Hypertensive disorders of pregnancy, particularly pre-eclampsia, are recognized not only as major obstetric complications but also as early indicators of future maternal cardiovascular and renal risk. Despite this, postpartum care remains centered on blood pressure surveillance, whereas kidney assessment is not consistently incorporated into routine obstetric follow-up. This narrative review examines the renal implications of hypertensive disorders of pregnancy beyond delivery and translates guidance and observational evidence into a practical obstetric approach to postpartum kidney assessment. Available data indicate that a clinically meaningful subgroup of women have persistent renal abnormalities in the early postpartum period, most often as albuminuria or proteinuria rather than as overt reduction in estimated glomerular filtration rate. Reliance on blood pressure or serum creatinine alone may therefore fail to identify incomplete renal recovery, pregnancy-unmasked chronic kidney disease, or women requiring closer reassessment. We also emphasize pregnancy-associated acute kidney injury as a high-priority phenotype, operationalized by creatinine rise or oliguria using Kidney Disease: Improving Global Outcomes (KDIGO)-type criteria and interpreted against pregnancy-specific creatinine physiology. Patients meriting greater attention include those with severe or preterm disease, persistent hypertension, antenatal renal abnormalities, pregnancy-associated acute kidney injury, or relevant pre-existing comorbidity. We propose a feasible postpartum framework based on blood pressure measurement, serum creatinine with estimated glomerular filtration rate, and urinary assessment of albuminuria or proteinuria, with repeat testing or specialist evaluation guided by postpartum findings and clinical risk. Rather than creating a parallel nephrology pathway, this approach supports obstetric services in identifying women whose renal recovery may be incomplete.

Diabetic kidney disease (DKD) is a type of chronic renal injury induced by diabetes mellitus and is characterized by persistent proteinuria and progressive decreases in the glomerular filtration rate. Recent studies have highlighted the significance of histone lactylation and necroptosis in the pathogenesis of DKD. We explored the mechanisms by which lactate-induced histone H3 lysine-18 lactylation (H3K18la) and H3K27la promote necroptosis in DKD. Lactate-induced H3K18la and H3K27la modulated Fas transcription, contributing to necroptosis and DKD progression. Moreover, keratin 18 (KRT18), identified as a lactyltransferase, regulated H3K18la and H3K27la levels, subsequently inducing Fas transcription and necroptosis. Furthermore, ginsenoside Rc (gRc) inhibited KRT18 lactyltransferase activity by competing for the lactate binding site in KRT18. Notably, gRc treatment reduced the KRT18, H3K18la, H3K27la, and Fas levels and alleviated necroptosis and renal dysfunction in DKD models. In conclusion, KRT18 functions as a lactyltransferase to induce Fas transcription and necroptosis. Moreover, inhibiting KRT18-mediated histone lactylation via gRc is a potential strategy for treating DKD.

Despite being an option for high-risk or inoperable cases, existing neoadjuvant therapies for hormone receptor-positive/human epidermal growth factor receptor 2-negative (HR+/HER2-) breast cancer yield suboptimal pathological responses, necessitating novel strategies. This prospective, phase II ACNTBC trial (NCT05558722) investigated the efficacy and safety of combining anlotinib with chemotherapy as a neoadjuvant treatment for HR+/HER2- breast cancer. Enrolled patients received 5 cycles of anlotinib (12 mg qd, d1‒14; q3w) plus 6 cycles of nab-paclitaxel (200 mg/m[2], q3w), pirarubicin (50 mg/m[2], q3w), and cyclophosphamide (500 mg/m[2], q3w). The primary endpoint was the total pathological complete response (tpCR) rate, with the major secondary endpoints including residual cancer burden (RCB) 0/I rate, objective response rate (ORR), and safety. The study enrolled 31 patients, and the ORR was 93.5% (29/31, 95% CI, 78.6-99.2). In the per-protocol set of 28 patients completing treatment and surgery, the tpCR rate was 14.3% (4/28, 95% CI, 4.0-32.7), with RCB 0/I rate of 25.0% (7/28, 95% CI, 10.7-44.9). Grade 3/4 adverse events included hematologic toxicities, hypertension, proteinuria, and headache, all manageable. Post-hoc biomarker analysis showed that high baseline VEGFR2 expression and microvessel density (MVD) were significantly associated with superior efficacy, and the treatment significantly reduced Ki-67 index, VEGFR2 expression, and MVD. Supporting evidence from an exploratory inverse probability of treatment weighting (IPTW) analysis using a real-world cohort receiving chemotherapy alone indicated a potential benefit of the combination over chemotherapy alone. In conclusion, neoadjuvant anlotinib plus chemotherapy demonstrates promising efficacy and manageable safety in HR+/HER2- breast cancer with a high Ki-67 index.

C3 glomerulopathy (C3G) is a clinicopathologic entity characterized by glomerular inflammation with dominant staining for C3 on immunofluorescence microscopy. Electron microscopy is used to determine the location and type of deposits, which further divides C3G into C3 glomerulonephritis (C3GN) and dense deposit disease (DDD) based on ultrastructural findings. Both entities are progressive, with about 60% of patients progressing to end-stage kidney disease (ESKD) within 10 years. Recurrence after kidney transplantation occurs in up to 60% of C3G cases. New knowledge about the pathophysiology-different patterns of injury, histopathological scoring, apolipoprotein E staining, dysregulation of the alternative complement pathway (including both autoantibodies to and mutations in complement regulatory factors), as well as proteomic analyses-has allowed a better understanding of different pathophysiological profiles and clinical presentations, enabling individualized treatment. The role of nephroprotection is well established in C3G, as it is for other glomerular diseases. Non-specific treatment with corticosteroids and immunosuppression is associated with a variable response rate. However, more recently, results from clinical trials with proximal complement inhibitors have shown significant improvement in proteinuria and attenuation of the decline in estimated glomerular filtration rate (eGFR). Based on the results of these trials involving drugs that specifically target the upstream complement pathways, including the alternative pathway, new treatment options have recently become available for patients with C3G.

Takayasu arteritis (TAK) is a large-vessel vasculitis in which glomerulonephritis is a rare complication with a poorly characterized clinical and histopathological profile. Patients with biopsy-proven glomerulonephritis were retrospectively identified from a single-center TAK cohort followed between 2014 and 2022. A systematic review of PubMed/MEDLINE, Scopus, and Web of Science for articles published up to December 2025 was conducted in parallel, excluding studies involving patients younger than 18 years and cases with confounding autoimmune conditions or non-classifiable biopsy findings. This case-based review was reported in accordance with the CABARET and PRISMA 2020 standards. Among 72 patients with TAK, three (4.2%) had biopsy-proven glomerulonephritis. The systematic review yielded 31 articles describing 39 additional cases (84.6% female; median age at TAK diagnosis 26 years; median age at glomerular disease diagnosis 33 years). Glomerular disease was diagnosed a median of 5 years (IQR 0-11) after TAK and most often presented as asymptomatic proteinuria or nephrotic syndrome. Mesangial proliferative glomerulonephritis was the most common subtype (35.9%), followed by AA amyloidosis (30.8%), membranoproliferative glomerulonephritis (12.8%), focal segmental glomerulosclerosis (10.3%), and membranous nephropathy (7.7%). Renal artery stenosis was absent in 69.2% of cases. Corticosteroids were used in 92.3% of cases and biologic agents in 10.3%. Glomerulonephritis is a rare but clinically significant late complication of TAK, characterized by a distinct histopathological spectrum dominated by mesangial lesions, AA amyloidosis, and membranoproliferative glomerulonephritis. Routine proteinuria screening in patients with TAK, including during clinical remission, is warranted to enable early detection and timely management.

To evaluate the emerging role of aldosterone synthase inhibitors (ASIs) in combination with sodium-glucose cotransporter 2 (SGLT2) inhibitors for the management of uncontrolled hypertension in patients with chronic kidney disease (CKD), and to assess their potential cardiorenal benefits.

This narrative review examines acute and chronic kidney injury following COVID-19 infection and vaccination, discussing the mechanism of SARS-CoV-2 entry into host cells through the ACE2 receptor - highly expressed in renal tissues - facilitating the viral invasion. Viral RNA has been detected in the urine of patients infected with SARS-CoV-2, suggesting direct renal involvement. The incidence of acute kidney injuriy (AKI) among hospitalized COVID-19 patients was particularly higher in the early stages of the pandemic and largely varied by 29%-46%, depending on population studied and COVID-19 wave. Pathological findings include acute tubular injury (ATI), collapsing glomerulopathy, and focal segmental glomerulosclerosis. Major risk factors for AKI comprise older age, male sex, diabetes, hypertension, cardiovascular disease, and preexisting Chronic Kidney Disease (CKD). AKI significantly increases mortality of COVID-19 patients, particularly in advanced stages of renal failure. CKD is also associated with severe COVID-19 outcomes, including increased hospitalization, intensive care admission, and mortality. Patients with CKD show a dose-dependent relationship between disease stage and adverse patient outcomes. This review further addresses renal complications following COVID-19 vaccination, which, although rare, encompass various immune-mediated glomerular diseases. Minimal Change Disease (MCD) is most frequently reported after COVID-19 vaccination, followed by IgA nephropathy, membranous nephropathy, anti-glomerular basement membrane (anti-GBM) nephritis, and ANCA-associated vasculitis. These conditions commonly present with hematuria, proteinuria, or nephrotic syndrome, and many respond to corticosteroid or immunosuppressive therapy. Other less frequent renal complications include thrombotic microangiopathy, acute tubulointerstitial nephritis, and IgG4-related nephritis. In conclusion, both COVID-19 infection and vaccination can be associated with a spectrum of renal manifestations ranging from AKI to CKD and immune-mediated glomerulopathies. Awareness, early detection, and multidisciplinary management are essential to reduce renal morbidity and improve patient outcomes.

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome characterized by diverse etiologies and a high risk of misdiagnosis. Autoinflammatory disorders, such as adult-onset Still's disease (AOSD), are often underrecognized as contributing factors. Minimal change disease (MCD) represents an exceedingly rare renal complication in the context of HLH. This report describes the case of an adult female diagnosed with Epstein-Barr virus (EBV)-associated HLH. Initial therapy with etoposide and dexamethasone yielded a partial response; however, disease relapse occurred, accompanied by the development of significant proteinuria. Renal biopsy confirmed a diagnosis of MCD. Administration of rituximab led to complete remission of the nephrotic syndrome, although HLH activity persisted. A subsequent skin biopsy revealed perivascular infiltration composed predominantly of lymphocytes and neutrophils. In combination with clinical features such as high-grade fever and rash, these findings supported a diagnosis of AOSD. Adjustment of the treatment regimen to include corticosteroids and methotrexate resulted in complete remission of HLH. This case underscores the importance of re-evaluating the underlying cause in patients with HLH who demonstrate an inadequate therapeutic response. MCD may represent a renal manifestation of immune dysregulation associated with HLH. A multidisciplinary approach is essential for improving diagnostic precision and optimizing treatment in complex presentations of HLH.

Background/Objectives: Immunoglobulin A nephropathy (IgAN) is a type of chronic kidney disease (CKD) and the most common cause of kidney failure in patients <40 years of age. Previous economic models in CKD have generally defined health states solely by the progression of CKD. This manuscript presents an alternative method which also considers the level of proteinuria in a CKD patient. Methods: A cohort-level state transition model was developed, comparing the health benefits of sparsentan, a dual endothelin angiotensin receptor antagonist, to irbesartan, an angiotensin receptor blocker, in IgAN. Within four UP/C (proteinuria) states, patients are assigned to three sub-health states according to CKD stage. Patients with end-stage renal disease are grouped together, irrespective of UP/C, and are stratified instead by renal replacement therapy modality. Transition matrices are derived from a combination of data from PROTECT, a clinical trial comparing sparsentan to irbesartan, and the UK RaDaR registry. Health-related quality of life data from a general CKD population is used as a proxy. Results: Patients with IgAN who were modelled to receive treatment with sparsentan had an estimated total undiscounted life years of 25.5 years, a gain of 0.9 years in comparison with irbesartan. Patients were also more likely to spend more time in earlier CKD stages while in pre-ESRD. This translated to significant quality-adjusted life year gains for patients treated with sparsentan in comparison with irbesartan. Conclusions: This study presents a new structure for health economic models in IgAN that more comprehensively captures the effect of proteinuria in combination with CKD progression. This new approach ultimately allows for the more robust implementation of clinical trial data in IgAN and estimates of the cost-effectiveness of new treatments.