Compensatory Growth and Other Growth Responses of the Kidney

Wesson, Laurence G.

doi:10.1159/000185282

Cited by 98 publications

(75 citation statements)

References 221 publications

(386 reference statements)

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“…Additionally, the progression of most renal diseases is more closely associated with morphological changes in the tubulo-interstitial environment rather than with alterations ofthe glomerular architecture (51)(52)(53). A sequence of events involving early compensatory tubular hypertrophy with subsequent atrophy and interstitial fibrosis has been observed in many models of chronic renal damage (2,5). It is intriguing to speculate that TGF-, may play a role in this chain of pathophysiological events leading to chronic renal failure (54).…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms inducing tubulo-epithelial cell hypertrophy are incompletely understood, and fundamental differences in the cell biology of this growth response as opposed to cellular hyperplasia (which occurs after acute tubular necrosis) have been sorted out (3,4). Although many investigators have tried to isolate and characterize putative humoral factors that may mediate hypertrophy, the so-called renotropins (5,6), the majority of these factors also induce cellular proliferation of cultured tubular cells (3,7). Only a few factors are hypertrophogenic for tubular cells in vitro.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Angiotensin II-induced hypertrophy of cultured murine proximal tubular cells is mediated by endogenous transforming growth factor-beta.

Wolf

Mueller²,

Stahl³

et al. 1993

J. Clin. Invest.

366

186

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Previous studies by our group have demonstrated that angiotensin II (ANG II), as a single factor in serum-free medium, induces cellular hypertrophy of a cultured murine proximal tubular cell line (MCT). The present study was performed to test the hypothesis that this growth effect was mediated by activation of endogenous transforming growth factor-,@ (TGF-,B). Exogenous TGF-#1 (1 ng/ml) mimicked the growth effects observed with 10i-M ANG II (inhibition of DNA synthesis and induction of cellular hypertrophy). A neutralizing anti-TGF-ft antibody attenuated the ANG II-induced increase in de novo protein and total RNA synthesis as well as total protein content. This antibody also abolished the ANG II-mediated inhibition of 13HIthymidine incorporation into quiescent MCT cells.Control IgG or an unrelated antibody had no effect. A bioassay for TGF-ft using mink lung epithelial cells revealed that MC`'

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Angiotensin II-induced hypertrophy of cultured murine proximal tubular cells is mediated by endogenous transforming growth factor-beta.

Wolf

Mueller²,

Stahl³

et al. 1993

J. Clin. Invest.

366

186

View full text Add to dashboard Cite

show abstract

“…[11][12] Based on previous studies, patients undergoing nephrectomy for any reason experience increasing blood flow to the remaining kidney, associated with induction of rapid compensatory growth and parenchymal hypertrophy with an unpredictable rate. 7,13,14 However, only limited data exist assessing hemodynamic changes of the remaining kidney, after removing a healthy kidney from a donor for transplant. [15][16][17] Color Doppler ultrasound, by evaluating the resistive indices of arteries, is an efficient means of assessing hemodynamic changes in any organ.…”

Section: Resistive Index Of the Remaining Kidney In Allograft Kidney mentioning

confidence: 99%

Resistive Index of the Remaining Kidney in Allograft Kidney Donors

Nekouei

Ahmadnia²,

Abedi³

et al. 2012

Exp Clin Transplant

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Objectives: Kidney transplant is the last resort in patients with end-stage renal disease. In living-kidney donors undergoing nephrectomy for transplant; however, morphologic and hemodynamic changes may occur in the remaining kidney with time. If there would be such a change, then it may alter the diagnostic utility of Doppler ultrasound in evaluating diseased conditions of the solitary kidney. Using Doppler ultrasound, this study sought to determine whether there are hemodynamic changes in the remaining kidney. Materials and Methods: Forty-one patients (38 men, 3 women) for kidney donation were examined using a MyLab 50 color Doppler apparatus with a convey 3.5-to 5-MHz probe. Resistive index values of the main renal, interlobar, and interlobular arteries in the remaining kidney were assessed before, and at 7 and 90 days after nephrectomy. The size and parenchymal thickness of the remaining kidney also were measured before and after nephrectomy. Results: At day 90, a statistically significant increase (P < .001) in resistive index was seen at all levels, compared with before and 7 days after nephrectomy. No significant changes, however, could be noticed on the day 7, when compared with before the nephrectomy. Renal size and parenchymal thickness remained constant over the time studied. Conclusions: Although a statistically significant increase in resistive index values of the remaining kidney was seen 90 days after the nephrectomy, these values have remained within the normal limits of renal resistive index. So, our findings indicate that resistive index measurement is useful in assessing the diseased condition of the remaining kidney after removing the contralateral kidney.

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“…THE MECHANISMS RESPONSIBLE for compensatory renal growth after uninephrectomy (UNX) include a number of endocrine, biochemical, and molecular changes (5,6,24). In adult male rats, UNX results in the rapid growth of the remaining kidney through hypertrophy, with only a minimal hyperplasic component (5,6,24).…”

mentioning

confidence: 99%

“…In adult male rats, UNX results in the rapid growth of the remaining kidney through hypertrophy, with only a minimal hyperplasic component (5,6,24). We have previously determined that this accelerated growth occurs via a growth hormone (GH)-dependent mechanism (8), independently of the IGF-I system (15,17).…”

mentioning

confidence: 99%

Growth hormone regulation of glomerular AT₁angiotensin receptors in adult uninephrectomized male rats

Mok¹,

Sandberg²,

Sweeny³

et al. 2003

American Journal of Physiology-Renal Physiology

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roney. Growth hormone regulation of glomerular AT1 angiotensin receptors in adult uninephrectomized male rats. Am J Physiol Renal Physiol 285: F1085-F1091, 2003. First published June 24, 2003 10.1152/ajprenal.00383.2002.-Sex differences exist in the mechanisms initiating early compensatory renal growth after unilateral nephrectomy (UNX); remnant kidney growth is growth hormone (GH) independent in adult female rats and GH dependent in adult male rats. The present study determined whether sex differences also exist in angiotensin type 1 receptor (AT1R) regulation during early remnant kidney (REM) growth after UNX, and if so, whether GH modulates AT1R expression after UNX in the male rat. Scatchard analysis of radioligand binding in glomeruli demonstrated that 48 h post-UNX, AT1R density (Bmax) was significantly decreased by 20% in female REM compared with control kidneys. In contrast, male REM glomerular Bmax was significantly increased by 28% compared with control kidneys. Furthermore, GH-suppressed male rats displayed attenuated REM growth, which was associated with a 35% decrease in AT1R Bmax. Losartan treatment also decreased REM AT1R Bmax by 55%. The activity of mRNA binding proteins that bind to the 5Ј leader sequence of the AT1R was regulated by UNX and GH treatment in an inverse manner to AT1R expression. These findings suggest that in rats 1) there are sex differences in the regulation of glomerular AT1R expression after UNX; 2) the increase in AT1R binding sites in the male REM is regulated by GH and mediates early remnant kidney growth; and 3) AT1R 5Ј leader sequence mRNA binding proteins play a role in UNX and GH regulation of glomerular AT 1Rs in both males and females.

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Compensatory Growth and Other Growth Responses of the Kidney

Cited by 98 publications

References 221 publications

Angiotensin II-induced hypertrophy of cultured murine proximal tubular cells is mediated by endogenous transforming growth factor-beta.

Angiotensin II-induced hypertrophy of cultured murine proximal tubular cells is mediated by endogenous transforming growth factor-beta.

Resistive Index of the Remaining Kidney in Allograft Kidney Donors

Growth hormone regulation of glomerular AT₁angiotensin receptors in adult uninephrectomized male rats

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Compensatory Growth and Other Growth Responses of the Kidney

Cited by 98 publications

References 221 publications

Angiotensin II-induced hypertrophy of cultured murine proximal tubular cells is mediated by endogenous transforming growth factor-beta.

Angiotensin II-induced hypertrophy of cultured murine proximal tubular cells is mediated by endogenous transforming growth factor-beta.

Resistive Index of the Remaining Kidney in Allograft Kidney Donors

Growth hormone regulation of glomerular AT1angiotensin receptors in adult uninephrectomized male rats

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Growth hormone regulation of glomerular AT₁angiotensin receptors in adult uninephrectomized male rats