الفهرس 
Material and methodsOnly 14 pages are availabe for public view
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Abstract
173
SUMMARY
This study includes 38 patients with CRF classified into
two groups :
1. Twenty patients under regular HD program :
These patients were classified into two subgroups :
a. Ten hypertensive patients.
b. Ten normotensive patients.
2. Eighteen patients managed by conservative measures :
They were classified into two subgroups :
a. Ten hypertensive patients.
b. Eight normotensive patients.
A group of ten normal adult subjects were studied as
control •
In group one peripheral PGE and PRA was measured before
and AHD
Renal venous blood samples were taken according to
Seldinger’s technique from eight patients in the second group.
PGE and PRA in renal venous plasma were compared with that
present in peripheral plasma
The results showed:
- For normal control, plasma PGE was 3.84 :!: 0.59 pg / ml
(mean + SE). PRA was 1.8 :!: 0.23 ng/ml/hr.
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- Group 1 patients on regular HD program :
Plasma PGE level BHD was 6.52 :!: 0.7 pg/ ml, this is H. significant
compared to the control subjects (p < 0.01). PRA
level was 3.17 :!: 0.4 ng/ml/hr. which is significantly higher
than the contrl (p < 0.025). Increased PRA in patients with
CRF may be due to a deficiency of a normally circulating renin
inhibitor in plasma of uremic patients (Kotehen et al.,1984) •
Increased PGE may result either from over production or
impaired inactivation of PGs • Also this may be a consequence
of chronic HD program in an attempt to modulate the
hemodynamic changes in CRF and to limit the magnitude of
vasoconstriction observed with renin overproduction
Regarding PGE plasma level and its relation to blood
pressure, hypertensive patients showed a lower PGE level
than normotensive ones. The difference was V.H. significant
(p <0.0005). This indicates that hypertension may
result from a decrease in the vasodilatory system allowing
the vasoconstrictor system to act unopposed with the ultimate
production of hypertension. HD was associated with increase
in plasma PGE and PRA. Plasma PGE increased to 9.59 + 0.92
pg / ml AHD. This is H. significant compared with the value
BHD. PRA increaed to 4.06 :!: 0.43 ng/ml/hr.
The change in PGE and PRA level AHD can be explained by
the fact that during HD there was a reduction of plasma volume,
this represents an adequate stimulus for the release of vasoactive
substances such as renin to produce peripheral vasoconstriction
in an attempt to support systemic blood pressure.
175
This vasoactive substance can directly stimulate PGE product
Lon ,
The increase in PGE and PRA after HD was observed more
in hypertensive patients than normotensive ones. This may
represent a protective or compensatory mechanism in the hypertensives
in an attempt to lower their blood pressure.
Despite the concomitant increase in PGE and PRA concentrations
observed AHD, no correlation between PGE and PRA
before and AHD was found whether in hypertensive or in the
normotensive patients. This finding suggests that other
factors such as norepinephrine or antidiuretic hormone may
also modulate plasma concentration of PGE.
- Group 2 patients managed by conservative measures :
This group also showed increase in PRA more than the control
Their mean PRA was 2.9 + 0.35 ng/ml/hr. which is significantly
higher compared with the control (p <0.025). However, PGE
was 3.23 ~ 0.36 pg/ml, this is lower than the control.
It is not possible to deduce the reason for suppression of
PGE synthesis in uremic patients under conservative measures
compared with control subjects and patients under HD.
Also in this group hypertensive patients showed a lower PGE
level than the normotensive ones, the difference was V.H.
significant (p < 0.0005). However, there was no significant
difference in PRA between hypertensive and normotensive
ones.
176
In this work the relation between PGE and PRA levels
in renal venous plasma was compared with that present in peripheral
plasma among eight patients under conservative measures.
a. PGE: there was a significant correlation between PGE level
in renal venous plasma with that of peripheral plasma (p
<0.05) with 47 % increase in renal venous plasma.
Renal venous PGE plasma level = 1.246 + 1.082 X
peripheral PGE value.
b. PRA: there was insignificant relation between PRA level
in renal venous plasma with that of peripheral plasma
(P>0.15) with 31% increase in renal venous plasma level.
Renal venous plasma level of ERA = 1.72 X peripheral
PRA 1.134
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Conclusion
* Prostaglandin E has an important antihypertensive role
in patients with chronic renal failure and hypertension
results from prostaglandin deficiency.
* Haemodialysis has a protective antihypertensive effect
as it is associated with increased PGE production in
accordance with activation of the vasoconstrictor system.
This may serve to offset the circulatory effects of
systemic and regional vasoconstriction. PGE may prevent
the overshooting rise in blood pressure especially in
hypertensive patients.
* A relation was found between PGE and BRA in renal venous
plasma with that present in peripheral plasma among eight
patients with chronic renal failure under conservative
measures Thus, by measuring PGE level in peripheral
plasma, renal venous level can be calculated 0
* Clinically, non-steroidal anti-inflammatory drugs should
be used with great caution in patients suffering from
diseases associated with decrease renal perfusion as they
lead to further deterioration in renal function.
Such diseases include chronic heart failure, liver cirrh178
osis, nephrotic syndrome, and patients with impaired renal
function. Moreover, non-steroidal anti-inflammatory drugs
should be used with great caution in hypertensive pat~ents
as they interfere with the therapy of hypertension.
Recommendations
Renal prostaglandins can affect and control the entire
renal physiologic processes. They affect water transport,
renal blood flow, sodium and potassium excretion, plasma
renin and erythropoetin production. This is an important
precaution to the physician against the use of non-steroidal
anti-inflammatory agents for an ever-increasing list of
indications.
Prostaglandin E may be used as an antihypertensive agent.
It may be used either through its selective stimulation or
its direct administration to improve the hemodynamic state
in chronic renal failure patients and to attenuate endogenous
neurohumoral vasoconstrictive effects of hyperreninemia.
As prostaglandins, especially PGE2 modulate the immune
response, future research may clarify the role of PGE
2
’
thromboxanes and leukotriene systems in the pathogenesis
of immunologic abnormalities of glomerular diseases.