Angiotensin Converting Enzyme Activity in Compensatory Renal Hypertrophy

Babić, Nermina; Huskić, Jasminko; Nakas-Ićindić, Emina

doi:10.17305/bjbms.2007.3098

Cited by 5 publications

(6 citation statements)

References 15 publications

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“…The mechanism for this large increase in GFR in the 1-K cilia (Ϫ) group is presently unknown. Reductions of renal mass lead to the activation of several growth factors, 14,[33][34][35] changes in renal nerve activity, 36 and alterations in mechanisms that control renal hemodynamics such as the tubuloglomerular feedback mechanism. 37,38 Augmented functional hypertrophy in the 1-K cilia (Ϫ) group at 3 weeks may represent an abnormal/exaggerated response to growth factor/vasodilator signaling acting at the level of the afferent arteriole or the macula densa in the absence of cilia.…”

Section: Discussionmentioning

confidence: 99%

Loss of Primary Cilia Upregulates Renal Hypertrophic Signaling and Promotes Cystogenesis

Bell¹,

Fitzgibbon²,

Sas³

et al. 2011

Journal of the American Society of Nephrology

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Primary cilia dysfunction alters renal tubular cell proliferation and differentiation and associates with accelerated cyst formation in polycystic kidney disease. However, the mechanism leading from primary ciliary dysfunction to renal cyst formation is unknown. We hypothesize that primary cilia prevent renal cyst formation by suppressing pathologic tubular cell hypertrophy and proliferation. Unilateral nephrectomy initiates tubular cell hypertrophy and proliferation in the contralateral kidney and provides a tool to examine primary cilia regulation of renal hypertrophy. Conditional knockout of the primary cilia ift88 gene leads to delayed, adult-onset renal cystic disease, which provides a window of opportunity to conduct unilateral nephrectomy and examine downstream kinetics of renal hypertrophy and cyst formation. In wild-type animals, unilateral nephrectomy activated the mTOR pathway and produced appropriate structural and functional hypertrophy without renal cyst formation. However, in ift88 conditional knockout animals, unilateral nephrectomy triggered increased renal hypertrophy and accelerated renal cyst formation, leading to renal dysfunction. mTOR signaling also increased compared with wild-type animals, suggesting a mechanistic cascade starting with primary ciliary dysfunction, leading to excessive mTOR signaling and renal hypertrophic signaling and culminating in cyst formation. These data suggest that events initiating hypertrophic signaling, such as structural or functional loss of renal mass, may accelerate progression of adult polycystic kidney disease toward end-stage renal disease.

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Section: Discussionmentioning

confidence: 99%

Loss of Primary Cilia Upregulates Renal Hypertrophic Signaling and Promotes Cystogenesis

Bell¹,

Fitzgibbon²,

Sas³

et al. 2011

Journal of the American Society of Nephrology

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“…In conscious lambs, blood pressure is low at birth and plasma renin activity is elevated but during the first 3 months of post-natal maturation, plasma renin activity decreases as blood pressure increases ( Monument and Smith, 2003 ; Velaphi et al, 2007 ). Additionally, in the early postnatal period in conscious lambs angiotensin II activation of AT1R regulates GFR and kidney injury associated with glomerular hyperfiltration and hypertrophy may be underpinned by RAS activation ( Babić et al, 2007 ; Vinturache and Smith, 2016 ).…”

Section: Mechanisms Facilitating Adaptations and Potentiating Kidney mentioning

confidence: 99%

Physiology and Pathophysiology of Compensatory Adaptations of a Solitary Functioning Kidney

et al. 2020

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Children born with a solitary functioning kidney (SFK) have an increased risk of hypertension and kidney disease from early in adulthood. In response to a reduction in kidney mass, the remaining kidney undergoes compensatory kidney growth. This is associated with both an increase in size of the kidney tubules and the glomeruli and an increase in single nephron glomerular filtration rate (SNGFR). The compensatory hypertrophy and increase in filtration at the level of the individual nephron results in normalization of total glomerular filtration rate (GFR). However, over time these same compensatory mechanisms may contribute to kidney injury and hypertension. Indeed, approximately 50% of children born with a SFK develop hypertension by the age of 18 and 20–40% require dialysis by the age of 30. The mechanisms that result in kidney injury are only partly understood, and early biomarkers that distinguish those at an elevated risk of kidney injury are needed. This review will outline the compensatory adaptations to a SFK, and outline how these adaptations may contribute to kidney injury and hypertension later in life. These will be based largely on the mechanisms we have identified from our studies in an ovine model of SFK, that implicate the renal nitric oxide system, the renin angiotensin system and the renal nerves to kidney disease and hypertension associated with SFK. This discussion will also evaluate current, and speculate on next generation, prognostic factors that may predict those children at a higher risk of future kidney disease and hypertension.

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“…2 After unilateral nephrectomy, the remaining kidney undergoes structural and functional changes as a pliant response to quench the increased functional demand to maintain the homeostasis of fluid and solutes in the body. 3,4 The compensatory renal hypertrophy causes an increase in weight and/ or volume of the remaining kidney of the adult animals. [5][6][7][8] The nephrogenesis in rats and mice is accomplished during their neonatal period, while in humans, it occurs prenatally, and therefore, the renal growth that occurs does not include new nephron formation.…”

Section: Introductionmentioning

confidence: 99%

“…4,12,25,26 At the histopathologic level, kidney weight was used as the main most prominent indicator of the compensatory hypertrophy. 3,8 The compensatory growth can affect the glomeruli, proximal and distal convoluted tubules and also the cortical collecting ducts, 7,[27][28][29][30] with reports specifying that this growth occurs primarily in the cortex, especially confined to the proximal convoluted tubules. 11 The growth pattern resembles that of the natural growth of kidney during the postnatal period where hypertrophy of the proximal tubules is more than that of distal tubules.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural changes and nestin expression accompanying compensatory renal growth after unilateral nephrectomy in adult rats

Eladl

Elsaed

Atef

et al. 2017

IJNRD

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Background: Several renal disorders affect the glomerular podocytes. Compensatory structural and functional changes have been observed in animals that have undergone unilateral renal ablation. These changes occur as a pliant response to quench the increased functional demand to maintain homeostasis of fluid and solutes. Nestin is an intermediate filament protein present in the glomerular podocytes of the adult kidney and is linked with the maintenance of its foot process structure. Structural changes in the podocytes ultimately restructure the filtration barrier. Very few studies related to the ultrastructural and histopathologic changes of the podocytes are documented. The present study aimed to assess the histopathologic changes at the ultrastructural level in the adapted kidney at different time intervals following unilateral renal ablation in adult rats and its relation with nestin. Methods: Forty-eight rats were divided into four groups (n=12 in each group). The animals of Group A were control naïve rats, while the group B, group C and group D animals underwent left unilateral nephrectomy and the remaining right kidney was removed on days 10, 20 and 30, respectively. Each group included four sham-operated rats, which were sacrificed at the same time as the naïve rats. Each nephrectomized sample was weighed and its sections were subjected to hematoxylin and eosin examination, transmission electron microscopic study as well as immunostaining using the intermediate filament protein nestin. Results: No difference was found between the kidney sections from the control group and the sham-operated groups. A significant increase in the weight of the right kidneys was noted in groups B, C and D (P<0.001). The ultrastructural adaptive changes seen in the glomeruli of group B were subsequently reduced in groups C and D. This finding corresponded to a similar pattern of nestin expression in the podocytes, which showed significant increase in group B followed by reduced expression in groups C and D. Histopathologic and transmission electron microscopic evaluation of group B showed signs of kidney injury. On the other hand, group C animals showed markedly reduced renal adaptive changes and similar changes were also noted in group D. Conclusion: Correlation between nestin expression and the ultrastructural changes confirms that nestin has a role in increasing the mechanical stability of the podocytes in order to enhance their morphologic changes in response to the tensile glomerular capillary wall. However, further studies investigating more remote ultrastructural changes and their relation with nestin expression are needed to confirm this relationship.

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Angiotensin Converting Enzyme Activity in Compensatory Renal Hypertrophy

Cited by 5 publications

References 15 publications

Loss of Primary Cilia Upregulates Renal Hypertrophic Signaling and Promotes Cystogenesis

Loss of Primary Cilia Upregulates Renal Hypertrophic Signaling and Promotes Cystogenesis

Physiology and Pathophysiology of Compensatory Adaptations of a Solitary Functioning Kidney

Ultrastructural changes and nestin expression accompanying compensatory renal growth after unilateral nephrectomy in adult rats

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