2. Anatomy of the kidney
• The kidney is a retroperitoneal
organ, about 150 gm in weight
(2 kidneys 0.5 % of the body
weight).
• It is covered by a renal capsule
and renal fascia.
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3. Structure of the kidney
• The kidney is divided into an outer cortex and
inner medulla.
- The medulla is composed of renal pyramids,
separated by renal columns.
- The renal pyramids empty urine into the
calyces that drain into the renal pelvis. From
there urine flows into the ureter and is
transported to the bladder to be stored.
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4. General function of the kidney
• Regulate ECF volume.
• Regulation of electrolytes.
• Regulation of arterial blood pressure.
• Regulation of pH (acid-base balance).
• Excretion of waste products.
• Endocrinal function (renin- erythropoietin- active vitamin D).
• Degradation of hormones.
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5. Functional organization of the kidney
• Renal cortex:
Red and dotted.
Contains glomeruli.
Contains proximal tubules,
distal convoluted tubules and
cortical collecting duct.
• Renal medulla:
Pale and radial.
Contains renal pyramids which
contain minor calyces that unite
to form major calyces.
Contains loop of Henle and
medulary collecting ducts.
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10. Nephron
it is the structural and functional unit of the kidney
Renal corpuscle
• Formed of:
1) glomerulus: 20-40 loop of
capillaries between afferent
and efferent arteriole.
2) Bowman’s capsule: which is
the blind end of the proximal
tubule.
Renal tubules
• Formed of:
1) Proximal tubule.
2) Intermediate tubule (loop of
Henle).
3) Distal tubule (distal
convoluted tubule, connecting
tubule and collecting duct.
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13. Types of nephrons
Superficial cortical
• 85-90 % .
• Glomerulus in the outer 2/3 of the
cortex.
• Loop of Henle is formed of DLH
and ALH.
• Loop of Henle makes a bend at the
junction between outer and inner
medulla.
• Small in size with low capacity to
reabsorb salt and water.
Juxta medullary
• 10-15 %.
• Glomerulus in the inner 1/3 of the
cortex.
• Loop of Henle is formed of DLH ,
thin ALH and thick ALH.
• Loop of Henle makes a bend at the
tip of inner medulla.
• Large in size with high capacity to
reabsorb Na and water.
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15. Juxta-glomerular apperatus
• It is system formed of modified:
1) Macula densa cells.
2) Juxta- glomerular granular
cells.
3) Extra-glomerular mesengial
cells.
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16. Macula densa cells
• Modified tubular epithelial cells.
• Present at the transitional zone between thick ALH and DCT.
• Monitor Na and chloride concentration in the tubular fluid.
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17. Juxta glomerular granular cells
• Present in the wall of the afferent arteriole.
• Smooth muscles with epitheliod apperance.
• Forms , stores and secretes renin.
• Contains B1 adrenergic receptors.
• Acts also as baroreceptors.
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18. Extraglomerular mesengial cells
• It is a continuation of the intraglomerular mesengial cells.
• It is in direct contact with the macula densa and juxtaglomerular
granular cells.
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19. Stimuli for renin release
• Sympathetic stimulation.
• Renal ischemia.
• Decrease Na+ and Cl- concentration in the tubular fluid.
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20. Mechanisms of stimulation:
Renin release
In cases of hemorrhage with
decreased circulating blood
volume stimulation of low
and high pressure
baroreceptors located in the
great vessels of the thorax
stimulation of the
sympathetic nervous system
stimulation of B receptors
on JGG cells renin
release
With renal artery stenosis or
thrombosis decreased
renal perfusion pressure
stimulation of the juxta
glomerular granular cells
renin release.
Decreases Na & Cl
concentration of the tubular
fluid stimulation of the
macula densa that
stimulates the JGGcells via
Prostaglandins renin
release.
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23. Function of the renin angiotensin system
Salt and water retention
1- angitensin II increases Na
reabsorption from proximal
tubules.
2- AII stimulates the zona
glomerulosa of the adrenal
cortex to secrete aldoseterone
that increases Na reabsorption
from distal tubules.
Vasoconstriction
1- arteriolar constriction
increasing the afterload (arterial
blood pressure).
2- Venoconstriction increasing the
preload (venous return).
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24. Pharmacological Inhibitors of the RAAS
• Angiotensin converting enzyme inhibitors: decreased the formation of
AII.
• Angiotensin II blockers: decreased aldosterone release.
• B- blockers.
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