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CHAPTER 26
have been significant contributions for a better understanding of the pathogenesis of renal
hypertension (Butler, 1937; Barker & Walters, 1940; Pickering & Heptinstall, 1953;
Holley
et al.,
1964; Heptinstall, 1966). In recent years, experimental and clinical studies
were concerned with the effects of changes in the renal artery blood flow due to renal
artery stenosis on the renin-angiotensin-aldosterone system which, according to Brest
et al.
(1965), is, at least in part, operative in the mechanism of renal arterial hypertension.
This view is in accordance with Genest's (1961) and Peart's (1965) work, who established
that angiotensin II, the most important aldosterone-stimulating hormone, is a potent
pressor substance which can significantly raise the arterial blood pressure.
This problem has recently been the subject of a Symposium on Hypertension held
in Montreal by 84 research workers (Ed. Genest and Koiw, 1972) which dealt with the
new advances made in the control of renin secretion and release, angiotensin I converting
enzyme activity and immuno-assay methods for the measurement of angiotensin I and
II. In addition, the disturbance of aldosterone regulation in early, uncomplicated benign
essential hypertension and the i8-hydrodroxy-corticosterone secretion rate in early
hypertension was also discussed. While these papers on experimental research will be
undoubtedly of great interest to research workers on prevention and treatment of hyper
tension and chronic pyelonephritis in paraplegia, this highly complex problem is still far
from solution. Irvine H. Page in his chapter 'The Remarkable Story of Hypertension'
summed up his views on recent research as follows: 'Error is inevitable if you are creative
and to err is human; to really foul things up requires a computer'.
Brest
et al.
(1965) also consider it likely that retention of sodium in the arterial
muscle walls may intensify the vasopressor effect of the circulating angiotensin in the
blood. On the other hand, Brest
et al.
consider the mechanism responsible for renal
parenchymal hypertension to be much less well defined than that of renal arterial hyper
tension. Amongst the factors which are responsible for this discrepancy, they consider
to be failure of kidneys to inactivate a pressure substance, deficient renal secretion of
vasodepressor material and sodium retention. Their own studies indicate that excess of
sodium rather than fluid plays the most important part in raising blood pressure, and
salt restriction by diet or salt withdrawal by dialysis will improve renal parenchymal
hypertension.
The greatly increased life-span of spinal paraplegics and tetraplegics after the
Second World War naturally makes renal deficiency an increasingly important problem,
whether this is caused by pyelonephritis with or without amyloidosis and/or hyper
tension. In a series of paraplegic patients, groups can be distinguished showing amyloi
dosis due to chronic sepsis, as a result of pressure sores and osteomyelitis, with relatively
unimportant upper urinary tract infection; other patients will show renal impairment
due to chronic pyelonephritis but no evidence of amyloidosis; yet another group will
show the two conditions co-existing. Future studies should aim to define the relationships
between renal amyloidosis, chronic pyelonephritis and hypertension in these various
groups of patients. Regular blood pressure readings from the early stages in patients with
pressure sores and in those with ascending urinary infection and throughout the later
stages of these complications are essential. Diastolic pressure of 90-95 mmHg in young
adults should be considered in accordance with Fishberg (1954) as abnormally high and
