{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T09:04:21Z","timestamp":1790845461053,"version":"4.1.0"},"reference-count":107,"publisher":"MDPI AG","issue":"18","license":[{"start":{"date-parts":[[2024,9,23]],"date-time":"2024-09-23T00:00:00Z","timestamp":1727049600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nutrients"],"abstract":"<jats:p>Polycystic kidney disease (PKD) includes autosomal dominant (ADPKD) and autosomal recessive (ARPKD) forms, both of which are primary genetic causes of kidney disease in adults and children. ADPKD is the most common hereditary kidney disease, with a prevalence of 329 cases per million in Europe. This condition accounts for 5\u201315% of end-stage chronic kidney disease (ESKD) cases, and in developed countries such as Poland, 8\u201310% of all dialysis patients have ESKD due to ADPKD. The disease is caused by mutations in the PKD1 and PKD2 genes, with PKD1 mutations responsible for 85% of cases, leading to a more aggressive disease course. Recent research suggests that ADPKD involves a metabolic defect contributing to cystic epithelial proliferation and cyst growth. Aim: This review explores the interplay between metabolism, obesity, and ADPKD, discussing dietary and pharmacological strategies that target these metabolic abnormalities to slow disease progression. Conclusion: Metabolic reprogramming therapies, including GLP-1 analogs and dual agonists of GIP\/GLP-1 or glucagon\/GLP-1 receptors, show promise, though further research is needed to understand their potential in ADPKD treatment fully.<\/jats:p>","DOI":"10.3390\/nu16183216","type":"journal-article","created":{"date-parts":[[2024,9,23]],"date-time":"2024-09-23T09:15:07Z","timestamp":1727082907000},"page":"3216","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["The Influence of Non-Pharmacological and Pharmacological Interventions on the Course of Autosomal Dominant Polycystic Kidney Disease"],"prefix":"10.3390","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5853-2147","authenticated-orcid":false,"given":"Karolina","family":"K\u0119dzierska-Kapuza","sequence":"first","affiliation":[{"name":"Department of Internal Diseases, Endocrinology and Diabetology, National Medical Institute of the Ministry of Interior and Administration, 137 Wo\u0142oska St., 02-507 Warsaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0002-9917","authenticated-orcid":false,"given":"Inga","family":"\u0141opuszy\u0144ska","sequence":"additional","affiliation":[{"name":"Department of Gastroenterological Surgery and Transplantology, National Medical Institute of the Ministry of Interior and Administration, 137 Wo\u0142oska St., 02-507 Warsaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grzegorz","family":"Niewi\u0144ski","sequence":"additional","affiliation":[{"name":"Department of Gastroenterological Surgery and Transplantology, National Medical Institute of the Ministry of Interior and Administration, 137 Wo\u0142oska St., 02-507 Warsaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward","family":"Franek","sequence":"additional","affiliation":[{"name":"Department of Internal Diseases, Endocrinology and Diabetology, National Medical Institute of the Ministry of Interior and Administration, 137 Wo\u0142oska St., 02-507 Warsaw, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9808-0624","authenticated-orcid":false,"given":"Ma\u0142gorzata","family":"Szczuko","sequence":"additional","affiliation":[{"name":"Department of Human Nutrition and Metabolomic, Pomeranian Medical University, 24 W. 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