Compensatory adaptation of structure and function following progressive renal ablation

Kaufman, Joel M.; DiMeola, H J; Siegel, Norman J.; Lytton, Bernard; Kashgarian, Michael; Hayslett, John P.

doi:10.1038/ki.1974.72

Cited by 143 publications

(61 citation statements)

References 14 publications

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“…A wealth of experimental data (1,2) and clinical observations (3)(4)(5) support the notion that an imbalance between basal metabolic rate and glomerular number leads to progression of chronic renal failure. Allometric studies have shown that metabolic rate is the primary process that sets GFR, and renal adaptation to body size between species is mainly due to an increased glomerular number and only marginally depends on glomerular volume enlargement (6).…”

mentioning

confidence: 84%

Estimation of Total Glomerular Number in Stable Renal Transplants

Fulladosa¹,

Moreso²,

Narváez

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Glomerular number (N g ) is considered a major determinant of renal function and outcome. In the dog, it has been shown that Ng can be estimated with reasonable precision in vivo by means of a renal biopsy and magnetic resonance imaging (MRI). Thus, this method was applied to study anatomoclinical correlations in stable human renal transplants. Thirty-nine stable renal transplants were included. A protocol renal allograft biopsy was done at 4 mo. Biopsies were evaluated according to Banff criteria. Glomerular volume fraction (VV glom/cortex ) was measured by means of a point-counting method, and mean glomerular volume (V g ) was estimated by means of Weibel and Gomez (V g -W&G) and maximal profile area (V g -MPA) methods. MRI was used to estimate renal cortical volume (V cortex ). N g was calculated as (VV glom/cortex ϫ V cortex )/V g . GFR was estimated by the inulin clearance. Ten age-matched donor biopsies served as controls for V g . Histologic diagnosis was as follows: normal (n ϭ 20), borderline (n ϭ 7), acute rejection (n ϭ 1), and chronic allograft nephropathy (n ϭ 11). VV glom/cortex was 3.4 Ϯ 1.1%, V cortex was 167 Ϯ 46 cm . A positive correlation between GFR and N g -W&G (r ϭ 0.47, P ϭ 0.002) was observed. Furthermore, the older the donor, the higher V g -W&G (r ϭ 0.37, P ϭ 0.01) and the lower N g -W&G (r ϭ Ϫ0.40, P ϭ 0.01). Total glomerular number can be estimated in stable renal allografts by means of a renal biopsy and MRI. Our data show that N g depends on donor age and positively correlates with GFR.

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mentioning

confidence: 84%

Estimation of Total Glomerular Number in Stable Renal Transplants

Fulladosa¹,

Moreso²,

Narváez

et al. 2003

Journal of the American Society of Nephrology

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“…Thus, a common process appears to underlie functional deterioration in various renal diseases, irrespective of cause. The hyperfiltration theory 1 proposes nonimmunological mechanisms underlying renal functional deterioration and is supported by many observations in animal models in which nephron numbers are reduced by simple excision of tissue [2][3][4] or by ligation of specific branches of the renal artery. [5][6][7] In these models, the remaining kidney is histologically normal at the beginning of progressive impairment of renal function.…”

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confidence: 95%

A Rat Model of Progressive Chronic Renal Failure Produced by Microembolism

Kimura

Suzuki

Hishida

1999

The American Journal of Pathology

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“…Free-flow micropuncture studies in rat remnant kidneys have shown, in the chronic state, that in the surviving remnant nephrons glomerular hyperfiltration is proportional to the extent of the initial reduction in renal mass (8) and maintained by significant increases in single nephron plasma flow (SNPF) and glomerular capillary hydrostatic pressure difference (AP) (4). Chronically, these glomerular hemodynamic alterations are the direct consequence of a proportionally greater vasodilation in afferent than in efferent arterioles (4,9,10).…”

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confidence: 99%

Glomerular and tubular adaptive responses to acute nephron loss in the rat. Effect of prostaglandin synthesis inhibition.

Pelayo¹,

Shanley²

1990

J. Clin. Invest.

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These studies, using in vivo micropuncture techniques in the Munich-Wistar rat, document the magnitude of changes in glomerular and tubular function and structure 24 h after -75% nephron loss (Nx) and compared these results with those obtained in sham-operated rats. The contribution of either nephron hypertrophy or renal prostaglandin to these adjustments in nephron function was also explored. After acute Nx, single nephron GFR (SNGFR) was increased, on average by -30%, due primarily to glomerular hyperperfusion and hypertension. The -45% reduction in preglomerular and the constancy in postglomerular vascular resistances was entirely responsible for these adaptations. Although increases in fluid reabsorption in proximal convoluted tubules correlated closely with increases in SNGFR, the fractional fluid reabsorption between late proximal and early distal tubular segments was depressed. Nephron hypertrophy could not be substantiated based on either measurements of protein content in renal tissue homogenates or morphometric analysis of proximal convoluted tubules. However, acute Nx was associated with increased urinary excretory rates per functional nephron for 6-keto-PGFI. and TXB2. Prostaglandin synthesis inhibition did not affect function in control nephrons, but this maneuver was associated with normaliztion of glomerular and tubular function in remnant nephrons. The results suggest that enhanced synthesis of cyclooxygenase-dependent products is one of the earliest responses to Nx, and even before hypertrophy the pathophysiologic effects of prostaglandin may be important contributors to the adaptations in remnant nephron function. (J. Clin. Invest.

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Compensatory adaptation of structure and function following progressive renal ablation

Cited by 143 publications

References 14 publications

Estimation of Total Glomerular Number in Stable Renal Transplants

Estimation of Total Glomerular Number in Stable Renal Transplants

A Rat Model of Progressive Chronic Renal Failure Produced by Microembolism

Glomerular and tubular adaptive responses to acute nephron loss in the rat. Effect of prostaglandin synthesis inhibition.

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