anatomy

1. ANATOMY AND
PHYSIOLOGY OF RENAL
SYSTEM
Moderator: Dr. Anupama Gupta
Presenter :Dr. Mahendra Kumar Sood

2. Kidneys
 Kidneys are a pair of excretory organs situated on the
posterior abdominal wall, extending from upper
border of T12 to L3 vertebra
 Right kidney is slightly lower than the left
 Each kidney is 11 cm long, 6 cm broad and 3 cm
thick, weight 150 g in males and 135 g in females
 Capsules or coverings of kidneys - Fibrous capsule,
Peri-renal fat, Renal fascia and Para-renal fat
 Coronal segment – cortex; medulla; renal sinus

3. Renal cortex
 Cortical lobules -
which form caps over
the bases of the
pyramids
 Renal columns -
which dip in between
the pyramids
Renal medulla
 has 10 conical masses
called renal pyramids,
their apices form renal
papillae
Renal sinus
 Space that extends into kidney from hilus
 Contains branches of renal artery and renal vein
 Renal pelvis divides into 2-3 major calices and these in turn divide
into 7-13 minor calices, each minor calyx (cup of flower) ends in an
expansion which is indented by 1-3 renal papillae

4.  Histologically, each kidney is composed 1-3 million
uriniferous tubules. Each consists of secretory part
which functional unit of kidney.
 Nephrons open in to collecting tubules. Many such tubules
unite to form the ducts of Bellini which open into minor
calices
Arterial Supply
 One renal artery on each side arising from abdominal
aorta
 At or near hilus, renal artery divides into anterior and
posterior branches giving rise to segmental arteries
Lymphatics
 Lateral aortic nodes
Nerve Supply
 Renal plexus (an off shoot of coeliac plexus, T10-L1)

5. Anatomical & Functional Division of Nephron
 Renal Corpuscles
(Glomerulus + Bowman’s
capsule)
 Proximal Tubule
 Loop of Henle
 Distal Tubule
 Collecting Duct
 JG Apparatus

6. Two types of nephrons are present
 Cortical nephrons with short loop of Henle
 Juxtamedullary nephrons with long loops of
Henle

7. Glomerulus - Five components
 Capillary endothelium – 70-
100 nm fenestrations – restrict
passage of cells
 Glomerular basement
membrane – filters plasma
proteins
 Visceral epithelium –
podocytes with foot processes
with 25-60 nm gaps,
permeability altered by
contraction of foot processes
 Parietal epithelium (Bowman’s
capsule)
 Mesangium (interstitial cells) –
pericytes, structural support,
phagocytosis, restricts blood
flow in response to
angiotensin-II
Filtration
barrier

8. Filtration barrier - Size and charge selective
 Charge: all 3 layers contain negatively charged
glycoproteins  restricts passage of other negatively
charge proteins
 Size: Molecules with radius <1.8 nm  water,
sodium, urea, glucose, inulin  freely filtered
 >3.6 nm  hemoglobin and albumin  not filtered
 Between 1.8-3.6  cations filtered, anions not
 Glomerulonephritis  negatively charged
glycoproteins destroyed polyanionic proteins
filtered  proteinuria

9. Tubule
Proximal Tubule (PCT)
 60-75% ultrafiltrate  reabsorb isotonically in PCT
 Reabsorption takes place through apical side of cell
membrane  basolateral cell membrane  renal
interstitium  peritubular capillaries
 Carbonic anhydrase inhibitors (acetazolamide)
interfere with Na+ reabsorption and H+ secretion in
PCT

10. Functions
Reabsorption
 NaCl
 Water
 Bicarbonate
 Glucose
 Proteins
 Aminoacids
 K+, Mg, PO4
+, uric acid,
urea
Secretion
 Organic anions
 Organic cations
 Ammonia products
Reabsorption of solutes in
PCT

11. Sodium reabsorption in PCT (65-75% of filtered Na+
load reabsorbed)
Na+ is actively transported out of proximal tubular cells at
their capillary sides by membrane bound Na+_ K+ ATPase

Resulting low intracellular concentration of Na+

Passive movement of Na+ down its gradient from tubular
fluid into epithelial cells

Na+ reabsorption is coupled with reabsorption of other
solutes and secretion of H+  reabsorption of 90% of
filtered HCO3 ions
Chloride absorption  passive  follows concentration
gradient  transverse tight junctions between adjacent
tubular epithelium

12.  Water  specialised channels composed of
membrane protein aquaporin-1 (apical membrane) 
facilitate water movement passively along osmotic
gradients
Secretion :
 Cations ( Creatinine, cimetidine, quinidine,) : share
same pump mechanism and interfere in excretion of
one another
 Anions include Urate, ketoacids, penicillins,
cephalosposins, diuretics, salicyclates and most x-ray
dyes

13. Loop of Henle
 Consists of descending and ascending portions.
 Maintaining a hypertonic medullary interstitium.
 The ascending portion consists of thin ascending limb, a
medullary thick ascending limb and a cortical thick
ascending limb.
 25-30% of ultrafiltrate reaches loop of Henle
 Only,15-20% filtered Na+ load is reabsorbed
 Solute and water reabsorption is passive and follows
concentration and osmotic gradients (except thick
ascending loop)

14. In Ascending thick segment,
 Sodium reabsorption is coupled to both K+ and Cl-
reabsorption
 Impermeable to water
 Important site for calcium and magnesium
reabsorption
 Parathyroid hormone  calcium reabsorption at this
site
 Loop diuretics inhibit Na+ and Cl- reabsorption in
TAL compete with Cl- for its binding site on carrier
protein

15. Sodium and chloride reabsorption in thick ascending
loop

16. Distal tubule
 Very tight junctions between tubular cells
relatively impermeable to water and Na+
 5% of filtered Na+ load  reabsorbed
 Major site of parathyroid hormone and Vit D
mediated calcium reabsorption
 The late distal segment (collecting segment)
 Hormone mediated Ca+2 reabsorption
 Aldosterone mediated Na+ reabsorption

17. Collecting tubule
 divided into cortical and medullary portions
 5-7% of filtered Na+ load is reabsorbed
Cortical collecting tubule – consists of
two types of cells:
Principal cells  secrete K+ and
aldosterone mediated Na+ reabsorption
Intercalated cells  acid base regulation

18. Secretion of hydrogen and reabsorption of
bicarbonate and potassium in cortical collecting
tubule

19. Aldosterone
 Enhances Na+ -K+ ATPase activity by  number of
open Na+ & K+ channels in luminal membrane
 Enhances H+ secreting ATPase on the luminal border
intercalated cells
 Because principal cells reabsorb Na+ via an
electrogenic pump
 Either Cl- must be reabsorbed
 K+ must be secreted to maintain electroneutrality
  intracellular K+ favours K+ secretion

20. K+ sparing diuretics
Competitive
 Spironolactone – aldosterone receptor antagonist
 Inhibits aldosterone mediated sodium reabsorption
and potassium secretion in collecting tubule
Non-competitive
 Triamterene and amiloride inhibits sodium
reabsorption and potassium secretion by decreasing
number of open channels in luminal membrane of
collecting tubule

21. Medullary collecting tubule
 Site of action of ADH or AVP (arginine vasopressin)
 stimulates expression of water channel protein,
aquaporin-2, in the cell membrane
 Dehydration   ADH secretion  luminal
membrane becomes permeable to water  water is
osmotically drawn out of tubular fluid passing
through the medulla  concentrated urine (upto 1400
mos)
 Adequate hydration – suppressed ADH secretion 
fluid in collecting tubule passes through medulla
unchanged and remains hypotonic (100-200 msom/l)
 Hydrogen ion secreted are excreted in the form of
titrable acids (phosphates) and ammonium ions

22. Countercurrent mechanism:
 Regulates tonicity of
tubular fluid and
medullary interstitium.
 Counter current
multiplier (loop of
Henle)
 Counter current
exchangers (cortical
and medullary
collecting tubules and
their respective
capillaries – vasa recta)

23.  Tubular fluid enters the distal PCT iso-osmotic with plasma (300
mOsm/kg) (1).
 Descending limb of Henle (2)  water rapidly diffuses out into
the increasingly hypertonic medulla and is removed by the vasa
recta
 Tubular fluid becomes hypertonic, largely because of conc. of
NaCl.
 Urea diffuses in from the hypertonic interstitium, further
increasing tubular fluid osmolality (1200 mOsm/kg).
 Thin ascending loop of Henle (3), NaCl passively diffuses into the
interstitium along its concentration gradient
 But water is trapped in the water-impermeable tubule, which
progressively decreases tubular fluid osmolality.
 Urea passively diffuses into the tubular fluid (urea recycling).
 Tubular dilution is accelerated by active reabsorption of NaCl in
the thick ascending loop and proximal distal tubule (4).

24.  Fluid entering distal tubule is quite hypo-osmotic (100 mOsm/kg)
 In the collecting segment (5), the osmolality of the tubular fluid
returns to that of plasma (300 mOsm/kg)
 But contents of the proximal tubule, the solute component consists
largely of urea, creatinine, and other excreted compounds.
 Increased plasma antidiuretic hormone (ADH) renders the cortical
and medullary collecting ducts (6) permeable to water, which
passively diffuses into the hypertonic medullary interstitium.
 Some urea diffuses out into the medulla, the maximal osmolality
of concentrated urine (7) approaches that of the hypertonic
medullary interstitium, about 1200 mOsm/kg
 In the absence of ADH, the collecting ducts remain impermeable
to water, and the urine is diluted.

25. Counter Current Exchange by Vasa Recta
• Is important component of
countercurrent mechanism and
maintain Hypertonicity of
countercurrent exchange.
• Permeable to salt, H20 (via
aquaporins), & urea
• Recirculates salt, trapping some
in medulla interstitial fluid
• Reabsorbs H20 coming out of
descending limb
• Descending section has urea
transporters
• Nacl and Water diffuse into
descending limb and diffuse
back into medullary tissue fluid.

26. Juxtaglomerular apparatus
 Macula densa – modified
portion of thick ascending limb
which is applied to glomerulus
at the vascular pole between the
afferent and efferent arterioles
containing chemoreceptor cells
which sense tubular
concentration of NaCl
 Granular cells – lies in wall of
afferent arteriole close to
macula densa.
Produce renin, which catalyses
the formation of angiotensin 
modulates efferent and afferent
arterial tone and GFR

27. Functions
Nephron regulates
 Intravascular volume, osmolality, acid base
balance, excrete the end product of metabolism
and drugs
 Urine is formed by combination of glomerular
ultrafiltration + tubular reabsorption and secretion
Nephron produces hormones
 Fluid homeostasis (renin, prostaglandins, kinins)
 Bone metabolism (1,25-dihydroxycholecalciferol)
 Hematopoiesis (erythropoietin) – produced by
interstitial cells in peritubular capillary bed (85%
 stimulus hypoxia

28. Circulation of renal blood flow Renal artery divides
serially into – interlobar
artery  arcuate 
interlobular arteries 
afferent arterioles 
capillary tufts of renal
glomeruli into outer
cortex  efferent
arterioles  in
juxtamedullary zone 
arterioles become vasa
recta (closely applied to
loop of henle)
Venous drainage:
Stelate veins 
interlobular veins 
arcuate veins 
interlobar veins

29. Cortex Medulla
Percent renal blood flow 94 6
Blood flow (mL/min/g) 5.0 0.03
PO2 (mm Hg) 50 8
O2 extraction ratio (VO2 /DO2 ) 0.18 0.79
Distribution of renal blood flow between the cortex &
medulla
 The renal medulla receives only a small fraction of the total
renal blood flow, and flow rates are extremely slow
 As a result, tissue oxygen tension is extremely low, and the
medulla extracts almost 80% of the oxygen delivered to it
 A very mild reduction in total and cortical renal blood flow
may therefore induce ischemia and hypoxia in the renal
medulla
DO2 = Oxygen delivery, VO2 = Oxygen consumption

30. RENAL BLOOD FLOW AND
GLOMERULAR FILTERATION
CLEARANCE:
o The renal clearance of a substance is the volume of
blood that is completely cleared of that substance
per unit time.
o Used in measurement of RBF and GFR.
RENAL BLOOD FLOW:
o Renal plasma flow(RPF) is most commonly
measured by p-aminohippurate(PAH) clearance.
o PAH at low plasma cone, assumed to be completely
cleared from plasma by filtration and secretion in
one passage through the kidneys.

31. 

32. 

33. o The ratio of GFR to RPF is called the filtration
fraction(FF) and is normally 20%.
o GFR is dependent on the relative tones of both the
afferent and efferent arterioles.
o Afferent arteriolar dilation or efferent arteriolar
vasoconstriction increase the FF and maintain GFR,
when RPF decreases.

34. Renal autoregulation
 Enables the kidney to maintain solute and water
regulation independently of fluctuations in arterial
blood pressure
 Kidney maintains a constant renal blood flow and
GFR through renal arterial range of 80-180 mmHg

35. Intrinsic Myogenic Regulation
Renal vascular resistance

Mediated by variable resistance of afferent arterioles

 mean arterial pressure

 renal vascular resistance
( tone, dilatation of afferent arterioles)

Myogenic response

Renal blood flow and GFR maintained

Vice versa, afferent arterioles constrict in response to  MAP

36. Tubuloglomerular feedback
 GFR

 delivery of NaCl to distal tubule

 Cl- sensed by macular Densa cells

Release of renin (from afferent arterioles)

Angiotensin II

Arteriolar constriction
 GFR and RBF

37.  Normally, a balance is present between systems promoting
renal vasoconstriction and sodium retention versus systems
promoting renal vasodilation and sodium excretion.
 Surgical stress, ischemia, and sepsis tip the balance in favor
of vasoconstriction and sodium retention.
 On the other hand, hypervolemia (or induction of atrial
stretch) tips the balance in favor of vasodilation and sodium
excretion.
Hormonal Regulation

38.  Angiotensin II causes generalised arterial
vasoconstriction and reduces RBF.
 Renal synthesis of vasodilating
prostaglandins(PGD2, PGE2 , PGI2 ) is an
important protective mechanism during periods
of systemic hypotension and renal ischemia.
 ANP released from atrial myocytesin response
to atrial distension, antagonizes the
vasoconstrictive action of angiotensin II and
relaxes mesangial cells, effectively increasing
GFR.

39. Neuronal Regulation
Sympathetic outflow from spinal
cord(T4-L1)

Celiac & renal plexus

Innervate the JG apparatus (β1 )
and renal vasculature (α1 )

α1 –receptors enhance sodium
reabsorption in PCT, whereas α2 –
receptors decrease reabsorption and
promote water excretion

40. Autoregulation impaired in
 Severe sepsis
 ARF
 During cardiopulmonary bypass
 Autoregulation is not abolished by most anaesthetic
agents

41. Regulation of Blood pressure and fluid balance by
Renin-angiotensin-aldosterone system

42. The Ureters
 Pair of muscular tubes
 Extend from renal pelvis to the bladder
 Peristaltic contractions force urine from the kidneys to the
urinary bladder
 Oblique entry into bladder prevents backflow of urine

43. Urinary Bladder
 A collapsible muscular
sac
 Stores and expels urine
 Full bladder – spherical
 Expands into the abdominal
cavity
 Empty bladder – lies
entirely within the pelvis
Figure 23.13

44. The urethra
 Extends from the urinary bladder to the exterior of the body
 Passes through urogenital diaphragm (external urinary sphincter)
 Differs in length and function in males (18-20cm)and females(4cm)
 Internal urethral sphincter - involuntary smooth muscle
 External urethral sphincter - voluntarily inhibits urination, relaxes when one
urinates

45. Effects Of Anesthesia And Surgery On
Renal Function
Reversible decreases in RBF, GFR, urinary flow and
sodium excretion occur during both regional and
general anesthesia.
Most of changes are indirect and are mediated by
autonomic and hormonal responses to surgery and
anesthesia.
INDIRECT EFFECTS
Cardiovascular: most inhalation and intravenous
agents and sympathetic blockade in spinal or epidural
anesthesia may cause drop in systemic blood pressure.

46. Decreases in blood pressure below limits of
autoregulation reduce RBF, GFR, urinary flow and
sodium excretion.
Neurologic: incresed sympathetic activity in
perioperative period due to anxiety, pain , light
anesthesia and surgical stimulation increases renal
vascular resistence and activates hormonal systems,
reducing RBF, GFR and urine output.
Endocrine : stress response to anxiety, pain, surgical
stimulation, hypoxia, acidosis and hypothermia
increases epinephrine, norepinephrine, renin,
angiotensin II, aldosterone, ADH, cortisol.

47. DIRECT ANESTHETIC EFFECTS
 Volatile agents decrease renal vascular
resistence.
 Ketamine minimally affects renal function and
preserve renal function during hemorrhagic
hypovolemia.
 NSAIDs prevents renal production of
vasodilatory prostaglandins.
 ACE inhibitors block the protective effects of
angiotensin II and may result in reduction in
GFR during anesthesia.

48. DIRECT SURGICAL EFFECTS
 The pneumoperitoneum produced during laproscopy
alter renal physiology.
 The increase in intraabdominal pressure typically
produces oliguria or anuria that is proportional to
insufflation pressure due to venous compression,
renal parenchymal compression, decreased cardiac
output, and increase in plasma renin, aldosterone and
ADH.
 Other surgical procedures that alter renal function
are:-
Cardiopulmonary bypass
Cross clamping of aorta
Dissection near the renal arteries.

49. References
 Miller’s Anaesthesia, 6th ed. Functional anatomy and
renal physiology.
 Wylie and Churchill Davidson’s. Functional anatomy and
renal physiology, 7th ed.
 Barash Clinical Anaesthesia, Functional anatomy and
renal physiology, 5th ed.
 Morgan. Clinical Anaesthesiology, 4th ed.
 Ganong WF. Review of Medical Physiology, 20th ed.