IGF-1 modulates kidney response to chronic ischemia

מתוך medicontext.co.il
By Will Boggs, MD

NEW YORK (Reuters Health) – Insulin-like growth factor-1 (IGF-1) levels determine whether kidneys will atrophy or hypertrophy in chronic renal ischemia, according to a report in the December 2001 issue of the American Journal of Hypertension.

In the so-called "two-kidney, one-clip" (2K1C) rat model of renovascular hypertension, the kidney with the constricting clip atrophies and the unclipped kidney hypertrophies, the authors explain, whereas the kidney in the one-kidney, one-clip (1K1C) model does not atrophy.

Hypothesizing that IGF-1 may play a role in the kidney's response to ischemia, Dr. Michael Bursztyn, from Hadassah University Hospital in Jerusalem, and colleagues measured the renal expression of the IGF-1 gene, along with the expression of genes for its receptor (IGF-IR) and its binding protein (IGFBP-1) in both models and in unilaterally nephrectomized rats.

The clipped kidney in the 2K1C model (which atrophied) showed persistent elevation of IGF-1 mRNA over that of the contralateral kidney and that of control animals, the authors report. In contrast, they found, the clipped kidney in the 1K1C model (which increased in size) showed similar IGF-1 mRNA levels to controls and significantly lower levels than the unclipped 2K1C and unilateral nephrectomy kidneys.

IGFBP-1 mRNA levels in the clipped 2K1C kidney were lower than controls at 3 days, unchanged at 10 days, and increased at 30 days, the researchers note.

IGF-1 levels also changed over time and did not reflect mRNA levels. According to the report, IGF-1 levels in clipped 2K1C kidneys were 47% lower than controls, 61% lower than in 1K1C kidneys, and 66% lower than in uninephrectomy kidneys by 30 days after clipping.

In contrast, kidneys from 1K1C and uninephrectomized rats had higher IGF-1 levels than controls did, the investigators say.

"We have shown that atrophy or hypertrophy of kidneys may be dependent on levels of IGF-1 early in the pathophysiologic process," the authors conclude. "Hypertrophy (on days 10 and 30) depended on increased levels already evident by day 3, whereas failure to increase IGF-1 levels (even in the face of a significantly increased message) may have promoted atrophy during chronic ischemia."

"I believe it may be too early for [our] research to have immediate clinical implications," Dr. Bursztyn told Reuters Health. "We shall need to do more research to find out if administration of IGF-1 may prevent such atrophy. If it does, then it might be considered for treatment in the relatively large number of older patients with 'ischemic' nephropathy."

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