title: Compensatory growth of congenital solitary kidneys in pigs reflects increased nephron numbers rather than hypertrophy.
abstract: BACKGROUND
  Patients with unilateral MultiCystic Kidney Dysplasia (MCKD) or unilateral renal agenesis (URA) have a congenital solitary functioning kidney (CSFK) that is compensatory enlarged. The question whether this enlargement is due to increased nephron numbers and/or to nephron hypertrophy is unresolved. This question is of utmost clinical importance, since hypertrophy is associated with a risk of developing hypertension and proteinuria later in life with consequent development of CKD and cardiovascular disease.
  
  
  RESULTS
  In a cohort of 32,000 slaughter pigs, 7 congenital solitary functioning kidneys and 7 control kidneys were identified and harvested. Cortex volume was measured and with a 3-dimensional stereologic technique the number and volume of glomeruli was determined and compared. The mean total cortex volume was increased by more than 80% and the mean number of glomeruli per kidney was 50% higher in CSFKs than in a single control kidney, equaling 75% of the total nephron number in both kidneys of control subjects. The mean total glomerular volume in the CSFKs was not increased relative to the controls.
  
  
  CONCLUSIONS
  Thus, in pigs, compensatory enlargement of a CSFK is based on increased nephron numbers. Extrapolation of these findings to the human situation suggests that patients with a CSFK might not be at increased risk for developing hyperfiltration-associated renal and cardiovascular disease in later life due to a lower nephron number.
authors.affiliation: Department of Pathology, University Medical Center, Utrecht, The Netherlands.
authors.forename: Stefan H
authors.initials: SH
authors.lastname: van Vuuren
authors.forename: Chalana M
authors.initials: CM
authors.lastname: Sol
authors.forename: Roel
authors.initials: R
authors.lastname: Broekhuizen
authors.forename: Marc R
authors.initials: MR
authors.lastname: Lilien
authors.forename: Michiel J S
authors.initials: MJ
authors.lastname: Oosterveld
authors.forename: Tri Q
authors.initials: TQ
authors.lastname: Nguyen
authors.forename: Roel
authors.initials: R
authors.lastname: Goldschmeding
authors.forename: Tom P V M
authors.initials: TP
authors.lastname: de Jong
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006984:Hypertrophy / Q000503:physiopathology*; D007668:Kidney / Q000473:pathology / Q000502:physiology*; D007674:Kidney Diseases / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000378:metabolism*; D015233:Models, Statistical; D009399:Nephrons / Q000502:physiology*; D015588:Observer Variation; D012306:Risk; D013552:Swine