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PURPOSE: Renovascular anatomical variations pose potential surgical challenges during paraaortic lymphadenectomy (PaLA) in gynecologic oncology. This study aimed to document the prevalence and intraoperative characteristics of renovascular variations encountered during PaLA, and to describe their management through detailed photographic documentation. METHODS: This retrospective single-center observational study included 42 patients with gynecologic malignancies (24 endometrial, 16 ovarian, 2 cervical cancers) who underwent PaLA at Ankara, Türkiye, between February 2024 and February 2025. Procedures were performed laparoscopically (n = 20, 47.6%) or via laparotomy (n = 22, 52.4%). Patients underwent preoperative contrast-enhanced abdominal CT (slice thickness ≤ 3 mm). Renovascular variations were identified intraoperatively, photographed, and classified anatomically. RESULTS: Renovascular variations were identified in 9 patients (21.4%). Inferior polar renal arteries occurred in 5 patients (11.9%): 2 bilateral, 3 unilateral right-sided. Retroaortic left renal vein was encountered in 4 patients (9.5%). Preoperative imaging identified variations in 8 of 9 cases (88.9%), with one small-caliber artery missed on imaging. No vascular injuries occurred in cases with recognized variations. All laparoscopic cases with variations (n = 4) were completed without conversion. CONCLUSION: Renovascular variations occurred in one-fifth of patients undergoing PaLA in this series. While preoperative imaging identified most variations, intraoperative vigilance remains essential. With careful surgical technique and anatomical awareness, these variations can be safely managed, though the small sample size limits generalizability. This series provides educational documentation for gynecologic oncologists.

Renovascular hypertension is the most common cause of secondary hypertension and occurs in 0.5% to 5% of individuals with hypertension. This is more common in individuals who have difficulty controlling their pressure or elderly patients with end-stage kidney disease. An evaluation for renovascular hypertension is indicated if there is a high level of clinical suspicion. The primary imaging modalities for assessing renovascular hypertension are ultrasound, CT, and MRI, and these options can vary depending on the patient's current renal status. Although ultrasound is beneficial since it uses nonionizing radiation, CT with contrast provides excellent spatial resolution. In patients with decreased renal function, MRI is a reliable alternative. The American College of Radiology Appropriateness Criteria are evidence-based guidelines for specific clinical conditions that are reviewed annually by a multidisciplinary expert panel. The guideline development and revision process support the systematic analysis of the medical literature from peer reviewed journals. Established methodology principles such as Grading of Recommendations Assessment, Development, and Evaluation or GRADE are adapted to evaluate the evidence. The RAND/UCLA Appropriateness Method User Manual provides the methodology to determine the appropriateness of imaging and treatment procedures for specific clinical scenarios. In those instances where peer reviewed literature is lacking or equivocal, experts may be the primary evidentiary source available to formulate a recommendation.

Posterior reversible encephalopathy syndrome (PRES) can develop in the setting of severe hypertension and may present with seizures and altered consciousness. We report the case of an 81-year-old woman who presented with impaired consciousness and generalized seizures during a hypertensive crisis. Brain magnetic resonance imaging revealed bilateral parieto-occipital subcortical hyperintensities. Diagnostic imaging revealed severe proximal stenosis of the right renal artery, complete occlusion of the left renal artery, and marked atrophy of the left kidney, suggesting renovascular hypertension due to renal artery stenosis in a solitary functioning kidney. Based on these findings, PRES secondary to renovascular hypertension was diagnosed, and percutaneous renal angioplasty was performed, resulting in stabilization of blood pressure and resolution of neurological symptoms. This case highlights the importance of considering renovascular hypertension as a reversible cause of PRES, especially in patients with a solitary kidney and marked blood pressure elevation and variability.

The present study investigated efficacy of Ocimum tenuiflorum fermented beverage in the amelioration of renovascular-hypertension in 2K1C model. Hypertension was induced by clipping the left renal artery. The hypertensive rats exhibited elevated systolic, diastolic, and mean arterial pressure; increased heart rate; activity of angiotensin-converting enzyme (ACE); and elevated serum and renal levels of angiotensin II. Additionally, liver and heart functions were impaired, accompanied by increased expression of α-skeletal actin, indicating organ damage associated with hypertension. However, administration of the fermented tulsi beverage for six weeks led to partial restoration of these parameters. The mechanism of action involves the suppression of ACE activity, as supported by gene expression analysis. The observed efficacy may be attributed to the beverage's rich polyphenolic content and high bioavailability. To our knowledge, this is the first report demonstrating the ameliorative potential of a fermented tulsi beverage against renovascular hypertension in a 2K1C rat model.

Percutaneous transluminal renal angioplasty (PTRA) is a treatment for renovascular hypertension due to renal artery stenosis. However, postoperative complications in stent re-stenosis/occlusion may occur frequently. A 60-year-old male patient presented to our hospital with uncontrolled hypertension and a deterioration of renal function. He had undergone an initial renal stenting 10 years earlier, followed by repeat PTRAs during follow-up for in-stent restenosis. The left renal stent was found to be completely occluded, while the right renal stent was found to be 75% stenosed. We performed an aorto-renal artery bypass. The bypass was patent without stenosis and the renovascular hypertension was recovered.

PURPOSE OF REVIEW: This narrative review aims to summarize what is currently understood about Neurofibromatosis Type 1 (NF-1) and renovascular hypertension (RVH) in children, including clinical presentation and diagnosis, epidemiology, genetics, and management considerations including advances in treatment modalities. RECENT FINDINGS: Most of what is currently understood about NF-1 and arterial dysplasia leading to RVH relies on the inclusion of patients with NF-1 in single-institution reports. The management of pediatric RVH often requires multi-modal therapies inclusive of anti-hypertensive medications and revascularization for refractory cases, through catheter-based (i.e., endovascular) and open surgical means. There is a need to develop genotype-targeted guidelines for the diagnosis and management of pediatric aorto-renal dysplasia resulting in RVH in patients with NF-1. While our understanding of pediatric RVH and NF-1 has evolved over the past decade, critical research questions have emerged that encompass epidemiology, etiology and genetics. These research questions require immediate attention to establish and optimize standardized diagnostic and treatment guidelines.

We evaluated kidney fibrosis in renovascular disease (RVD) using quantitative (q) and semi-quantitative magnetization-transfer (MT) magnetic resonance imaging (MRI). Ten RVD patients and 22 healthy volunteers (HVs) were prospectively enrolled. Of HVs, 10 (HV-1) underwent imaging studies whereas plasma samples were collected from 12 others (HV-2). The qMT-derived bound-pool fraction (f) was compared to MRI-based MT imaging (MTI)-derived MT ratio (MTR), blood oxygenation-level-dependent (BOLD) R2*, and diffusion-weighted imaging (DWI) apparent diffusion coefficient (ADC). MTR was assessed at offset frequencies of 600 Hz and 1000 Hz, and RVD qMT and MTI on both 1.5T and 3.0T MRI. Additionally, we measured plasma and urinary levels of fibrogenic cytokines and micro-RNAs, and stenotic kidney (STK) perfusion and volume with multidetector computed-tomography (MDCT). At 3.0T-MRI, STK cortex and medulla qMT-f were higher in RVD vs. HV-1 (p = 0.01, p = 0.05, respectively), as was MTR-600 Hz, whereas BOLD-R2* and the DWI ADC were not different. MTR and f measured at 1.5T were comparable to those obtained at 3.0T. STK blood flow was decreased vs. the contralateral kidney (CLK) (p = 0.033) but plasma and urinary fibrogenic indices were unchanged in RVD vs. HV-2. Both f and MTI at 3.0T-MRI may be useful for noninvasive assessment of STK fibrosis, independent of magnetic-field strength. MTI is potentially more sensitive than fibrogenic cytokine levels for detecting mild RVD-related fibrosis changes.

Background: Scattered tubular-like cells (STCs) are dedifferentiated renal tubular cells that repair other damaged kidney cells. STCs may be damaged and rendered ineffective by renovascular disease (RVD), but the underlying mechanisms remain unknown. We hypothesized that RVD induces changes in methylated (5mC) and hydroxymethylated (5hmC) DNA and modulates the transcriptomic profile and functional properties of swine STCs. Methods: CD24+/CD133+ STCs were harvested from pig kidneys after 10 weeks of RVD or sham (n=6 each) and their 5mC and 5hmC profiles of individual peaks were examined by immunoprecipitation sequencing (MeDIP-/hMeDIP-seq, respectively, n=3 each). Integrated (MeDIP/hMeDIPseq/mRNA-seq) analysis was performed followed by functional analysis of overlapping differentially expressed (DE) genes. STC-protective effects were assessed in vitro before and after epigenetic (Bobcat339) modulation. Results: MeDIP-seq analysis identified 1,362 hyper-methylated and 1,432 hypo-methylated peaks in RVD-STCs compared to Normal-STCs, which correlated with 80 upregulated and 55 downregulated genes in RVD-STCs. hMeDIP-seq revealed 1,447 hyper-hydroxymethylated and 765 hypo-hydroxymethylated peaks in RVD-STCs versus Normal-STCs, which correlated with 80 genes upregulated and 53 downregulated in RVD-STCs. Overlapping upregulated genes were mainly implicated in the regulation of oxidative phosphorylation, apoptosis, and lipid metabolism (e.g., STAT6), whereas overlapping downregulated genes were mainly involved in cell proliferation. Importantly, RVD increased STAT6 protein expression and impaired the proliferative capacity of STCs, which were partially reversed by treatment with Bobcat339, which also enhanced the ability of RVD-STCs to promote the viability of injured tubular epithelial cells. Conclusions: Renal ischemia induces locus-specific epigenetic alterations, associated with transcriptomic changes and impaired reparative function of swine STCs. These observations may contribute to develop novel approaches to preserve the reparative capacity of STCs in individuals with RVD.

Renovascular hypertension can be clinically challenging to diagnose. The most common etiology remains atherosclerotic disease. When medical management fails, renal artery revascularization is considered. Since the advent of endovascular interventions and the outcomes of CORAL (Benefits of Medical Therapy Plus Stenting for Renal Atherosclerotic Lesions), surgical management of renal artery stenosis has shown a decrease in prevalence. Our experience demonstrates a viable solution for patients requiring open surgery with limited inflow options.

Median Arcuate Ligament Syndrome (MALS) typically causes gastrointestinal symptoms due to celiac artery compression. Rarely, extrinsic compression of the renal artery may lead to renovascular hypertension. We report a 15-year-old boy with progressive renal asymmetry and poorly controlled hypertension without abdominal symptoms. Imaging demonstrated compression of the celiac trunk and left renal artery by the median arcuate ligament and diaphragmatic crura. Open surgical decompression restored renal artery flow and normalized blood pressure. This case highlights an unusual pediatric presentation of MALS and emphasizes that early recognition and timely surgical intervention can prevent irreversible renal vascular damage.

Immunoglobulin A vasculitis (IgAV) is the most common cause of vasculitis among children. However, it is a very rare cause of large artery vasculitis. The histopathology of immunoglobulin A vasculitis typically involves IgA deposits in small vessels of the dermis, joints, kidneys, and gastrointestinal tract. These deposits induce an inflammatory response, activating the complement system, which explains the variety of symptoms and signs. A 14-year-old Levantine Arab male with malignant refractory hypertension and prior left nephrectomy was referred for evaluation. The initial presentation at the age of 4 years revealed severe bilateral renal artery stenosis, left ventricular hypertrophy, and reduced ejection fraction (31%), which improved with medical therapy. Parents declined vascular interventions. At the age of 7 years, left kidney atrophy and total occlusion of the left renal artery led to nephrectomy. At the age of 14 years, hypertension worsened despite multiple antihypertensives. Imaging showed total occlusion of the right renal artery. A multidisciplinary team recommended autotransplantation of the solitary right kidney to the left iliac fossa. Postoperative recovery included transient anuria, followed by normalization of renal function and blood pressure. Histopathology revealed IgA-mediated vascular changes without amyloid deposition. The 1-month follow-up showed controlled blood pressure (130/80 mmHg) on reduced antihypertensive therapy. This rare case sheds light on malignant renovascular hypertension in a young male, possibly due to IgA deposition in the right renal artery after a previous left nephrectomy. The surgical decision took into consideration the young age of the patient and the eventual characteristics of the renal artery, in addition to the size of the artery; therefore, we preferred and proceeded to an auto kidney transplant rather than aortorenal bypass, believing that the arterial anastomosis, which is the most important, could be more convenient from the hemodynamic point of view.

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Renal artery stenosis is one of the severe secondary hypertension (HTN) causes in children and may lead to hypertension-mediated organ damage (HMOD), including left ventricle hypertrophy (LVH). We describe a case of a 4-year-old boy with severe renovascular HTN and LVH during infancy. Genetic testing revealed variant of unknown significance in SMAD3, a gene linked to Loeys-Dietz syndrome. The patient was treated with intensive pharmacotherapy and percutaneous intravascular intervention. Early onset of HTN and HMOD should prompt consideration of genetic evaluation to aid diagnosis and management. In this case, a heterozygous SMAD3 variant coexisted with renal artery stenosis without the development of aortic aneurysms.

Atherosclerotic renal artery stenosis (ARAS) remains a complex contributor to hypertension and kidney disease. Although randomized trials failed to show benefit of revascularization on top of medical therapy over medical therapy alone, mounting evidence suggests that earlier stages of ARAS may still be clinically relevant. In this review, we will reevaluate assumptions about the relationship between lesion severity and clinical outcomes and highlight the discrepancy between angiographic definitions of significant stenosis and functional renal impairment. We suggest that with all degrees of angiographically identified ARAS, particularly in patients with refractory hypertension, Kidney failure, or flash pulmonary edema, the hemodynamic importance of the stenosis should be estimated. In this regard, a pressure drop of 10% or more across the stenosis is an indication that hypertension may be related to the obstruction. Because the classical definition of a hemodynamically significant stenosis precludes earlier and potentially more adequate opportunities for intervention, it is presently unknown if patients with ARAS of less than 60% stenosis would benefit from mechanical treatment. We suggest reevaluating the thresholds for intervention and call for new trials focused on early-stage atherosclerotic renal vascular disease.

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In middle-aged and older atherosclerotic renal artery stenosis (ARAS), the anatomical severity of stenosis is a poor surrogate for microvascular competence, and the renal benefit of revascularization is unpredictable. We developed Renal-Video-AI, a self-supervised deep learning framework (Video Swin Transformer with VideoMAE pretraining) that extracts spatiotemporal hemodynamic features from contrast-enhanced ultrasound, and applied it to a multi-center Discovery Cohort (N = 1,226), an independent External Validation Cohort (N = 122), a prospective Multimodal Cohort with paired 10x Visium spatial transcriptomics (N = 57), and an aged two-kidney-one-clip (2K1C) murine model. Unsupervised phenomapping identified 3 intrinsic hemodynamic phenotypes-Preserved, Delayed, and Rarefied. The Rarefied phenotype predicted major adverse renal events (MAREs) independently of anatomical stenosis [hazard ratio (HR) 4.82, 95% confidence interval (CI) 3.10 to 6.50; Fine-Gray subdistribution HR (sHR) 5.1], and adding the phenotype to a standard clinical model improved the C-statistic from 0.72 to 0.88. A significant phenotype-by-treatment interaction (P < 0.01) showed that stenting reduced events only in the Delayed phenotype (HR 0.52, 95% CI 0.35 to 0.78), not in the Preserved (HR 0.98) or Rarefied (HR 1.05) phenotypes. In absolute terms, stenting reduced the 3-year cumulative incidence of MARE in the Delayed phenotype from 25.4% to 13.2% (absolute risk reduction 12.2%; number needed to treat = 8, 95% CI 6 to 13), with no benefit in the Preserved (8.4% versus 8.0%) or Rarefied (38.6% versus 39.4%) phenotypes. Spatial transcriptomics localized a hypoxia and pyroptosis signature to rarefied tissue, and the aged 2K1C model revealed a mitochondrial reactive oxygen species (ROS)-NLRP3-pyroptosis axis whose pharmacological inhibition (MCC950) restored microvascular perfusion. AI video-phenomapping thus reframes the revascularization decision around microvascular competence rather than anatomy, identifying both therapeutic futility (Rarefied) and a treatable window (Delayed), and nominates NLRP3-driven pyroptosis as a therapeutic target.

Anlotinib is a multi-target tyrosine kinase inhibitor that has been approved in China as a third-line treatment for advanced non-small cell lung cancer. It exerts anti-tumor effects by inhibiting tumor growth and tumor angiogenesis, and its toxicity also arises from this mechanism. Anlotinib can damage vascular endothelium, thereby inducing cardiovascular toxicity, which leads to hypertension, hyperlipidemia, accelerated atherosclerosis, and the initiation of atherosclerotic cardiovascular disease, ultimately resulting in life-threatening cardiovascular events. To the best of our knowledge, this study is the first case report documenting the development of hypertension, hyperlipidemia, hypothyroidism, subsequent discovery of bilateral renal artery stenosis, and acute myocardial infarction in a young patient receiving anlotinib treatment. This showed anlotinib may accelerate systemic large/medium-sized artery atherosclerosis in the context of complex tumor therapy, causing life-threatening cardiovascular events. Besides, it highlights the necessity of regular monitoring of relevant indicators during follow-up for patients undergoing anlotinib therapy, enabling early detection of warning signs and timely intervention.