114
BRIAN POOLE
embryo and of whole embryo minus homologous tissue. In the cultures with
whole embryo extract, kidney tubule differentiation was reduced. This was
taken to indicate an increased rate of growth in the kidney tissue in the
presence of homologous tissue extract. Similar effects were obtained with
heart cells. There is an interesting report that minor injury to one kidney
with a hypodermic needle causes an eightfold increase in the mitotic index
of the intact opposite kidney (Argyris, 1961).
The injection of serum from normal or unilaterally nephrectomized
rats has been reported to have no effect on the mitotic index of unilaterally
nephrectomized rats (Goss, 1963; G. E. G. Williams, 1962a). Lowenstein
and Stern (1963) report increased DNA synthesis in kidneys of intact rats
after injection of serum from unilaterally nephrectomized rats. Ogawa
and Nowinski (1958) reported that serum from unilaterally nephrectomized
rats selectively stimulates growth of kidney tissue in vitro.
D. Summary
There are many fewer reports of experimental studies of kidney hypertrophy than there are of liver hypertrophy. However, we can draw several
conclusions. Clearly the pituitary, thyroid, adrenals, and gonads are not
the source of the hypertrophic stimulus, although the gonads may have
drastic effects on kidney mitotic activity, as discussed in the Introduction
(Section I). The stimulus to hypertrophy is independent of kidney innervation, and the increased excretory function of the remaining kidney is not
the source of the hypertrophic stimulus, although there is some evidence
that the stimulus is humoral. The theory of humoral feedback is in agreement with all the experimental evidence, except for the serum injection
work which is subject to many uncertainties, as discussed above. The
response of the kidney remaining after unilateral nephrectomy is rather
slow, and we cannot exclude the possibility that it is the overload of some
metabolic kidney function which causes the hypertrophy, although there
is no evidence to suggest this.
VI. Conclusion
A. Similarity of Growth Control in Liver and Kidney
There are two alleged differences between the processes of hypertrophic
growth in liver and kidney which have led most authors to consider them
as qualitatively different phenomena. It is frequently stated that kidney
hypertrophy is merely an increase in the size of structures already present,
whereas liver restoration is a hyperplasia or "regeneration" involving cell
proliferation and the formation of new lobules. However, there is usaully
cell division associated with kidney hypertrophy, and the formation of new
BRIAN POOLE
embryo and of whole embryo minus homologous tissue. In the cultures with
whole embryo extract, kidney tubule differentiation was reduced. This was
taken to indicate an increased rate of growth in the kidney tissue in the
presence of homologous tissue extract. Similar effects were obtained with
heart cells. There is an interesting report that minor injury to one kidney
with a hypodermic needle causes an eightfold increase in the mitotic index
of the intact opposite kidney (Argyris, 1961).
The injection of serum from normal or unilaterally nephrectomized
rats has been reported to have no effect on the mitotic index of unilaterally
nephrectomized rats (Goss, 1963; G. E. G. Williams, 1962a). Lowenstein
and Stern (1963) report increased DNA synthesis in kidneys of intact rats
after injection of serum from unilaterally nephrectomized rats. Ogawa
and Nowinski (1958) reported that serum from unilaterally nephrectomized
rats selectively stimulates growth of kidney tissue in vitro.
D. Summary
There are many fewer reports of experimental studies of kidney hypertrophy than there are of liver hypertrophy. However, we can draw several
conclusions. Clearly the pituitary, thyroid, adrenals, and gonads are not
the source of the hypertrophic stimulus, although the gonads may have
drastic effects on kidney mitotic activity, as discussed in the Introduction
(Section I). The stimulus to hypertrophy is independent of kidney innervation, and the increased excretory function of the remaining kidney is not
the source of the hypertrophic stimulus, although there is some evidence
that the stimulus is humoral. The theory of humoral feedback is in agreement with all the experimental evidence, except for the serum injection
work which is subject to many uncertainties, as discussed above. The
response of the kidney remaining after unilateral nephrectomy is rather
slow, and we cannot exclude the possibility that it is the overload of some
metabolic kidney function which causes the hypertrophy, although there
is no evidence to suggest this.
VI. Conclusion
A. Similarity of Growth Control in Liver and Kidney
There are two alleged differences between the processes of hypertrophic
growth in liver and kidney which have led most authors to consider them
as qualitatively different phenomena. It is frequently stated that kidney
hypertrophy is merely an increase in the size of structures already present,
whereas liver restoration is a hyperplasia or "regeneration" involving cell
proliferation and the formation of new lobules. However, there is usaully
cell division associated with kidney hypertrophy, and the formation of new