Perspectives in Renal Medicine
Kidney International (2001) 59, 2005–2022; doi:10.1046/j.1523-1755.2001.00716.x
Treatment prospects for autosomal-dominant polycystic kidney disease
Qi Qian, Peter C Harris and Vicente E Torres
Mayo Clinic/Mayo Foundation, Rochester, Minnesota, USA
Correspondence: Vicente E. Torres, M.D., Eisenberg S33B, Nephrology, Mayo Clinic, 200 First St SW, Rochester, Minnesota 55905, USA. E-mail: torres.vicente@mayo.edu
Received 29 September 2000; Revised 22 November 2000; Accepted 1 December 2000.
Abstract
Treatment prospects for autosomal-dominant polycystic kidney disease. An increased understanding of the molecular genetic and cellular pathophysiologic mechanisms responsible for the development of autosomal-dominant polycystic kidney disease (ADPKD), made possible by the advances in molecular biology and genetics of the last three decades, has laid the foundation for the development of effective therapies. As the concept that a polycystic kidney is a neoplasm in disguise is becoming increasingly accepted, the development of therapies for ADPKD may benefit greatly from the expanding body of information on cancer chemoprevention and chemosuppression. This review summarizes the observations that already have been made and discusses therapies for PKD that deserve investigation.
Keywords:
antimutagens, antioxidants, soy protein, fish oil, EGF receptor, tyrosine kinase inhibitors
Abbreviations:
AA, arachidonic acid; ADPKD, autosomal-dominant polycystic kidney disease; Ang, angiotensin; APC, adenomatous polyposis coli; ARPKD, autosomal-recessive polycystic kidney disease; AT1, angiotensin II type 1; ATP, adenosine 5'-triphosphate; AVP-V2R, arginine vasopressin-V2 receptor; CAF, cyst activating factor; CAM, cell adhesion molecule; cAMP, cyclic adenosine-3', 5' monophosphate; CFTR, cystic fibrosis transmembrane conductance regulator; COX-2, cyclooxygenase-2; DAG, diacylglycerol; DHA, docosahexaenoic acid; Dvl, Discheveled (receptor); EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; EPA, eicosapentaenoic acid; ERK, extracellular signal-regulated kinase; FA, fatty acid; FAK, focal adhesion kinase; GDP, guanosine diphosphate; GFR, glomerular filtration rate; GTP, guanosine triphosphate; GTPase, endogenous guanosine triphosphatase; HMG-CoA, 3-hydroxy-3-methylglutaryl coenzyme A; IL, interleukin; LA, 
-6 linoleic acid; LEF-1, lymphoid-enhancing transcription factor; LNA, -3 linolenic acid; L-NAME, NG-nitro-L-arginine methyl ester; LT, leukotriene; MAPK, mitogen activated protein kinase; MCP, monocyte chemotactic protein; MEK, mitogen extracellular kinase; MMP, matrix metalloproteinase; NO, nitric oxide; OPN, osteopontin; PG, prostaglandin; PI3K, phosphatidylinositol-3 kinase; PI3P, phosphatidylinositol-3 phosphate; PIP2, phosphatidylinositol (4,5)-bisphosphate; PKA, protein kinase A; PKA-1, protein kinase A type 1 isoform; PKA-2, protein kinase A type 2 isoform; PKB, protein kinase B; PKD, polycystic kidney disease; PLC
, phospholipase C; RAR, retinoid acid receptor; RXR, retinoid X-receptor; TACE, tumor necrosis factor-
converting enzyme; TCF, T cell factor; TIMP, tissue inhibitor of matrix metalloproteinase; TNF-, tumor necrosis factor-
