Citations

Resistant hypertension (RH) is a high-risk phenotype characterized by blood pressure readings ≥130/80 mmHg despite maximally tolerated therapy with three antihypertensive agents, including a diuretic, or controlled blood pressure requiring four or more medications. The diagnosis of RH requires a structured evaluation that confirms accurate blood pressure measurement, excludes pseudoresistance—particularly nonadherence and white coat hypertension—and identifies secondary causes such as obstructive sleep apnea, primary aldosteronism, renovascular disease, pheochromocytoma, and Cushing syndrome. RH arises from overlapping mechanisms, including activation of the renin–angiotensin–aldosterone system (RAAS), sympathetic overactivity, arterial stiffness, volume expansion, and immune-mediated pathways. Management begins with lifestyle modification and optimized triple therapy, followed by mineralocorticoid receptor antagonists as the preferred fourth-line treatment. Emerging pharmacological options, such as sodium–glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, endothelin receptor antagonists, aldosterone synthase inhibitors, and angiotensin receptor and neprilysin inhibitors (ARNIs), offer additional therapeutic potential; meanwhile, device-based interventions, including renal denervation and baroreflex activation therapy, have shown sustained blood pressure reductions in selected patients. Future directions highlight precision medicine, digital health technologies, and artificial intelligence as methods to improve diagnosis, guide individualized therapy, and enhance long-term blood pressure control.

Immunotherapy has transformed oncology, yet kidney complications increasingly affect outcomes. This review summarizes nephrotoxicity from immune checkpoint inhibitors (ICIs), chimeric antigen receptor T-cell (CAR-T) therapies, and bispecific T-cell engagers (BiTEs). ICIs remain most used, with acute interstitial nephritis (AIN) as the hallmark lesion, while glomerular diseases and electrolyte abnormalities are less common. CAR-T therapy, though highly effective in hematologic cancers, carries risks of cytokine release syndrome, tumor lysis syndrome, and acute kidney injury (AKI). BiTEs, particularly teclistamab, show higher AKI rates than CAR-T, though mechanisms remain unclear. Early recognition, tailored management, and multidisciplinary collaboration are essential to ensure safe therapy and preserve kidney function.

Background: Vascular endothelial growth factor inhibitors (VEGF-I) are frequently used for cancer treatment. VEGF-I can cause proteinuria and acute kidney injury (AKI) with thrombotic microangiopathy (TMA) as a commonly described pathology, but other glomerular pathologies are not well characterized. We aim to describe the clinical characteristics and glomerular lesions associated with VEFG-I in a single center cohort. Methods: We performed a retrospective chart review of patients treated with VEGF-I and underwent kidney biopsies from 2010 to 2022 at the Mayo Clinic, Rochester, MN. Biopsy findings were reviewed by our pathologists. Data on patients’ characteristics, clinical course, and outcomes were abstracted. Descriptive statistics were used to report relevant patient characteristics and findings. Results: From 2010 to 2022, 19 kidney biopsies were performed for kidney dysfunction in patients on VEGF-I. Eleven had complete data, with a median age of 62 years (interquartile range 58–66 years); renal cell carcinoma (RCC) was the most common cancer (4 of 11 patients). TMA was noted in 8 of the 11 biopsies, with proteinuria as the most frequent indication for biopsy in these cases. Three patients had findings other than TMA. One developed anti-phospholipase A2 receptor negative membranous nephropathy; VEGF-I and pembrolizumab were discontinued, and prednisone improved proteinuria. Another patient had known cryoglobulinemia with nephrotic range proteinuria which was exacerbated by VEGF-I peaking at 11 g/day. Despite stopping VEGF-I and treating with prednisone and rituximab, kidney dysfunction progressed to end stage kidney disease (ESKD). A third patient had IgA nephropathy with concurrent diabetic changes, but proteinuria progressed even after stopping VEGF-I. Conclusion: In this case-series of patients treated with VEGF-I undergoing kidney biopsy, we describe the pathological characteristics, clinical course, and outcomes of patients with pathologies other than TMA. Our study adds information to the sparse literature on patients with renal dysfunction after receiving VEGF-I.

Abstract Background: Chronic kidney disease (CKD) has been associated with higher risk of gastrointestinal disorders, particularly Gastroesophageal reflux disease (GERD). However, the magnitude of this association and the underlying mechanisms remains unclear. Methods: A systematic search was conducted across major databases from inception to November 2024. We included cross-sectional and case-control studies evaluating the relationship between CKD and GERD. Data were extracted and analyzed using a random-effects model to calculate pooled odds ratios (ORs) and prevalence rates. Study quality was assessed using the Newcastle-Ottawa Scale, and heterogeneity was evaluated using the Cochran’s Q test and I² statistic. Results: Nine studies involving 4,650,709 participants were included. The pooled prevalence of GERD among CKD patients was 18% (95% CI: 0.10–0.26, I² =93.64%). The pooled crude OR for the association between CKD and GERD was 2.53 (95% CI: 1.30–4.92) and adjusted OR was 1.48 (95% CI: 1.05–2.08). Conclusion: This meta-analysis reveals a marginally significant association between CKD and GERD, highlighting higher prevalence of GERD among individuals with CKD. Furthers studies are needed to elucidate the underlying pathophysiological mechanisms and potential clinical implications.

ABSTRACT Background and Hypothesis Teclistamab, a novel bispecific monoclonal antibody targeting CD3 and B cell maturation antigen (BCMA), and chimeric antigen receptor T cell (CAR-T) therapy are promising options for treating relapsed/refractory multiple myeloma (MM). However, the rates of acute kidney injury (AKI) associated with teclistamab remain inadequately characterized. This study aims to compare the incidence, severity, and outcomes of AKI between patients receiving teclistamab and CAR-T therapy. Methods This was a retrospective study involving 64 patients with relapsed/refractory MM treated with either teclistamab or CAR-T therapy. All patients had previously received at least four lines of chemotherapy before being treated with either teclistamab or CAR-T. The primary outcome was the incidence of AKI, and secondary outcomes included AKI severity, kidney recovery rates, and mortality. Kaplan–Meier estimates for AKI-free survival were calculated, and hazard ratios (HRs) for AKI risk were determined using Cox proportional hazards models. Results Sixty-four patients met inclusion criteria for this study (30 received CAR-T and 34 received teclistamab therapy). Among these patients, 14 AKI events occurred in total (22%), with 10 events (29%) in the teclistamab group and four events (13%) in the CAR-T group. AKI-free survival estimates at 180 days after treatment initiation were 68% [95% confidence interval (CI): 53%–87%] for teclistamab patients and 90% (95% CI: 79%–100%) for CAR-T patients. While patients receiving teclistamab were found to have an increased risk of an AKI event compared to those receiving CAR-T therapy, the results were not statistically significant [HR (95% CI): 3.38 (0.93–12.31), P = .065]. Conclusions This study suggests that patients treated with teclistamab may experience a higher incidence of AKI compared to those receiving CAR-T therapy. However, further research is required to determine whether this increased risk is attributable to disease progression or teclistamab itself. These results highlight the need for close kidney function monitoring in patients receiving teclistamab.

ABSTRACT We report a case of acute interstitial nephritis (AIN) in a 68-year-old male with squamous cell carcinoma (SCC) and relapsed/refractory multiple myeloma (RRMM) who developed acute kidney injury (AKI) shortly after starting teclistamab for RRMM. Despite stable renal function on immune checkpoint inhibitor (ICI) therapy for SCC, proton pump inhibitors and trimethoprim-sulfamethoxazole for 3 years, AKI only occurred post-teclistamab initiation. Biopsy-confirmed AIN with serum creatinine improved only after pulse-dose steroids. This case highlights a potential synergistic nephrotoxic effect of teclistamab and ICIs, warranting further investigation into teclistamab's renal safety.