title: Method of renal mass reduction is a critical modulator of subsequent hypertension and glomerular injury.
abstract: The hypertension, proteinuria, and glomerulosclerosis that develop in the remnant kidney model (uninephrectomy plus infarction of approximately 2/3 of the other kidney) have been generally considered to represent the adverse consequences of a severe reduction in nephron number. To differentiate the blood pressure (BP) responses to infarction from those of reduced renal mass per se, BP was continuously monitored radiotelemetrically in rats whose total renal mass was reduced by 2/3 (infarction) and by 5/6 (infarction or surgical excision of both poles) and in sham-operated controls. Hypertension only developed in the two infarcted groups. Overall averages of systolic BP monitored every 10 min over 6 wk were 144 +/- 8 and 156 +/- 5 mm Hg in the 2/3 and 5/6 infarction groups (N = 10 each), respectively, as compared with 120 +/- 2 mm Hg (N = 12) in the approximately 5/6 surgical excision group (P < 0.01) and 117 +/- 5 mm Hg (N = 8) in controls. Changes in kidney weights, glomerular volumes, RBF, GFR, and renal autoregulatory ability after renal mass reduction by the two methods were qualitatively similar in additional animals from each group monitored for 2, 4, or 6 wk without radiotelemetry. Significant proteinuria and glomerulosclerosis only developed in the two infarction (hypertensive) groups. At 6 wk, 18 +/- 4 and 19 +/- 3% of the glomeruli exhibited injury in the 2/3 (N = 22) and the 5/6 infarction groups (N = 21), respectively, in contrast to 3 +/- 1% glomerular injury in the 5/6 surgical excision group (N = 24) (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Loyola University Medical Center, Maywood, IL.
authors.forename: K A
authors.initials: KA
authors.lastname: Griffin
authors.forename: M
authors.initials: M
authors.lastname: Picken
authors.forename: A K
authors.initials: AK
authors.lastname: Bidani
mesh_terms: D000818:Animals; D001835:Body Weight; D005923:Glomerulosclerosis, Focal Segmental / Q000209:etiology*; D006977:Hypertension, Renal / Q000209:etiology*; D007238:Infarction / Q000473:pathology*; D007668:Kidney / Q000098:blood supply* / Q000473:pathology; D007678:Kidney Glomerulus / Q000473:pathology*; D008297:Male; D009392:Nephrectomy / Q000009:adverse effects / Q000379:methods*; D011507:Proteinuria / Q000209:etiology; D051381:Rats; D017207:Rats, Sprague-Dawley