RENAL PHYSIOLOGY REVISION NOTES
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The document details the anatomy and physiology of the renal system, including the structure and function of nephron components, renal blood flow, glomerulotubular balance, and the mechanisms of solute and water reabsorption. It describes various transporter proteins involved in sodium and glucose reabsorption, the effects of hormones like ADH on renal function, and the actions of natriuretic peptides. Additionally, it covers the regulation of urine concentration, micturition reflex, and the impact of conditions like oliguria and neurogenic bladder on kidney function.
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• GFR = Kf [(PGC – PT) – (πGC – πT)]](https://image.slidesharecdn.com/renalsystem-180417042207/85/RENAL-PHYSIOLOGY-REVISION-NOTES-58-320.jpg)
RENAL PHYSIOLOGY REVISION NOTES
- 1. Renal system
- 4. • 1-1.3 million nepron in each kidney
- 6. Total length of nephron 45-65mm • Longest • 15mm Proximal tubule • 5mm Distal tubule • 20mm Collecting duct
- 14. Malphigian corpuscle = glomerulus+ bowmans capsule
- 16. Glomerular membrane is formed by • Glomerular capillary endothelium with gaps in b/w 100nm • Basement membrane • No anatomical pores but only functional • Bowmans visceral 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 2nd half of PCT + 1st half of PST • S3 segment 2nd 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 /lacis cells
- 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 arterioleLacis cells
- 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 themacula densa cells 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 densa cells 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 densa cells 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 densa cells 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
- 44. Glomerulotubular balance • 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 glomerulotubular balance, 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)]
- 66. Filtration fraction • The ratio of the GFR to the RPF, the fltration fraction, 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 • Hb in RBC is not excreted
- 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 filtred water 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 + & othe rions occurs & 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 rebsorption in descending limb of LOH
- 89. K+ reabsorption • Only electrolyte that is reabsorbed as well as secreted
- 92. Hypokalemia causes 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 ias absorbed 100 % in proximal tubule
- 95. glucose transport • The TmG glucose • Maxm rate 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 frst appears 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/dL of 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 heterogenecity of nephrons ie not all nephrons have TmG of 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 aminoacids are 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 suprachiasamatic N (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 osmolarity of urine > 300 mOsm, when ADH is high and water is conserved, plasma osmolarity is decreased. • Positive free water clearance (dilute urine) is seen with osmolarity of urine < 300 mOsm, when ADH is low and free water is removed from body, plasma osmolarity is 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 • Cacitriol increases 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 rebsorption of 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 titrable acid+ excreted NH4 – excreted HCO3
- 123. Titrable acid • H2PO4 largest component of titrable acidity
- 125. • H+ is not absorbed by nephron anywhere • Substance reabsorbed & secreted by nephron uric acid creatinine K+
- 129. Countercurrent mechanism • Countercurrent multiplier • 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 • Countercurrent exchanger vasa recta
- 131. Countercurrent multiplier system in LOH
- 132. • Countercurrent multiplier is active process • Countercurrent exchanger 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-Horsfall glycoprotein 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 centers damaged • Motor Neurogenic Bladder = Efferents damage • 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 centers and leads to retention. Damage at any level above the conus medularis causes what's called Spastic bladder in which manual stimulation results in a reflex forceful contraction of the detruser muscle. • 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