Renal function before and after unilateral ephrectomy in renal donors

Pabico, Rufino C.; McKenna, Barbara A.; Freeman, Richard B.

doi:10.1038/ki.1975.96

Cited by 122 publications

(68 citation statements)

References 24 publications

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“…1). Moreover, the single kidney model that we employed did not influence expression of these abnormalities in spite of contrary observations in other animal species (30). Indeed, we found that uninephrectomy and/or renal transplantation between matched murine models did not negatively influence the GFR or alter phosphate clearance in the resultant single kidney.…”

Section: Discussionmentioning

confidence: 60%

Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.

Nesbitt¹,

Coffman²,

Griffiths³

et al. 1992

J. Clin. Invest.

209

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Although deranged phosphate transport is the fundamental abnormality in X-linked hypophosphatemic (XLH) rickets, it remains unknown if this defect is the consequence of an intrinsic kidney abnormality or aberrant production of a humoral factor. To discriminate between these possibilities, we examined phosphate homeostasis in normal and Hyp mice, subjected to renal crosstransplantation. We initially evaluated the effects of uninephrectomy on the indices of phosphate metabolism that identify the mutant biochemical phenotype. No

show abstract

Section: Discussionmentioning

confidence: 60%

Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.

Nesbitt¹,

Coffman²,

Griffiths³

et al. 1992

J. Clin. Invest.

209

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show abstract

“…12,13 Also consistent with a renal hypertrophic response, the increase in GFR in healthy LDs is accompanied by a proportional increase in tubular maximal reabsorptive function, demonstrating preservation of glomerulotubular balance. 3 Absolute increases in single-kidney uric acid and phosphate clearance, as well as acid excretion, however, cannot be attributed solely to the increase in GFR; these increases therefore reflect additional homeostatic adaptations in tubular function after nephrectomy. 3 Donor age and obesity are important modulators of adaptation in the single kidney.…”

Section: Physiologic Adaptations After Uninephrectomy In Healthy Donorsmentioning

confidence: 99%

“…3 Absolute increases in single-kidney uric acid and phosphate clearance, as well as acid excretion, however, cannot be attributed solely to the increase in GFR; these increases therefore reflect additional homeostatic adaptations in tubular function after nephrectomy. 3 Donor age and obesity are important modulators of adaptation in the single kidney. Despite a similar baseline adaptive renal response after nephrectomy, RFR measured by dopamine infusion 2 months after donation was significantly reduced in obese donors (body mass index .…”

Section: Physiologic Adaptations After Uninephrectomy In Healthy Donorsmentioning

confidence: 99%

“…7 The central role of increased perfusion in the early functional adaptation in humans is supported by the observed increase in renal plasma flow (RPF) after nephrectomy, of a magnitude similar to or greater than the percentage change in GFR (Table 1). 2,3,5,8 To investigate the hemodynamic mechanisms whereby GFR increases after nephrectomy, renal functional reserve capacity (RFR), defined as percentage increase in GFR after infusion of lowdose dopamine or amino acids, was evaluated in 15 LDs before donation and at a mean 6 SEM of 1.360.3 months and 4.960.8 years after donation (Table 1). 9 At both time points, the percentage increase in GFR induced by dopamine was half of that measured before donation, whereas the percentage change induced by amino acid infusion was similar before and after donation.…”

Section: Physiologic Adaptations After Uninephrectomy In Healthy Donorsmentioning

confidence: 99%

“…[2][3][4][5][6] The rapidity and reproducibility of this early increase in GFR after nephrectomy suggest a predominantly hemodynamic response.…”

Section: Physiologic Adaptations After Uninephrectomy In Healthy Donorsmentioning

confidence: 99%

See 2 more Smart Citations

The Natural History of Residual Renal Function in Transplant Donors

Mueller

Luyckx

2012

Journal of the American Society of Nephrology

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After uninephrectomy, GFR in the remaining kidney increases to 60%-70% of the predonation value, largely because of a substantial increase in renal blood flow. Donor kidney function is then generally maintained over many years. Hypertension and proteinuria are common among living donors but do not appear to negatively affect long-term renal function. Loss of reserve capacity regarding renal function in some subgroups after donation, particularly in obese and older donors, raises questions about limitations of the renal adaptive response and suggests caution in generalization of current outcome data to more marginal donors not well represented in older studies.

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Cre/loxP approach‐mediated downregulation of Pik3c3 inhibits the hypertrophic growth of renal proximal tubule cells

Liu

Yuan

Dai

et al. 2020

Journal Cellular Physiology

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Nephron loss stimulates residual functioning nephrons to undergo compensatory growth. Excessive nephron growth may be a maladaptive response that sets the stage for progressive nephron damage, leading to kidney failure. To date, however, the mechanism of nephron growth remains incompletely understood. Our previous study revealed that class III phosphatidylinositol‐3‐kinase (Pik3c3) is activated in the remaining kidney after unilateral nephrectomy (UNX)‐induced nephron loss, but previous studies failed to generate a Pik3c3 gene knockout animal model. Global Pik3c3 deletion results in embryonic lethality. Given that renal proximal tubule cells make up the bulk of the kidney and undergo the most prominent hypertrophic growth after UNX, in this study we used Cre‐loxP‐based approaches to demonstrate for the first time that tamoxifen‐inducible SLC34a1 promoter‐driven CreERT2 recombinase‐mediated downregulation of Pik3c3 expression in renal proximal tubule cells alone is sufficient to inhibit UNX‐ or amino acid‐induced hypertrophic nephron growth. Furthermore, our mechanistic studies unveiled that the SLC34a1‐CreERT2 recombinase‐mediated Pik3c3 downregulation inhibited UNX‐ or amino acid‐stimulated lysosomal localization and signaling activation of mechanistic target of rapamycin complex 1 (mTORC1) in the renal proximal tubules. Moreover, our additional cell culture experiments using RNAi confirmed that knocking down Pik3c3 expression inhibited amino acid‐stimulated mTORC1 signaling and blunted cellular growth in primary cultures of renal proximal tubule cells. Together, both our in vivo and in vitro experimental results indicate that Pik3c3 is a major mechanistic mediator responsible for sensing amino acid availability and initiating hypertrophic growth of renal proximal tubule cells by activation of the mTORC1–S6K1–rpS6 signaling pathway.

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Renal function before and after unilateral ephrectomy in renal donors

Cited by 122 publications

References 24 publications

Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.

Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.

The Natural History of Residual Renal Function in Transplant Donors

Cre/loxP approach‐mediated downregulation of Pik3c3 inhibits the hypertrophic growth of renal proximal tubule cells

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