IGF-I inhibitors reduce compensatory hyperfiltration in the isolated rat kidney following unilateral nephrectomy
Related Experiment Video
Updated: Oct 18, 2026

Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
Published on: August 9, 2013
J L Haylor1, I H McKillop, S D Oldroyd
1Sheffield Kidney Institute, Northern General Hospital, Sheffield, UK.
Background:
A role for insulin-like growth factor-I (IGF-I) as a mediator of renal hyperfiltration and hyperperfusion following unilateral nephrectomy (UNx) has been examined.
Methods:
Adult male Wistar rats were subjected to either left UNx or sham operation. Twenty one days after surgery, the right kidney was removed under barbiturate anaesthesia, and renal function was measured ex vivo using an isolated rat kidney perfusion system. The glomerular filtration rate was assessed from the renal clearance of [(14)C]inulin.
Results:
UNx stimulated renal growth as shown by a significantly higher (P<0.02) tissue dry weight in kidneys from UNx (0.45+/-0.02 g) than from sham-operated rats (0.31+/-0.02 g). Compensatory hyperfiltration could be detected ex vivo; kidneys obtained from UNx rats having a significantly higher (P<0.05) [(14)C]inulin clearance (0.75+/-0.08 ml/min, n=8) than kidneys obtained from sham-operated animals (0.39+/-0.05 ml/min, n=8). Compensatory hyperperfusion was also detected ex vivo; kidneys obtained from UNx rats having a significantly higher (P<0.05) renal perfusate flow (28.2+/-2.7 ml/min) than kidneys obtained from sham-operated rats (22.5+/-0.8 ml/min). Following perfusion with either 50 microg monoclonal IGF-I antibody (n=4) or 6.5 microM genistein (n=4), an inhibitor of tyrosine kinase, no significant difference in [(14)C]inulin was observed between kidneys obtained from either UNx or sham-operated rats. In contrast to hyperfiltration, renal hyperperfusion remained unaffected by the IGF-I antibody and was only reduced by 30% following genistein administration.
Conclusions:
The results suggest a role for renal IGF-I as a mediator of compensatory hyperfiltration in the rat.
Related Concept Videos
Antihypertensive Drugs: Direct Renin Inhibitors
Acute Kidney Injury IV: Diagnostic Studies and Prevention
Acute Kidney Injury V: Interprofessional Care
Acute Kidney Injury II: Pathophysiology
Glomerular Filtration Rate and its Regulation
GFR regulation involves two primary intrinsic controls: the myogenic and tubuloglomerular feedback mechanisms.
The myogenic...
Acute Kidney Injury I: Introduction
