Kamal et al. J Nephrol Ther 2015, 6:1
DOI: 10.4172/2161-0959.1000231
Open Access Review Article
Volume 6 • Issue 1 • 1000231
J Nephrol Ther
ISSN: 2161-0959 JNT, an open access journal
Kidneys: The Victim Of Hypertension: Review
Islam Kamal*, Rehab Hamdy and Nourhan M.sayed
Kasr Alainy Faculty of Medicine, Cairo University, Egypt
*Corresponding author: Islam Kamal, Medical Student, Kasr Alainy Faculty of
Medicine, Cairo University, Egypt, Tel: 20 10 60 55056; E-mail: Islam.k.hamouda@
students.kasralainy.edu.eg
Received: December 02, 2015; Accepted: December 23, 2015; Published: December 30, 2015
Citation: Kamal I, Hamdy R, Mohamed N (2015) Kidneys: The Victim Of Hypertension:
Review. J Nephrol Ther 6: 231. doi:10.4172/2161-0959.1000231
Copyright: © 2015 Kamal I, et al. This is an open-access article distributed under
the terms of the Creative Commons Attribution License, which permits unrestricted
use, distribution, and reproduction in any medium, provided the original author and
source are credited.
Keywords: Blood pressure dependency; Hypertension; Chronic
renal failure; Renal denervation
Introduction
Normal blood pressure means the pressure that the blood afecting
the normal body vessels and depends on many items like: cardiac
output, vascular resistance and the total blood volume. In normal
healthy people it should be below than 120 mmhg “systolic” and below
than 80 mmhg “diastolic”. When your blood pressure rises more than
140/90 it means that you are hypertensive [1]. Hypertension is one of
the most leading causes of non-infectious death all over the world and
considered one of the most common conditions that doctors can see in
the primary care. Hypertension has many serious efects as coronary
artery disease, chronic renal failure, myocardial infarction, cerebral
stroke, aortic aneurysm and so on.
Kidneys are responsible for long term controlling blood pressure,
except in hypotension, through the rennin angiotensin aldosterone
system (RAAS) as follow (Figure 1): rennin is released form
juxtaglomerular apparatus of the kidney which lead to cleavage of the
angiotensinogen, secreted by the liver into blood, to form angiotensin1
and through angiotensin converting enzyme, produced by the lungs,
which induce production of angiotensin2 from angiotensin1.
ACE has many actions through its efect on AT1 & AT2, but mainly
on AT1:
On kidney: prevent natriuresis and cause vasoconstriction.
-On blood vessels: cause potent vasoconstriction.
-On adrenal cortex: increase release of aldosterone which stimulates
sodium reabsorption from distal nephron.
-On brain: have vasopressor action when injected intraventricular
[2]
Diabetes is the frst cause of CKD then HTN is the second one [3,4]
also increase age has a role in such disease, CKD is defned as persistent
kidney damage accompanied by reduction GFR and presence of
albuminuria, So the damaged kidney fail to flter the blood from wastes
and fuid, lead to increase the blood volume which cause increase in
blood pressure (HTN), HTN has been found to occur in 85% to 95% of
patients with CKD (stages 3-5) [5].
Te uncontrolled hypertensive patients have an increased
intraglomerularal pressure that lead to damage of glomeruli & increase
protein fltration, so this shows the relation between HTN and CKD,
how both of them can cause the other Figure 2, and the importance of
maintaining BP normal to decrease renal disease and cardiovascular
morbidity and mortality [3].
Reno vascular hypertension refects the relation between
anatomically evident artero-occulosion disease and hypertension.
Approximately two third of renovascular hypertension caused by
atherosclerosis of renal artery and the other one third caused by fbro
muscular disease and other congenital anomalies [6]. Tere are other
clinical entities as: acute renal thrombosis, embolism, cholesterol
embolic disease, aortic dissection and so on.
Renal artery stenosis (RAS) is one of the commonest causes of
renovascular hypertension, its prevalence increases by aging and many
risk factors especially smoking but doesn’t depend on race [6],
RAS is characterized by narrow arterial lumen by formation of
atherosclerotic plaque due to increase the permeability of plasma
macromolecules as LDL and increase of cells as macrophages, smooth
muscle cells & endothelial cells, which lead to this lesion when these
Abstract
Background & objectives: Our review discuss the relation between hypertension and the renal system ,and show
the cyclic effect of both hypertension and chronic kidney damage on each other, our objectives are to control the high
blood pressure with minimal renal affection due to side effects of medications.
Materials & methods: many studies and trials compare between different antihypertensive drugs and their effects
on kidneys which may decrease their effciency.
Results: Angiotensin converting enzyme inhibitor (ACE-Is), angiotensin II receptor blocker (ARBs), Beta-blockers
and calcium channel blockers are identifed to be the second line of treatment of hypertension according to a network
meta-analysis conducted in 2003, ACE-Is were found to show a signifcant effect in slowing the progression of
nephrosclerosis and slower declining of GFR more than β-blocker or calcium channel blocker.
Conclusion: Kidney is indispensable organ in the body that we must protect it from the irreversible macroscopic
and microscopic changes pathological as : macroscopic (small size, fnely granular surface, adherent and diffculty
stripped capsule, fbrotic, atrophic, not demarcated cortex on cut section, thick prominent arterioles and increased
peripelvic fat) and microscopic (afferent and efferent arterioles show benign arteriosclerosis, gradual ischemic
atrophy and fbrosis of the glomeruli, atrophy of non-functioning tubules related to atrophic glomeruli, may undergo
compensatory cystic dilatation of tubule related to functioning glomeruli). ACE-Is is considered the drug of choice in
hypertensive patients complicated with chronic kidney disease, In hypertensive patients that are refractory to medical
treatment, renal sympathetic denervation is a safe alternative.
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ISSN: 2161-0959
Journal of Nephrology & Therapeutics