title: Polycystic kidneys have decreased vascular density: a micro-CT study.
abstract: OBJECTIVE
  Polycystic kidney disease (PKD) is a common cause of end-stage renal failure and many of these patients suffer vascular dysfunction and hypertension. It remains unclear whether PKD is associated with abnormal microvascular structure. Thus, this study examined the renovascular structure in PKD.
  
  
  METHODS
  PKD rats (PCK model) and controls were studied at 10 weeks of age, and mean arterial pressure (MAP), renal blood flow, and creatinine clearance were measured. Microvascular architecture and cyst number and volume were assessed using micro-computed tomography, and angiogenic pathways evaluated.
  
  
  RESULTS
  Compared with controls, PKD animals had an increase in MAP (126.4 ± 4.0 vs. 126.2 ± 2.7 mmHg) and decreased clearance of creatinine (0.39 ± 0.09 vs. 0.30 ± 0.05 mL/min), associated with a decrease in microvascular density, both in the cortex (256 ± 22 vs. 136 ± 20 vessels per cm2) and medullar (114 ± 14 vs. 50 ± 9 vessels/cm2) and an increase in the average diameter of glomeruli (104.14 ± 2.94 vs. 125.76 ± 9.06 mm). PKD animals had increased fibrosis (2.2 ± 0.2 fold vs. control) and a decrease in the cortical expression in hypoxia inducible factor 1-α and vascular endothelial growth factor.
  
  
  CONCLUSIONS
  PKD animals have impaired renal vascular architecture, which can have significant functional consequences. The PKD microvasculature could represent a therapeutic target to decrease the impact of this disease.
authors.affiliation: Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA.
authors.forename: Rende
authors.initials: R
authors.lastname: Xu
authors.forename: Federico
authors.initials: F
authors.lastname: Franchi
authors.forename: Brent
authors.initials: B
authors.lastname: Miller
authors.forename: John A
authors.initials: JA
authors.lastname: Crane
authors.forename: Karen M
authors.initials: KM
authors.lastname: Peterson
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Psaltis
authors.forename: Peter C
authors.initials: PC
authors.lastname: Harris
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
authors.forename: Martin
authors.initials: M
authors.lastname: Rodriguez-Porcel
mesh_terms: D000581:Amidohydrolases / Q000097:blood; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D007672:Kidney Cortex / Q000098:blood supply / Q000000981:diagnostic imaging / Q000473:pathology; D007678:Kidney Glomerulus / Q000098:blood supply / Q000000981:diagnostic imaging / Q000473:pathology; D007679:Kidney Medulla / Q000098:blood supply / Q000000981:diagnostic imaging / Q000473:pathology; D008222:Lymphokines; D008833:Microcirculation / Q000502:physiology*; D009389:Neovascularization, Pathologic / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology*; D007690:Polycystic Kidney Diseases / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D011922:Rats, Mutant Strains; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000502:physiology*; D055114:X-Ray Microtomography
chemical_list: D008222:Lymphokines; C092591:fibrosin; D000581:Amidohydrolases; C019946:creatininase