the management of immune-mediated and genetic-mediated nephropathy, with an emphasis on the restoration of podocyte cytoskeletal integrity and inhibition of apoptosis. The clinical management of diabetic nephropathy with tacrolimus remains challenging because of the risk of worsening hyperglycemia and infection. We developed two RGD-HSA-TAC nanoparticles designed for targeted delivery of tacrolimus to podocytes. Administration of SANPs and CNPs resulted in elevated levels of tacrolimus in podocytes, leading to a reduction in podocyte damage and albuminuria in diabetic nephropathy mice. Furthermore, the use of SANPs and CNPs resulted in a decrease in tacrolimus accumulation in the pancreas, lymph nodes, and thymus, thereby reducing the potential to exacerbate hyperglycemia and infection. Importantly, compared to tacrolimus alone, both SANPs and CNPs demonstrated superior therapeutic efficacy, with CNPs exhibiting a greater advantage over SANPs. Compared to tacrolimus, SANPs and CNPs demonstrated superior therapeutic efficacy and a reduced incidence of adverse effects in the treatment of diabetic nephropathy.

Diabetic kidney disease (DKD) is the main cause of end-stage kidney disease, and podocyte injury is an important factor in the development of DKD. Mitophagy is severely inhibited in the podocytes of patients. Damaged mitochondria aggregate in the cytoplasm and can not be removed effectively. Restoring mitophagy may be a novel strategy for the treatment of DKD. In this study, Regulatory T cells (Tregs) are found to reduce podocyte injury in DKD through exosomes. Sequencing and cross-sectional analysis revealed that exosomes from Tregs delivered miR-218-5p to increase mitophagy in podocytes by inhibiting the TNC/TLR4/SRC/FUNDC1 pathway. Treg-Exos are engineered to express RGD peptides on the membrane surface. RGD-Treg-Exos bind to integrins on the surface of podocytes and effectively target podocytes for the delivery of miR-218-5p, thus increasing mitophagy in podocytes, reducing cell apoptosis, and alleviating podocyte injury. In summary, this study revealed that engineered RGD-Treg-Exos effectively ameliorated podocyte injury in DKD, thus constituting a novel method for DKD treatment.

Aims:To explore the clinicopathological features and renal outcome in patients with cryoglobulinemic glomerulonephritis (Cryo-GN) without confirmed systemic autoimmune diseases. Methods:Sixty-nine patients with Cryo-GN from a single center were recruited in this retrospective study. Their clinical, pathologic, and follow-up data were collected and analyzed. According to whether the serum monoclonal immunoglobulin (MIg) and HBV-DNA/HBV markers or HCV-RNA/anti-HCV antibodies were positive or not, they were classified into four groups: positive serum MIg only (MIg group), positive HBV-DNA/HBV markers or HCV-RNA/anti-HCV antibodies (HBV/HCV) only (HBV/HCV group), positive serum MIg and HBV/HCV (MIg+HBV/HCV group), and all MIg/HBV/HCV negative group. Results:The male-to-female ratio was 1.38:1 with a mean age of 50.4 ± 14.7 years in the patient cohort. Hypertension was presented in 59.4% of cases, anemia in 73.9%, renal insufficiency in 60.9%, nephrotic proteinuria in 44.9% and microscopic hematuria in 94.2%. The MIg group had significantly lower eGFR levels, higher cryoglobulin levels, and higher rates of abnormal serum-free light chain ratios than the MIg/HBV/HCV negative group. The most common histological pattern of Cryo-GN was membranoproliferative glomerulonephritis (MPGN), and the MIg group had significantly higher scores of the severity of intracapillary cryo-Plugs than the MIg+HBV/HCV group and the MIg/HBV/HCV negative group. Immunohistochemical staining of 29 patients revealed a significant infiltration of CD68+ cells within the glomeruli. Further multiplex immunohistochemical staining of 4 of these patients showed that the infiltrating cells within the glomeruli in Cryo-GN were predominantly CD68+CD163+ cells. Sixty-seven patients had a median follow-up of 31.7 months, and 23.9% of them progressed to end-stage renal disease (ESRD). The renal survival was inferior for MIg group than HBV/HCV group. Multivariate analysis showed that serum MIg and eGFR were independent prognostic factors. Conclusion:Regardless of the presence of HBV/HCV infection, non-systemic autoimmune diseases related Cryo-GN patients with serum MIg had worse renal function and renal survival. Patients with a large number of pseudothrombi in the glomerular capillary lumens tend to have worse renal outcomes. Serum MIg and eGFR were independent risk factors for renal survival in Cryo-GN patients without autoimmune diseases.

Anti-glomerular basement membrane glomerulonephritis (anti-GBM GN) is a rare autoimmune disease that often progresses to end-stage renal disease (ESRD). Complement activation and anti-GBM GN are closely related, as evidenced by the renal pathological characteristics of patients with anti-GBM GN, which include the linear deposition of immunoglobulin G (IgG) and C3 along the GBM. Increasing evidence suggests that all three pathways of complement activation may be involved in the pathogenesis and progression of anti-GBM GN. Anti-GBM GN’s clinical symptoms are linked to complement-related proteins, which are risk factors that impact the disease’s prognosis. This suggests that complement activation and activity may be the primary causes of renal damage in anti-GBM GN. Therefore, biomarkers of complement activation can identify anti-GBM GN cases that may progress to severe renal damage, and complement inhibition may become a new strategy for the clinical treatment of anti-GBM GN.

Background:Tyrosine kinase inhibitors (TKIs) are essential anticancer agents associated with substantial nephrotoxic potential. Although TKI-induced renal injury is increasingly recognized, comprehensive histopathological characterization remains limited due to insufficient renal biopsy data. This study characterizes the clinicopathological spectrum and outcomes of biopsy-proven TKI nephrotoxicity. Methods:This retrospective study analyzed 21 patients with biopsy-proven TKI-associated renal injury identified between 2015 and 2025. Demographic characteristics, renal function indices, oncological profiles and histopathological features were analyzed. Results:The cohort included 16 patients with solid tumors and 5 with hematologic malignancies exposed to four major TKI classes: vascular endothelial growth factor receptor, platelet-derived growth factor receptor, human epidermal growth factor receptor and Bruton's tyrosine kinase TKIs. The median time from TKI initiation to symptom onset was 9.5 months. Clinical manifestations included proteinuria (95%), edema (52%) and new-onset/worsened hypertension (47%). At biopsy, median serum creatinine was 1.07 mg/dL (94.6 µmol/L) and proteinuria was 1.83 g/day. Histopathological analysis demonstrated thrombotic microangiopathy (TMA)-like lesions in 17 of 21 cases (80%), with concurrent immunoglobulin A nephropathy in 3 cases and focal segmental glomerulosclerosis in 3 cases. Among 18 patients with available follow-up data, 14 discontinued their initial TKI therapy, with 5 transitioning to alternative TKIs. Treatment strategies included angiotensin-converting enzyme inhibitor/angiotensin-receptor blocker monotherapy (n = 13) and combination therapy with corticosteroids/immunosuppressants (n = 5). During a median follow-up period of 9.5 months, complete and partial proteinuria remission occurred in five cases each. Four patients died due to cancer progression, while renal function remained stable in the remaining patients without progression to end-stage renal disease. Conclusion:TKI-induced renal injury characteristically presents with edema, hypertension and significant proteinuria, with renal-limited TMA as the predominant histopathological finding. Timely recognition and prompt discontinuation of the offending TKI, coupled with appropriate supportive nephroprotective management, generally yield favorable long-term renal outcomes with preservation of kidney function.

Separate renal function assessment is important in clinical decision making. The single-photon emission computed tomography is commonly used for the assessment although radioactive, tedious and of high cost. This study aimed to automatically assess the separate renal function using plain CT images and artificial intelligence methods, including deep learning-based automatic segmentation and radiomics modeling. We performed a retrospective study on 281 patients with nephrarctia or hydronephrosis from two centers (Training set: 159 patients from Center I; Test set: 122 patients from Center II). The renal parenchyma and hydronephrosis regions in plain CT images were automatically segmented using deep learning-based U-Net transformers (UNETR). Radiomic features were extracted from the two regions and used to build radiomic signature using the ElasticNet, then further combined with clinical characteristics using multivariable logistic regression to obtain an integrated model. The automatic segmentation was evaluated using the dice similarity coefficient (DSC). The mean DSC of automatic kidney segmentation based on UNETR was 0.894 and 0.881 in the training and test sets. The average time of automatic and manual segmentation was 3.4 s/case and 1477.9 s/case. The AUC of radiomic signature was 0.778 in the training set and 0.801 in the test set. The AUC of the integrated model was 0.792 and 0.825 in the training and test sets. It is feasible to assess the renal function of each kidney separately using plain CT and AI methods. Our method can minimize the radiation risk, improve the diagnostic efficiency and reduce the costs.

The KDIGO 2021 guidelines suggest that individuals who test positive for serum anti-phospholipase A2 receptor (anti-PLA2R) antibodies may not require a renal biopsy to establish a diagnosis of membranous nephropathy (MN). However, it is imperative to acknowledge that MN can coexist with other chronic kidney diseases. In instances where MN is comorbid with IgA nephropathy, diabetic nephropathy, or focal segmental glomerulosclerosis, the therapeutic approach tends to be analogous. Nevertheless, there is a significant disparity in both the treatment regimen and the prognosis between MN and renal amyloidosis, with variations existing even among distinct subtypes of renal amyloidosis. Given that both MN and renal amyloidosis exhibit a predilection for the geriatric population, it is prudent to consider the possibility of MN concurrent with renal amyloidosis in elderly patients who test positive for serum anti-PLA2R antibodies. This consideration should precede a straightforward MN treatment strategy. In this report, we present six patients with MN concurrent with renal amyloidosis identified at our center over the past 14 years; in five of whom were positive for serum anti-PLA2R antibodies. We further elucidated the divergent clinicopathological characteristics and prognostic implications of these cases.