الفهرس 
Chronic kidney diseaseOnly 14 pages are availabe for public view
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Abstract
The dialysis procedure aids in hypertension management in most
hemodialysis patients, inducing blood pressure decreases from beginning to end.
The phenomenon of intradialytic hypertension (IH), where blood pressure
increases throughout dialysis, has intrigued nephrologists for years due to its
deviation from the expected response to dialysis and the evidence that patients
with recurrent IH have higher risk for long term complications. Initial research in
IH focused on potential biologic mechanisms to explain the acute rise in blood
pressure.
Endothelial cell dysfunction in IH has been studied for more than a decade
directed at changes and imbalances in known endothelial cell-derived
vasoconstrictors (endothelin-1 (ET-1), asymmetric dimethylarginine (ADMA))
and vasodilators (nitric oxide (NO)).
There is strong evidence that extracellular volume excess is a consistent
phenotype in IH patients. While the role of ET-1 continues to be revisited, other
mechanisms including the role of dialysate sodium and extracellular osmolarity
have been explored.
Our results showed that;
Both groups were comparable in age and gender distribution as the mean
age in IDH group was 58 ± 11.426 years and 58.43 ±11.504 in the non-IDH group
and the majority of cases were male (70% and 60%) in group I&II respectively.
The duration of dialysis ranged between 4 months and 13 years in IFH
group and between 6 months and 11 years in the non-IDH group with no
significant difference between the two groups.
The main associated comorbidities included DM (32.5% and 30% in the
IDH and non-IDH group respectively) none significantly differed. On the other
hands, number of HTN patients were significantly higher (82.5%) in the IDH and
(65%) in non-IDH group while number of cardiac patients were significantly
lower in IDH group (2.5%) than non IDH group (22.5%).
The predialysis and post dialysis MBP in the IDH group (107.73 ±3.297 &
114.70 ± 3.283 respectively) was significantly higher than in the non-IDH group
(91.08 ±4.827 & 93.25 ± 4.037 respectively).
There was significant higher level of sodium in IDH group (136.80 ±
2.18&141.65 ±1.875) than none IDH group (134.98±1.89 &137.75±1.71) at
predialysis and post dialysis respectively.
The dose of EPO was significantly higher in IDH group (7120 ± 3560)
than in non-IDH group (4960 ± 2880) and the mean platelets count (236.55 ±
95.39) in the IDH significantly higher than non-IDH group (187.98 ± 51.22).
WBC, HGB, and HR, albumin, UPR & pre serum creatinine didn‟t show
significant difference between the two groups.
The volume of UF was 2946 38 ± 328.55 ml in the IDH group and
3045.31 ± 345.16 ml in the non-IDH group with no significant difference between
the two groups.
Summary
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There is no significant difference in the different causes of renal failure
between the two groups (IDH & non IDH) including HTN, DM, combined HTN
with DM and use of analgesics other etiologies as CKD, pyelonephritis, AKI,
cyst, stones, glomerulonephritis,pre-eclampsia& polycystic kidney (p> 0.05).
The mean Ca levels, Po4 levels and K levels didn‟t show significant
difference between the two groups (p > 0.05).While PTH was significantly higher
in IDH (355.21 ± 336.11) than non IDH (291.82±330.06)
The mean NO level in the IDH group was 2.10 ± 1.23 was significantly
lower than in the non-IDH (3.84 ± 1.59) as (p< 0.001).
The percentages of cases that use BB were statistically significant higher
in the IDH group (52.5% vs 32.5% respectively) and CCBs (37.5% vs 10%
respectively) than non-IDH group.
The best cutoff point of NO to differentiate between cases with IDH and
without IDH was 2.52 with 85% sensitivity and 80% specificity. The AUC was
0.844 with high significant value (p=0.844).
Associated HTN, MBP, Na levels, platelets count and NO levels were
shown to be risk factors for IDH. With multivariate regression analysis, the
associated HTN and NO levels were the independent risk factors for IDH.
We concluded that;
In our study, we found that one marker of endothelial dysfunction in
intradialytic hypertension is NO. Our findings support previous research regarding
the involvement of endothelial dysfunction and higher sodium in intradialytic
hypertension. This study also found that one of the factors leading to decreased
NO is excessive of UF during hemodialysis. The decrease in NO interferes with
smooth muscle vasodilation, resulting in vasoconstriction which plays a role in
increasing blood pressure during HD.