RENAL PHYSIOLOGY REVISION NOTES

LAST MINUTE REVISION NOTES OF PHYSIOLOGY BASED ON LECTURE NOTES AND HIGH YIELD TOPICS
BASED ON PREVIOUS YEAR QUESTIONS
IMAGE BASED QUESTIONS

1. Renal system

4. •1-1.3 million nepronin each kidney

6. Total length of nephron 45-65mm
•Longest
•15mm
Proximal tubule
•5mm
Distal tubule
•20mm
Collecting duct

14. Malphigiancorpuscle = glomerulus+
bowmanscapsule

16. Glomerular membrane is formed by
•Glomerular capillary endothelium
with gaps in b/w 100nm
•Basement membrane
•No anatomical pores but only
functional
•Bowmansvisceral epithelium
(podocytes)
•Podocytes with filtration slits of size
25nm

19. •Substances less than 8nm can cross membrane
•If <4nm irrespective of charge they can cross
•If b/w 4-8nm cations cross easily & anions crosses with difficulty
GLOMERULAR MEMBRANE IS NEGATIVELY CHARGED

20. Slit diaphragm b/w podocytes

21. Proximal tubule
•S1 segment 1st part of
PCT
•S2 segment 2
nd
half of
PCT + 1
st
half of PST
•S3 segment 2
nd
half of
PST

22. •PCT

23. Collecting duct
•Cortical collecting duct
•Outer medullary collecting duct
•Inner medullary collecting duct

24. 2 types of cells in collecting duct
Principal (P) cells
•For Na + reabsorption
•K+ secretion
•H2O absorption
Intercalated (I)cells
•2 types
•Alpha cells acid secretion
•Beta cells Bicarbonate secretion

26. Juxtaglomerular apparatus
•Juxtaglomerular cells
(modified cells in tunica
media of afferent
arteriole)
•Macula densa(modified
distal tubule lining)
•Interstitial cells /laciscells

28. •Modified smooth muscle cells in tunica media of afferent arteriole
•Senses decreased pressure in afferent arteriole & produces renin act on
afferent arteriole
•Contains granules which secrete renin
•Innervated by sympathetic nerve produce renin on sympathetic discharge
JG cells
•Modified cells of distal tubule in contact with afferent arteriole
•Chemoreceptors detect low sodium in distal tubule
Macula
densa
•Extraglomerular mesangial cells
•In space b/w afferent & efferent arteriole Laciscells

30. Tubuloglomerularfeedback

31. •The sensor for this response is the macula densa. The amount of fluid
entering the distal tubule at the end of the thick ascending limb of the loop
of Henle depends on the amount of Na+ and Cl–in it.
•The Na+ and Cl–enter themaculadensacells via the Na–K–2Cl
cotransporter in their apical membranes. The increased Na+ causes
increased Na, K ATPase activity and the resultant increased ATP hydrolysis
causes more adenosine to be formed.
•Presumably, adenosine is secreted from the basal membrane of the cells. It
acts via adenosine A 1 receptors on the macula densacells to increase their
release of Ca2+ to the vascular smooth muscle in the afferent arterioles. Tis
causes afferent vasoconstriction and a resultant decrease in GFR

32. The Na+ and Cl–enter the macula densacells via the Na–K–2Cl cotransporter in their apical membranes
The increased Na+ causes increased Na, K ATPase activity ↑ATP hydrolysis more adenosine to be
formed.
Adenosine adenosine 1 receptors on the macula densacells to increase their release of Ca2+ to the
vascular smooth muscle in the afferent arterioles
afferent vasoconstriction and a resultant decrease in GFR

39. •Renal blood flow = 1260 ml =1.1 L-1.3 L (22 –25 % CO)
•Renal plasma flow = 700ml/min
•PAH is a substance that is

40. •O2 consumption
•Total 18 mL/min
•Cortex 9ml/min
•Inner medulla 9mL/min
•Artery –venous O2 difference = 14ml/l

41. Autoregulation of renal blood flow

43. Glomerulotubularbalance

44. Glomerulotubularbalance
•an increase in GFR causes an increase in the reabsorption of solutes,
and consequently of water, primarily in the proximal tubule, so that in
general the percentage of the solute reabsorbed is held constant. Tis
process is called glomerulotubularbalance, and it is particularly
prominent for Na
•one mediating factor is the oncotic pressure in the peritubular
capillaries. When the GFR is high, there is a relatively large increase in
the oncotic pressure of the plasma leaving the glomeruli via the
efferent arterioles and hence in their capillary branches. This
increases the reabsorption of Na+ from the tubule

58. GFR
•GFR = Kf[(PGC –PT) –(πGC –πT)]

59. Factors affecting GFR

66. Filtration fraction
•The ratio of the GFR to the RPF, the fltrationfraction, is normally
0.16–0.20

68. Filterability of a substance
•Water is freely filterable through glomerular membrane
•Filterability of 1 means substance is freely filterable as water
•Na glucose bicarbonate inulin creatinine
•Not filterable
•Albumin
•Myoglobin is partially filterable
•Free Hb(in plasma ) is excreted in urine
•Hbin RBC is not excreted

69. Tubular reabsorption

70. Proximal tubule
•60-70 % of glomerular filtrate is reabsorbed
•Proximal tubule is the site where enormous volume of glomerular
filtrate is reduced to one third
•60-70 % of solute & 60 -70 % of filtredwater are reabsorbed
•Therefore fluid leaving proximal tubule is isotonic to plasma

72. Thin descending limb of LOH
•Highly permeable to water (through aquaporin1)
•Relatively impermeable to sodium chloride & urea
•No active secretion or reabsorption
•FLUID IN DESCENDING LIMB BECOMES HYPERTONIC

73. Thin ascending limb of LOH
•Less permeable to water
•But more permeable to NaCl
•Thin segment of LOH is present only in juxtamedullary nephron (15 %)

74. THICK ASCENDING LOH
•Almost totally impermeable to water
•Active absorption of Na + & otherionsoccurs & water is not
reabsorbed therefore tubular fluid is hypotonic to plasma

79. Reabsorption of sodium
•65 % reabsorption
•NHE3 transporter
(Na+ entry coupled
to secretion of H+)
•Also secondary
active transport with
glucose aa
Proximal
Tubule
•30 % of na
reabsorption
•NKCC
transporter
Thick
ascending
limb of
LOH
•7 % of
reabsorption
•NCC
DCT
No sodium rebsorptionin descending limb of LOH

89. K+ reabsorption
•Only electrolyte that is reabsorbed as well as secreted

92. Hypokalemiacauses alkalosis hyperkalemia
causes acidosis

94. Glucose reabsorption
•By secondary active transport
•SGLT2 in PCT SGLT1 in PST
•Mutation of SGLT2 renal
glycosuria
•GLUT 2 is present in basolateral
membrane
•Glucose iasabsorbed 100 % in
proximal tubule

95. glucose transport
•The TmGglucose
•Maxmrate of absorption of glucose by tubule
•is about 375 mg/min in men and 300 mg/min in women

96. •The renal threshold for glucose is the plasma level at which the
glucose frstappears in the urine in more than the normal minute
amounts.
•One would predict that the renal threshold would be about 300
mg/dL, that is, 375 mg/min (TmG) divided by 125 mL/min (GFR).
However, the actual renal threshold is about 200 mg/dLof arterial
plasma, which corresponds to a venous level of about 180 mg/dL

98. Splay
•The “ideal” curve shown in this diagram would be obtained if the TmG
in all the tubules was identical and if all the glucose were removed
from each tubule when the amount filtered was below the TmG.
•This is not the case, and in humans, for example, the actual curve is
rounded and deviates considerably from the “ideal” curve. This
deviation is called splay.
•d/t heterogenecityof nephrons ienot all nephrons have TmGof 375mg/min
•Not all nephrons are not maximally active
•The magnitude of the splay is inversely proportional to the avidity
with which the transport mechanism binds the substance it
transports

101. •Glucose and aminoacidsare
completely reabsorbed in
proximal tubule along with
Na+ in secondary active
transport (100 % of glucose
and aa in proximal tubule )
•HCO3 is also reabsorbed in
PCT (90%)

102. Co transport with Na
•Glucose
•Aminoacids
•Phosphates

103. Water reabsorption
•Water reabsorption is facilitated by aquaporins

105. •PCT 60 –70 %
•LOH 15 %
•Distal tubule 20 %
•DCT 5 %
•CD 15 %
Obligatory
Facultative

106. Obligatory
•Total 85 %
•Irrespective of osmolality of
blood
•Independent of ADH
Facultative
•15 –18 % from CD
•Depends on blood osmolality
•Depends on ADH

107. Aquaporin for water reabsorption

109. ADH acts on late distal tubule

110. ADH formed in suprachiasamaticN (secreted
in posterior pituitary)

111. •Main action of ADH is on medullary collecting duct where maximum
concentration of urine occurs

112. FREE WATER CLEARANCE
•measure of ability to dilute urine
•equal to the volume of plasma cleared of pure water per unit time
Equation
free water clearance (CH2O) = urine flow rate (V) -water occupied with solute (Cosm)
• Cosm= UosmV/Posm
ADH
with ADH
• CH2O < 0
• retention of free water
without ADH
• CH2O > 0
• excretion of free water
Loop diuretics
• produce isotonic urine
• CH2O = 0

114. •Negative free water clearance (concentrated urine) is seen with
osmolarityof urine > 300 mOsm, when ADH is high and water is
conserved, plasma osmolarityis decreased.
•Positive free water clearance (dilute urine) is seen with osmolarityof
urine < 300 mOsm, when ADH is low and free water is removed from
body, plasma osmolarityis increased.

115. Free water clearance = 0
•chronic renal failure is zero
•Loop diuretics

117. CA2+ REABSORPTION

118. •99 % ca2+ is reabsorbed in nephron
•Maximum ca2+ is reabsorbed in PCT
•PTH increases ca2+ reabsorption from TAL & distal tubules
•Cacitriolincreases ca2+ reabsorption in TAL & distal tubule

119. H+ secretion in PCT
•In PCT H+ is secreted by Na+ -H+ exchanger(secondary active
transport)
•Maximum H+ secretion by this transporter
•H+ secreted in PCT does not acidify urine
•Helps in rebsorptionof HCO3

121. H+ secretion in DCT or CD
•ATP driven H+-K+ ATPase
•This H+ helps in acidification of urine

122. •Net acid secretion = excretable titrableacid+ excreted NH4 –excreted
HCO3

123. Titrableacid
•H2PO4 largest component of titrableacidity

124. Reabsorption of HCO3-

125. •H+ is not absorbed by nephron anywhere
•Substance reabsorbed & secreted by nephronuric acid creatinine
K+

128. Countercurrentmechanism

129. Countercurrentmechanism
•Countercurrentmultiplier
•TAL
•Na + K + Cl-symporter
•Collecting duct
•Active transport of Na+
•Medullary collecting duct facilitated diffusion of urea
•Ascending thin segment diffusion of Nacl:little role
•Countercurrentexchanger vasa recta

130. Countercurrentmechanism

131. Countercurrentmultiplier system in LOH

132. •Countercurrentmultiplier is active process
•Countercurrentexchanger is passive process

133. Most important substance for medullary
tonicity is urea

134. Erythropoetin

135. •Source of erythropoietin
•In kidney 85 %
•In liver 15 %
•Stimulus for EPO secretion
•Hypoxia (main cause)
•Cobalt salt
•Androgen
•Catechoalmines

138. Oliguria
•<500ml in 24 hour

139. •Cells in the thick ascending limb produce Tamm-Horsfallglycoprotein
and secrete it into the tubular fluid

142. Micturition reflex

147. •The first urge to void is felt at a bladder volume of about 150 mL, and
a marked sense of fullness at about 400 mL

148. •Lower Motor Neuron Damage
•Autonomous Neurogenic Bladder = Sacral spinal centersdamaged
•Motor Neurogenic Bladder = Efferentsdamage
•Sensory Neurogenic Bladder = Afferents damage (no stretch sensation conveyed to spinal cord)(atonic bladder)
•All of the three cause distended bladder with overflow incontinence and dribbling and predisposition to
infection. The autonomous variety may show some spinal cord lesions on MRI.
•Upper Motor Neuron Damage
•Automatic Neurogenic Bladder = is loss of brain stem control over the spinal centersand leads to retention. Damage at any
level above the conus medulariscauses what's calledSpastic bladder in which manual stimulation results in a reflex forceful
contraction of the detrusermuscle.
•Uninhibited Neurogenic Bladder = is no cortical control over the brain stem centers. Voiding mechanics is normal but
uninhibited at misappropriate times and places. example children before toilet training and frontal lobe lesions.

149. Natriuretic peptides

154. Effects of ANP are in opposite to angiotensin
II

155. Actions of ANP
./
Natriuresis Dilate afferent arteriole & relaxation of mesangial clels
Increase GFR & increase Na+ excretion
Decrease BP Increase in capillary permeability & vasodilatin
extravasation of fluid
Prevent remodelling in heart