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176 Cards in this Set
- Front
- Back
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kidney location
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between body wall and peritoneum
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major functions of the kidney
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1. rids body of wast
(from protein met. removes urea and creatine, and removes toxins/drugs) 2. maintain stable ICF and ECF by regulating excretion of solutes and water to balance intakes 3. during prolonges fasting kidney does gluconeogenisis from aa 4. make and release hormone |
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Failure of what function is most critical consequence of kidney failure
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failure to maintain a stable ICF and ECF. Can cause hypo/hypercalcemia, acidosis, alkolosis, or dehydration
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hormones made in the kidney
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erythropoeitin stimulates RBC production
1,25 kihydroxy vitamin D3 allows Ca absorption in GI |
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amount of salt kidney filters per day
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3 lbs or 1.5 kg
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amount of plasma kidney filters per day
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50 G/ day
or 2 G/hour |
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what must patient do if kidney fails?
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change diet by resticting proteins, salts and monitor water consumption
dialysis so solutes excreted can move across membrane and down a conc. gradient |
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hemodialysis
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blood is removed from circulation through a tube to artifical membrane that is permeable to small solutes. blood is then returned to the body
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pertioneal dialysis
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fluid in injected and removed from the peritoneal cavity. the membranes are the natural membranes of the peritoneum.
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outer layer of the kidney
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cortex
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functional unit of the kidney
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nephron
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blood supply to the nephron
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afferent arteriole gives rise to the glomerular capillary. the glomerulus is drained by another cap called the efferent artiole
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2 segement of the nephron
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renal corpuscle and the renal tubule
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renal corpuscle
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segment of the nephron. composed of glomerulus, bowman' capsule, and bowmans space
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renal tubule
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segment of the nephron. composed of proximal tubule, thin descending limb of the loop of henle, thin ascending limb of the loop of henle, thick ascending limb of the loop of henle, distal convoluted tubule, and the collecting duct.
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juxtaglomerular apparatus
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occurs where the thick ascneding limb of the loop of henle at junction of distal convoluted tubule comes into close contact with the renal corpuscle and contacts the afferent arteriole
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specialized cells in the nephron
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cells in the tubule called macula densa
cells in afferent arteriole called jaxtaglomerular cells |
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What does the cortex, the outermost layer of the kidney contain?
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renal corpuscles, proximal and distal convoluted tubules, superficial portions of the loop of henle and the Collecting ducts
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what does the medulla, the deep layer of the kidney contain?
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tad bit of the proximal tubule, deeper portions of the loop of henle and collectin duct.
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are there renal corpuscles in the medulla?
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No only in the cortex
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describe cortical nephrons
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v. superficial. renal corpuscle is near the kidney surface of the loop of henle does not penetrate into medulla
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describe juxtamedullary nephron
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renal corpuscle is v. close to the medulla and the loop of henle goes deep into the medulla
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what does pelvis, innermost layer of kidney conain?
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urine before it leaves to the ureter.
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region where the ureter leaves the kidney
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hilum. this is where bloodvessles, lymph, and nerves enter and exit the kidney too
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amount of CO fro kidneys
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20%
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bf from the renal arterie to the afferent arteriole
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from larger to smaller: goes from renal a. to interlobar a. in medulla, then to arcutate a. in medulla, then to interlobular a. in cortex
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How can BF to kidney be regulated?
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by smooth muscle in the afferent and efferent arterioles.
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what caps does the efferent arteriole give rise to?
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peritubular caps. fluid reabsorbed from the nephron is returned to the peritubular caps.
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caps the run parallel to the loop of henle
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peritubular caps(vasa recta). so stuff from tube is reabsorbed into these caps. this helps make urine with hi solute conc.
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Renal corpuscle physical adaptations for filtration
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bowmans capsule is in an epithelial sac.
glomerulus is cap loops v. close to epithelial sac. plasma is filtered into bowmans capsule. filtered fluid goes into the renal tubule |
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how does the glomerular cap contrast with other cap. beds?
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it is highly permeable due to fenestration that are 70-100 nm in diameter, therefore, solutes as large as plasma proteins can pass through
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describe basement membrane between cap endothelium and bowmans capsule
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gel like made from glycoproteins, proteoglycans like laminin.
v. thick negative charge so repels negatively charged plasma proteins |
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what acts as a barrier to filtration of plasma protiens?
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the basement membrane having a negative charge
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describe epithelium on bowmans capsule
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has podocytes that are elaborate thick foot like processes. there are filtration slits between the podocytes so larger molecules can be filtered
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hydrostatic and osmotic forces that allow filtration from glomerular cap into bowmans capsule
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cap hydrostatic pressure is 60 mmHg
cap protein osmotic pressure is 29 mmHg Bowmans hydrostatic pressure is 15 mmHg Bowmans osmotic pressure is 0 mmHg (60-29)-(15-0)= 16 mmHg net force favors filtration |
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why is glomerular cap. protein osmotic pressure high compared to other caps?
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bc of filtration of fluid filtered but proteins are left behind so hi solute conc.
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Why is bowmans space protein osmotic pressure 0?
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bc no proteins are filtered
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glomerular filtration rate (GFR) per day
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125 mL/min or 180 L/day
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typcial plasma flow to the nephrons
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600 ml/min or 900 L/day
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% of plasma flow to the nephrons that is filtered
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20%
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Amount of time it takes to filter all the plama in the body
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less than 30 min so plasma filters approx. 50 times a day
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ohms law
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flow=pressure/resistance
if pressure increases and flow does not change, then resistance must have also increased |
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autoregulation
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the ability of nephrons to regualte blood flow to a constant value at different levels of arterial pressure
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what pressure does kidney regulate blood flow?
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between 80-180 mmHg
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myogenic hypothesis of autoregulation
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as pressure rises the afferent arteriolar smooth muscle contracts and increases arteriolar resistance. this keeps blood flow and hydrostatic pressure in glomeruli from increasing
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tubulogomerular feedback
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increase in GFR due to increase in pressure with increase delivery of solute to juxtaglomerular apparatus and macula densa. the macula densa secretes a mediator (arachadonic acid or ATP) to cause afferent arteriole constriction to increase resistance to bring GFR back down
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what does constriction of afferent arteriole cause?
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decrease in pressure in glomerular caps. so for any given pressure, GFR is decreased and flow is reduced.
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what does constrictio of the efferent arteriole cause?
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increase in pressure in glomerular caps. For any given pressure, GFR is increased since net filtration pressure is increased but BF is decreased
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what causes constriction of afferent and efferent arterioles?
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sympathetic nerve activity. the increase in resistance causes reduction in blood flow, even if pressure increases.
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besides symp NS what other vasoconstrictors affect afferent and/or efferent arterioles?
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angiotensin II, ADH, cortisol
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How is GFR reduced with angiotensin II?
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mesangial cells which support glomerular capilllary loops can contract and reduce GFR
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vasodilators to the kidney
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prostaglandins increase BF during intense symp vasoconstriction so GFR wont shut down
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Effect of moderate increase in symp activity
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decrease blood flow but does not change GFR bc of constriction of both afferent and efferent arterioles
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effect of severe increase in symp activity
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reduces BF and GFR
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amount of Na+ and water reabsorbed in the proximal tubule
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67% or 2/3
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amount of filtered K+ that is reabsorbed in the proximal tubule
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60%
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4 main things that occur in proximal tubule
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1. reabsorbs 67% of filtered Na+ and H2O and 60% of filtered K+
2. reabsorbs all glucose & aa 3. secretes metabolic end products and toxins 4. preferential reabsorbtion of HCO3-; Cl- conc. rises |
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structure of tubular epithelium
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luminal membrane, basolateral membrane, tight junctions between cells, interstial fluid surrounds the tubule (peritubular fluid)
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How is Na+ reabsorbed in proximal tubule?
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Na+ in tube moves into tubular epithelial cells through luminal membrane down conc and electrical gradient (passive transport)
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tube lumin conc of Na?
promial tubular epithelial cell Na conc? |
luminal conc of Na is 140 mM/L and inside cell is 20mM/L. so Na want to move into the tubular epithelial cells.
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How does Na+ get from proximal tubular epithelial cell to the interstial fluid then into the peritubular cap. for reabsorbtion?
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Na+/K+ ATPase paump is on basolateral membrane of proximal tube epithelial cell. So Na+ are pumped into ISF and K+ are pumped into cell causing decrease of Na+ osmolarity in cell and increase in Na+ osmolarity in ISF. this causes water to move to ISF too through aquaporin channels and tight junctions. ISF moves into caps bc hydrostatic pressure is hi in ISF and lo in caps which promotes reabsorbtion of water and Na+.
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Na+conc by the end of the proximal tubule
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Na+ conc is the same as in the orginally filtered plasma by the end of the proximal tubule due to Na+ being isosmotically reabsorbed
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volume of fluid at end of proximal tubule
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1/3 less volume by the end of proximal tubule due to H2O and Na+ reabsorbtion
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How is K+ reabsorbed in the proximal tubule?
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K+ is NOT actively reabsorbed
As fluit leaves the tube, K+ is in the tube and it is concentrated in the tube. K+ then moves across tight junctions and into the ISF and into peritubular caps |
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How are glucose and aa reabsorbed in the proximal tubule?
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passive movement of Na+ across the lumin and into the epithelial cell uses cotransporter to bring glucose and aa with it. Once these solutes enter the cell, specific transporters extrude theses substances at basolateral membrane into ISF. the substances then enter peritubular cap.
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describe glucose reabsorbtion with diabetes
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glucose is higher than 200mg/dL a day so cotransporters are saturated and glucose cannot be reabsorbed so glucose is excreted in the urine (more glucose filtered than reabsorbed)
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What happens when certain drugs are secreted by the kidney to rapidly?
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an inhibitor of secretion like probenicid can be given to hel p maintain the plasma level
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How is H+ secreted into proximal tube?
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When Na+ passively moves out of lumen and into the cell it is coupled with H+ secretion into the lumen (Na+/H+ contransporter)
This allows H+ removal from plasma and HCO3- reabsorbtion |
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What increases H+ secretion in proximal tubule?
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peptide angitensin II bc it increases Na+ and H2O reabsorbtion by proximal tubule which is coupled with H+ secretion
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PAH in proximal tubule
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filtered and secreted. almost completely cleared from peritubular caps and into tube
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inulin in proximal tubule
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only filtered. so remains in tube to be excreted
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creatine in prxoimal tubule
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just filtered
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sodium in proximal tubule
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reabsorbed with water
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What remains in the tube at the end of the proximal tubule?
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33% of filtered Na+
33% of filtered H2O 40% of filtered K+ 0% glucose |
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amount of Na+ and K+ orginally filtered that is reabsorbed in the loop of henle
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25% Na+ and 25% K+
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only part of loop of henle that allows H2O reabsorbtion
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thin descending limb is v. permeable to water
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What part of the loop of henle is v. permeable to Na+ and Cl-?
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the ascending limb is not permeabel to water but is v. permeable to Na+ and Cl-. this aids in concentrating and diluting the urine
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What does thick ascending loop of henle do?
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creates a hypoosmotic tubular fluid bc it is impermeable to water but Na+, K+, and Cl- are reabsorbed. So salts leave and water remains.
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What does amount of water reabsorbtion in the thin descending limb of the loop of henle depend on?
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its location. whether it is among juxtamedually and superfical nephrons.
Juxtamedullary reabsorbs over 20% while superficial reabsorbe less than 10% |
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How are Na, Cl, and K reabsorbed in the thick ascending loop of henle?
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on luminal membrane Na+ movement is coupled with cotransporter that carries 1 K+ and 2 Cl-. A tad K+ leaks back into lumen. since water is not reabsorbed but solutes leave, the tube conc. decreases.
From cell to ISF. Na gets into ISF from Na/K ATPase. Cl-, and K+ diffuse through. |
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conc of tube by end of the thick ascending loop of henle
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150 mOsm/L which is hypoosmotic bc solutes are leaving the tube and water is remaining
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most typical mechanism of action of diuretics
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normally reabsorbed solutes remain in tubule bc solute reabsorbtion is inhibited. leading to increased solute and water excretion
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how does alchol act like a diuretic?
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it interferes with water reabsorbtion
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how does mannitol act like a diuretic?
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bc it cannot be reabsorbed
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Loop diuretics
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work in the thick ascending limp of the loop of henle by blockin Cl- binding site on the cotransporter so normal reabsorption of Na+, K+, and Cl- in thick ascending limb of the loop of henle isdecreased with a loop diuretic and these solutes will be excreted
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by the time tubular fluid leaves the distal convoluted tubule and collecting duct as urine, how much filtered Na+ and Water has been reabsorbed?
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99% or Na+ and 99% of water has been reabsorbed
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amount of Na reabsorbed in Distal convoluted tubule and colecting duct
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7%
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after the loop of henle, where is most water reabsorbed?
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well the distal convoluted tubule is impermeable to water so the collecting ducts reabsorb most water remaining in the tube
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How is Na+ reabsorbed in the distal convoluted tubule
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Na+ and Cl- cotransporter to get Na and Cl from tube into cell. At cell requires the Na+/K+ ATPase pump at the basolateral membrane to get Na into ISF and K into cell. Cl- isreabsorbed throught tight junctions between cells
tube fluid becomes hypoosmotic bc solutes are leaving and water remains |
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Thiazide diuretics
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block the NaCl cotransporter at DCT. So excretion of Na+, Cl-, K+, and Water are increased
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Amiloride and triamterene
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block the luminal membrane Na+ channels (called K+ sparing) so Na+ not reabsorbed and K+ is not secreted at DCT. More water is elminated in the urine as NaCl excretion is increased. these diuretics spare K+ bc K+ is not secreted into lumen
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When is K+ reabsorbed?
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K+ can be reabsorbed by intercalated cells in the collecting duct when K+ is low. There is a K+/H+ exchanger on the luminal membrane so K+ will come into cell aa H+ leaves cell and goes into tube. K+ will diffuse out of intercalated cell at the basolateral membrane
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Purpose of aldosterone
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steriod hormone that is released from the adrenal cortex when the body needs to retain sodium. Aldosterone binds to receptor and causes signal to nucleus which activates receptors which promote protein synthesis. Mainly acts on principle cells and increases Na reabsorbtion.
Increases luminal Na channels increase Na/K ATPase on baloateral side increase citric acid cycle enzymes so more ATP for Na/K Activate luminal K+channels More Na reabsorbed and more K+secreted |
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spironolactone
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prevnets aldosterone from entering the cell nucleus
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what is in the tube at the end of the loop of henle/
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8% of filtered Na
10% of filtered K 16-% of filtered water |
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what is in tube at the end of the collecting tube (in urine)?
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<1% filtered Na
1-80% K (variable) <1% filtered water |
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if urine is hypoosmotic, what does this mean?
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hi water intake w/ hyposmotic urine and lo wate intake with hyperosmotic urine
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when is tubular fluid concentrated?
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as it flows through collecting duct into the renal medulla
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How does urine become hyperosmotic in the collecting ducts into the renal medulla?
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tube fluid enters the collecting ducts as very hypoosmotic w/ respect to plasma.
osmolarity of ISF in the medulla around collecting ducts is hi (1200 mOsm/L) permeability of collecting duct to water is hi so water leaves tube and goes into ISF This increases tube conc. when tube fluid reaches the pelvis ist is hyperosmotic and excreted as urine |
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How is hyperosmotic condition of ISF created?
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by loop of henle
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how does loop of henle concentrate the ISF?
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thick ascending limb reabsorbs NaCl by juxtamedullary nephrons to increase NaCL conc in the ISF by 150-200 mOsm/L above level in tube. tube has lo permeability to water so NaCl conc decreases wi tube and increases in ISF
thin descending loop is close to ascending limb and is permeable to water but not NaCl so water leaves tube and solutes remain. thin ascending limb is permeable to NaCl but impermeable to water so NaCl goes into ISF. |
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where is NaCl conc highest in the ISF?
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inner medulla
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where is NaCl conc lowest in the ISF?
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renal cortex
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besides help from the loop of henle, how is ISF osmolarity further increased?
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by urea in ISF in inner medulla
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Max osmolarity of inner medulla
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over 1200 mOsm/L
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What keeps the solute gradient from being washedout of the ISF by peritubular cap?
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Caps are unusually arranged in that they are parrallel to the loop of henle (vasa recta loops) This minimezes the loss of solute throught cap blood
also the lo level of blood throgh the vasa recta (5% of kidney blood flow) reduces chance of cap washing out gradient |
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ADH
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made by PP. increasing plasma ADH increases permeabilty of collecting ducts to water so water will leave tube and enter ISF to conserve water. Without ADH the colllecting ducts are impermeable to water
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How is water reabsorbed from collecting duct?
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ADH signals receptor (V2) it is coupled with G protein receptors cAMP is made by activating adenyl cyclase to activate protein kinase A. proteins are phosphorylated causing insertion of water channels into luminal membrane. water flows out of collecting duct bc of large conc gradient and into ISF
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What does ADH do to NaCL?
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ADH increases NaCl reabsorption in the thick ascending loop of henle to icrease osmolarity of ISF in inner medulla to help with gradient so water will flow from CD into ISF
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Absence of ADH at Collecting ducts
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water permeability v. low from thick ascending loop of henle to CD so water trapped in tube but NaCl can be reabsorbed so tube fluid becomes progressively hypoosmotic
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diabetes insipidus
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extreme circumstances when ADH cant be released into the circulation there is no collect duct reabsorption of water
NaCL reabsorbtion causes lowere osmolarity in CD lumen ISF in medulla is less concentrated urin v. hypoosmotic with hi volume |
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When looking at kidney performance what should be looked at?
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GFR
BF to kidney tubules substances in urine |
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clearance equals plasma flow through kidney
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means substance is entirely removed from plasma. filtered and secreted so volume equla to entire plasma flow through the kidney has been cleared of that substance
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clearance equals GFR
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substance only filtered not secreted not reabsorbed. vol equal to GFR has been cleared
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What does the amount of substance entireely cleared from a volume of plasma over time equal to?
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plasma vol eintirely cleared of that substance
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clearance calculation
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amount of substance lost from plasma is same as amount of substance in urin
C= Urine conc x urine vol/[P] |
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using inulin to check clearnace
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inulin is filtered but not reabsorbed or secreted by kidney so allows dr to check GFR.
using C=UxV/P C should be .125 l/min=GFR |
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using creatine to check clearance
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creatine is filtered (secreted a tad) and made by body.
normal plasma conc is 1 mg/dl |
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what does it mean if plasma creatine is 3 mg/dl?
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well plasma creatine should only be 1 mg/dl so that means plasma is higher and GFR is lower by 1/3
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using PAH to check clearance
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PAH is filtered by glomerulus and secreted into tube so almost all PAH is removed from plasma
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glucose clearance
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0 bc filtered amount is entirely reabsorbed by proximal tubule
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sodium clearance
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99% of filtered is reabsorbed so plasma vol cleared is v. low
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where are osmoreceptors in brain?
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suproptic and paraventricula nuclei in hypothalmus and they activate the PP to release ADH
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Normal range of plasma osmolality
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280-290 mOsm/Kg differ from osmolarity which is 300 mOsm/L
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When does ADH secretion increase?
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when plasma osmolalities are above 275 mOsm/Kg
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When is ADH secretion surpressed?
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when plasma osmolality is below 275 mOsm/Kg
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flow chart: drink excess water
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decrease body fluid osmolarity bc hi water conc.
decrease firing of hypothalmic osmolrecetors decrease ADH release from PP Decrease plasma ADH Decrease permeablity to water at CD increase water excretion (urine hypoosmotic) |
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Flow chart with dehydration
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increase body osmolarity
increase firing of osmoreceptors in hypothalmus increase ADH release by PP Increase plasma ADH Increase CD permeabilty to water Increase water reabsorbtion decrease water excretion (urine is hyperosmotic) |
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How does kidney maintain extracellular vol ie blood vol?
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by regulating Na conc in vascualr component of ECM bc Na is major cation so increase or decreasing Na changes vol.
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What happens when kidney dectects low Na+ vol?
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sensors dectrect lo Na in extracellular space which means low water vol so effects of osmoreceptors bring plasma osmolality back up to normal
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high pressure arterial baroreceptors
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carotid and aortic
stimulated by stretch, when stretched, means hi Na+ and carotid stretch receptor releases ANP |
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Low pressure baroreceptors
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in great veins of chest or atria of heart. they are stimulated by increased stretch
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neural signal pathway to CNS from high pressure arterial barorecptors
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carotid-glossopharyangeal n.
aortic uses vagas n. |
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What happens when pressure is reduced in kidney?
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barorecptors in afferent arteriole of nephron produces a humoral signal resulting in release of renin
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How does juxtaglomerular apparatus ajust to lo NaCl levels?
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humoral signal causes release of renin
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where are osmoreceptors for juxtaglomerular apparatus?
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in macula densa
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Where does juxtaglomerular apparatus respond to delivery of NaCl?
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at ascending limb of loop of henle before junction with distal convoluted tubule
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What happens to GFR with hi vascular pressure?
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decrease symp NS to kidney
arteriolar constriction is decreased causing increase in GFR with increase excretion of Na+ and water |
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What happens to GFR with lo vascular pressure?
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arteriolar constriction is increased so decrease in GFR and decrease excretion of Na+ and water
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describe activation of renin-angiotensin system that leads to secretion of aldosterone
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juxtaglomerular cells of juxtaglomerular apparatus secrete renin which splits angiotensinogin to angiotensin I. In lungs, angiotensin I is converted to angionstensin II by angiontensin converting enzyme. Angiotensin II stimulates secretion of aldosterone from the adrenal cortex
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Function of aldosterone
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increase Na+ reabsorbtion and K+ secretion by collectin duct cells
so less Na+ is excreted and more in conserved |
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what stimulates juxtaglomerular apparatus to release renin?
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decrease in BP or blood vol.
decrease perfustion of baroreceptors |
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3 ways renin release from juxtaglomerular apparatus is stimulated
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1. increase in symp outflow to kidny is decreased causing beta adrengeric stimulation of juxtaglomerular cells
2.decrease in GFR, decreases NaCl to macula densa of ascending limb of loop so increases renin secretion in juxtaglomerular apparatus bc macula densa signal jux. cell through prostaglandins 3. barorecptors in jux. cells in afferent arteriole of nephron produces singan for increased renin as vascular pressure falls |
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how does angiotensin II directly promote Na+ and water reabsorbtion?
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by activating Na+/H+ exchanger in proximal tubule
so Na+ and Water are retained in the body |
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What causes ADH to be releasedd?
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decrease in barorectors stimulation with reduction in BP and vol cause PP to release ADH
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ADH function
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increase permeabilty of collecting duct to water and water reabsorbtion will be increased
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When Is ANP released?
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with hi stretch to atria due to BP and vol increased
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ANP functions
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increases GFR by dialating afferent arteriole and constricting efferent arteriole
decreases renin secretion by juxtaglomerular cells so this will decrease aldosterone and reduce Na+ reabsorbtion promotes Na+ excretion |
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amount of Ca in plasma
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10 mg/dl 40% is bound to protein
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where is most Extracellular Ca?
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99% in bone
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Ca functions
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deposition and maintainance of bone
second messenger intracellular signaling |
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hypocalcemia
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ionized Ca levels too low so get muscle spasms and bone reabsorbtion
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hypercalcemia
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inonized Ca levels too hi so get cardiac arrgythmias and reduced neuromuscular excitability
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what does plasma Ca regulation depend on?
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kidney
GI tract endocrine systems Ca in bone |
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most critical regulation of Ca in plasma
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Parathyroid glands which makes PTH
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When is PTH secreted?
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when Ca plasma levels are low
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What does PTH act on?
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bone
GI Kidney |
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PTH effects on bone
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stimulates osteoclast activity indirectly through actions on osteoblasts
bone reabsorbtion increases conc of plasma Ca |
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What does bone consist of?
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collagon matrix which is mineralized and demineralized by osteocytes, osteoblasts, and osteoclasts
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what other hormones increase bone reabsorbtion other than PTH?
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cortisol and thyroid hormone
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PTH effects on Ca absorbtion in GI
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indirect effect PTH causes enzymatic conversion of Vit D to active form 1,25 OhD3 in proximal tubule of kidney
1,25 OHD3 promotes GI absorbtion of Ca and P |
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PTH effects on renal handling of Ca
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only 1% of filtered Ca is excreted
the entire renal tubule reabsorbs Ca with 2/3 of Ca reabsorbed in proximal tube and 25% reabsorbed in loop of henle |
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How is Ca reabsorbed in kidney?
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Ca enter kidney tube cell at luminal membrane by moving down electrochem gradient. Ca gets out of cell and into ISF by either Ca ATPase or by Ca/Na exchanger (one Ca out for 3 Na in cell)
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PTH effect on kidney
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increaes reabsorbtion of Ca in thick ascending limb of loop of henle and distal convoluted tubule.
It promotes excretion of Phosphate through actions on proximal tubule the suppress phosphate reabsorbtion |
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Where is calcitonin secreted?
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by parafollicular cells of thyroid when plasma Ca conc is HI
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calcitonin function
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increases mineralization of bone by inhibitying osteoclasts
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hormones that increase bone mineralization
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calcitonin, insulin, GH, estrogen, testosterone
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Osteoporosis
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mineralization of bone matrix is decreased to point that bone easily fractures
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ostoporosis risk factors
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femal
post menopausal small frame lo weight low Ca intake |
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Treatment of osteoporosis
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biphosphonates to kill osteoclasts
estrogen calcitonin PTH |
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primary hyperparathyroidism
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parathyroid tumor cause excessive PTH releae so increse bone reabsorbtion, incease Ca uptake by gut, and increase renal reabsorbtion of Ca. Cause hypercalcemia
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main causes of hypocalcemia
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primary cause is by removal of parathyroid glands
secondary cause by malabsorption of vit D by gut, kidney disease which reduces D3 conversion |
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what does mechanism to reabsorb filtered bicarbonate depend on?
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conversion of CO2 and water wi tube cells into H+ and HCO3-
H+ is seceted into tube H+ combines with HCO3- in tube to make CO2 CO2 returns to cell |
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How is HCO3- reabsorbed?
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by contransport with Na+ or by exchange for Cl-
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2 mechanisms to add new HCO3- to plasma and make net excretion of H+ by kidney
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1. depends on H+ and HCO3- made in tube cells from intracellular CO2 after all HCO3- is reabsorbed. The H+ secreted into the tube combines with another anion like PO4- so the H+ is excreted. the HCO3- is reabsorbed (new bc made in cell)
2. glutamine is reabsorbed with Na into cell. Glutamine is broken down into ammonia and aKG. ammonia gets H+ to make ammonium which is secreted. HCO3- is reabsorbed (this is new) |
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How do kidneys maintian pH
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H+ made as result of metabolism is excreted
HCO3- reabsorbed and made by kidney to raise pH CO2 is eliminated by lungs |
