Renal Growth Factor

Malt, Ronald A.

doi:10.1016/b978-0-12-453801-6.50019-8

Cited by 6 publications

(3 citation statements)

References 78 publications

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“…Likewise, unilateral ureteroperitoneal fistula neither enhances renal DNA synthesis [40] nor mitotic rate [41] in the same manner as unilateral nephrectomy. As a first approximation, it appears that changes in renal mass rather than alterations in renal function trigger compensatory renal growth [22,42,43], In 1958 Braun-Menéndez [1] postulated that a circu lating substance controlled renal growth. He proposed that this humoral regulator, which he called renotropin, played a key role in both renal growth and hypertension.…”

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confidence: 99%

Humoral Regulation of Renal Growth

Austin¹,

Goldin²,

Preuss³

1981

Nephron

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The stimuli for compensatory renal growth following a decrease in functioning renal mass have interested a number of investigators. The existence of a humoral incitor and/or regulator of renal growth, renotropin, has been postulated; and three types of experiments have been performed to determine its existence. These include parabiotic, in vivo, and in vitro assays. In general, the three different methodologies support the existence of a renotropic factor (or factors) but further investigations are needed to clarify its precise roles in compensatory renal growth.

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confidence: 99%

Humoral Regulation of Renal Growth

Austin¹,

Goldin²,

Preuss³

1981

Nephron

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“…Long known as compensatory hypertrophy, the enlargement of one kidney after the other has been removed is an example of adaptive growth (Goss, 1964). Many aspects of the process are still poorly understood, including the nature of the stimulus to which the kidney responds by growth (Goss & Dittmer, 1969;Bucher & Malt, 1971;Malt, 1973;Lytton, 1974).…”

Section: Discussionmentioning

confidence: 99%

“…The term 'renotrophin', suggested by Braun-Menendez (1952, 1958, covers both these possibilities. However, the evidence for the presence of renotrophic agents in the blood after mononephrectomy is incomplete (Malt, 1973).…”

Section: Discussionmentioning

confidence: 99%

Growth of rats' kidneys after unilateral uretero‐caval anastomosis.

Morris¹

1976

The Journal of Physiology

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SUMMARY1. The relative significance of reduced excretion of urinary constituents and reduced renal mass, as stimuli to growth of one kidney after the other has been removed, has been investigated.2. To abolish the excretory function of one kidney without removing it, the right ureter was drained into the vena cava through a compound cannula for 6 weeks. Uretero-caval anastomoses, were performed in twenty-four male rats at 10 weeks of age: six survived without evidence of ureteric obstruction (and a further five with minimal obstruction).3. The rats with anastomoses. grew less than six other rats from which the right kidney had been removed or six which had been submitted to a sham operation, and their plasma urea and creatinine concentrations were higher.4. Relative to body weight, the dry weight of each kidney after ureterocaval anastomosis. without obstruction was 18 % greater than after sham operation; taking both kidneys together, the total increase was almost as much as in the left kidney alone after right nephrectomy (46%).5. Histologically and in terms of DNA concentration, the growth of both kidneys after uretero-caval anastomosis was of the same kind as in the left kidney after right nephrectomy.6. The return of urine from one kidney into the blood provided a powerful stimulus to renal growth in spite of the restraining effect of increased renal mass.

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