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16 Cards in this Set
- Front
- Back
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Sodium |
- main electrolyte determining BP, plasma volume and urinary concentration - completely filtered at glomerular level, 99% is transients and 1% is found in urine - sodium can’t be actively secreted in the urine and only the amount of reabsorption can be modified by stopping it - the fractional excretion of sodium is the % of sodium filtered by the kidney which is excreted in the urine - the filtered sodium can be calculated as the product of GFR (estimated from creatinine clearance) and the sodium concentration in the plasma, while the excreted sodium as the sodium in the urine is multiplied by the urinary flow rate |
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Renal tubules |
- made from 4 types of cells working at the same time 1) proximal convoluted tubules cells (65% of total sodium reabsorption) 2) loop of Henle cells (25%) 3) distal tubular cells (5%) 4) collecting duct cells (5%) - they are epithelial cells that express transporters on their surface according to local signals - active transport is the same in all tubular cells, passive transport is different according to the segment - distal tubular cells and collecting duct cells are the most important for specific sodium handling |
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Sodium and water reabsorption |
- sodium and water reabsorption are a linked phenomena and the link varies in different segments of kidney tubules: 1) PCT: isoosmotic water reabsorption 2) Loop of Henle: water reabsorption varies according to osmolarity 3) DCT and CT: reabsorption is influenced by hormones (regulating BP, volume and calcium homeostasis) - sodium is more concentrated outside of the cells (140 vs 20) while potassium is the opposite (3.5-5 vs 100) - the sodium potassium pump is found towards the interstitial side of the tubule is the main driving force in sodium reabsorption and its energy dependent, working against concentration - In case of ischemic injury= impairment in tubular function, sodium increases inside the cells. - different tubular segments have different passive transporters located in the luminal space |
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Proximal convoluted tubule: luminal side |
- glucose, amino acids, uric acid and glucose phosphate co transporters are found - it has a buffering function: bicarbonate production - co transporters are targets for anti-diabetic drugs relevant in CKD in fanconi disease= damage in PCT cells= glucose in urine without diabetes |
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Loop of Henle |
- descending, permeable to water - ascending, sodium reabsorption - the driving force for sodium reabsorption is the sodium potassium pump= gradient, all other transports are passive - a transporters allows for sodium, potassium and chloride symports and its the target of a very important anti-diuretic fuoresimde (LASIX)= hypokalemia and decreased chloride - ROMK: family of channels=potassium flow towards the lumen or the interstitial depending on location - in the PCT and loop of Henle: water passes through tight junctions= paracellular transport |
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Distal cells |
- closely associated to the juxtaglomerular apparatus (sensing sodium and chloride concentration and producing renin) and can be divided into: A) DTC 1= non-hormone sensitive characterized by sodium potassium pump and sodium chloride passive co transport regulated by wink through angiotensin II. It’s the targets of thiazide anti-diuretics revenant for BP and does not affect potassium B) DTC 2 = hormone-sensitive - calcium is also reabsorbed at this level. Aldosterone and angiotensin II are the most important to regulate BP but also PTH vasopressin and calcitriol. There are also a group of kinases able to regulate the aldosterone function. |
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Collecting duct |
1- principal cells (DTC2) that are sensitive to hormones like aldosterone 2- intercalated cells for pH regulation. At the level of the principle cells, aldosterone regulates ENAC (channel located in luminal district made of 3 subunits made of 3 genes that can mutate). In the collecting duct, there’s a possibility to regulate water reabsorption thanks to ADH modulating aqua potion expression, angiotensin II can increase aquaporin formation = increase in plasma volume |
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Kinases |
- WNK modulates symports in the loop of Henle, co transport in distal tubular cells and ROMK in collecting ducts - act before the long genomic action of aldosterone = increasing ENAC number WNK kinases open/close channels and increase/decrease activity of co transport. |
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Drugs that can block the system |
1- AMYLORIDE can close ENAC 2- anti-aldosteronic drugs/potassium sparing diuretics = antagonize aldosterone at the receptor level 3- blockers of 11-beta-hydroxysteroid-dehydrogenase |
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Potassium reabsorption and secretion |
- potassium excretion is modulated by moving ROMK towards interstitial space, angiotensin II is the only one involved - according to what we eat, the excretion of potassium will change |
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BP regulation and role of renin/angiotensin system |
- kidney is the most important in pressure regulation and pressure alteration, BP measurement requires closing the artery properly - systolic BP (SBP)= pressure in the arteries when heart beats, first number - DBP: 2nd number, pressure during diastolic period - pulse pressure: difference btw SBP DBP, relevant in CV damage - mean arterial pressure: diastolic pressure + 1/3 pulse pressure and should be between 70 and 100. Important to evaluate organ perfusion and below 70= kidney would not filter - SBP increases in adolescents. In the elderly= dramatic increase - DBP increases in adults and decreases in the elderly - pulse pressure increases with age - mean arterial pressure decreases reducing organ perfusion - in females: the stable period for SBP is shorter than for males and decrease starts at pre-menopausal period (the decrease in diastolic is less relevant) |
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Main actors in BP control |
1- cardiac output= SV and HR dependent, HR depends on cardiac function and nervous system control. SV is dependent in intravascular volume regulated by the kidney. During cardiac decrease, a decrease in BP is expected. 2- peripheral resistance depending on length and diameter of the vascular bed, dependent on renin/angiotensin system - the kidney is able to regulate both |
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Short vs intermediate vs long term control |
- short: second, minutes= baroreceptors and chemoreceptors reflexes that mainly decrease in BP - intermediate: 30 mins or hours = renin/angiotensin - long term: vasoactive compounds - maintain the perfusion to the brain = main goal |
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Regulation through the renin/angiotensin system |
- decrease in BP - lower GFR - decreased sodium/chloride flow to macula dense - renin release - increased angiotensin II if ACE works |
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Angiotensin functions |
- systemic vasoconstriction and increasing resistance and BP - vasoconstriction of renal EA and vasodilation of AA to maintain GFR even if decrease in BP - aldosterone secretion, activation and aquaporin production = increase in blood volume |
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Renin functions |
- the stimulus is not only macula sends but also baroreceptors, sympathetic nervous system, renal hypoperfusion - the renin system can work properly only if the liver is functioning well because its the provider of angiotensinogen in cases like liver cirrhosis, BP will drop - decreased water in the body: increased water reabsorption through sensing of osmolarity in the brain and heart centers - ANP is secreted by arterial cells and closes ENAC - if there’s decreased blood volume= reduced ANP= increased ENAC activity, sodium reabsorption |
