Polycystic kidney disease (PKD) is one of the most common hereditary kidney diseases, which is characterized by progressive cyst growth and secondary hypertension. In addition to cystogenesis and renal abnormalities, patients with PKD can develop vascular abnormalities and cardiovascular complications. Progressive cyst growth substantially alters renal structure and culminates into end-stage renal disease. There remains no cure beyond renal transplantation, and treatment options remain largely limited to chronic renal replacement therapy. In addition to end-stage renal disease, patients with PKD also present with hypertension and cardiovascular disease, yet the timing and interactions between the cardiovascular and renal effects of PKD progression are understudied. Here, we review the vascular dysfunction found in clinical and preclinical models of PKD, including the clinical manifestations and relationship to hypertension, stroke, and related cardiovascular diseases. Finally, our discussion also highlights the critical questions and emerging areas in vascular research in PKD.
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http://dx.doi.org/10.1159/000531647 | DOI Listing |
Am Fam Physician
January 2025
Western University Schulich School of Medicine and Dentistry, London, Ontario, Canada.
Vision loss affects more than 7 million Americans and impacts quality of life, independence, social functioning, and overall health. Common and dangerous conditions causing sudden vision loss include acute angle-closure glaucoma, retinal detachment, retinal artery occlusion, giant cell arteritis, and optic neuritis. Acute angle-closure glaucoma features ocular pain, headache, and nausea; treatment includes pilocarpine eye drops, oral or intravenous acetazolamide, and intravenous mannitol.
View Article and Find Full Text PDFStem Cells Transl Med
January 2025
Developmental and Stem Cell Biology Program, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON, Canada M5G 0A4.
Disruption of developmental processes affecting the fetal lung leads to pulmonary hypoplasia. Pulmonary hypoplasia results from several conditions including congenital diaphragmatic hernia (CDH) and oligohydramnios. Both entities have high morbidity and mortality, and no effective therapy that fully restores normal lung development.
View Article and Find Full Text PDFOpen Med (Wars)
January 2025
Endocrine Department, 920th Hospital of Joint Logistics Support Force, PLA, No. 212 Daguan Road, Xishan District, Kunming, 650000, Yunnan, China.
Background: Diabetes-related cognitive impairment is increasingly recognized as a significant complication, profoundly impacting patients' quality of life. This review aims to examine the pathophysiological mechanisms, clinical manifestations, risk factors, assessment and diagnosis, management strategies, and future research directions of cognitive impairment in diabetes.
Methodology: A comprehensive literature search was conducted using PubMed, Medline, and other medical databases to identify, review, and evaluate published articles on cognitive impairment in diabetes.
Adv Ther (Weinh)
January 2025
Department of Urology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Division of Pediatric Urology, Department of Surgery, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL 60611, USA; Center for Regenerative Nanomedicine, Northwestern University, Chicago, IL 60611, USA; Department of Biomedical Engineering, McCormick School of Engineering, Northwestern University, Evanston, IL 60208, USA.
Impaired bladder compliance secondary to congenital or acquired bladder dysfunction can lead to irreversible kidney damage. This is managed with surgical augmentation utilizing intestinal tissue, which can cause stone formation, infections, and malignant transformation. Co-seeded bone marrow mesenchymal stem cell (MSC)/CD34+ hematopoietic stem cell (HSPC) scaffolds (PRS) have been successful in regenerating bladder tissue.
View Article and Find Full Text PDFMedComm (2020)
February 2025
Pulmonary endothelial cell (EC) activation is a key factor in acute respiratory distress syndrome (ARDS). In sepsis, increased glycolysis leads to lactate buildup, which induces lysine lactylation (Kla) on histones and other proteins. However, the role of protein lactylation in EC dysfunction during sepsis-induced ARDS remains unclear.
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