Kidney Flashcards
Autoregulation of renal circulation
Independent of the systemic circulation. Blood flow of the kidney consistently adapts to the demand of the excretion => achieve its excretory function
Filtration
- CFC (capillary filtration coefficient): ultrafiltration in renal glomerulus is 100X higher than in any other capillary, due to the (-) charge of its lamina densa which strongly reflects the proteins.
- EFP (effective filtration pressure): extent of ultrafiltration depends on pressure gradient, components: Phydrostatic of glomerulus, Bowman’s sheath P, colloid-osmotic P of plasma
EFP = GP - (CP + GCP)
Reabsorptin
Extremly large filtration rate => fatal loss of fluid.
2 main pathways: paracellular, transcellular
Secretion
From plasma leaving the glomerulus (eff arteriole). Some after filtration + reabsorption, some directly. Transcellular + paracellular
Excretion
Filtration, reabsorption, secretion => secondary filtrate of urine
Rate= urine / selected material excreted. 2-3 mL/min/100 kg bwt urine
Glomerular filtration rate
Amount of filtrate produced/t. Material which is ONLY filtrated and its load + rate has to be equal to the amount appearing in urine/t (eg.insulin = 120mL/min/100 kg bwt)
Autoregulation of GFR: constant (myogenic mechanism, tubulo-glomerular feedback)
Extraction
Elimination of a substance.
[substance] in renal a -> kidney -> same/reduced amount leaves through the v
Max: when substance doesn’t appear at all on the venous side (E=1)
Min: entire amount appears on the venous side + nothing un urine (E=0).
E = Pa - Pv / Pa
Clearance
Remove a substance from the plasma + forward it to the urine.
- Exclusively filtered (neither absorbed nor secreted) => clearance = GFR
- Entirely secreted (eg.p-aminohippuric acid)- clearance => RPF
▪️PAH: const in low [], in higher clearance decreases
▪️insulin: its [] does not influence its clearance
▪️urea: freely filtered, unlimited capacity of filtration
▪️glucose: freely filtered, normal plasma [] => clearance = 0. In diabetes glucose appears in the urine (no reabsorption)
Renal plasma flow
Amount of plasma flowing around the kidney Flick principle (law of conservation of matter): amount of substance entering the kidney (arterial side) must = amount leaving (venous side + urine) RPF = U X V / (Pa - Pv)
Loop of Henle and distal tubule
30% of Na is reabsorbed here.
- Thick descending limb: NO active transport, high permeability, electrical potential gradient bw the lumen + interstitium
- Thick ascending limb: 25% of the filtered amount is reabsorbed here
Na/K-ATPase pump: Na- cell -> interstitium + K- interstitium -> cell
Na can be reabsorbed in the luminal side + excess K via K channels leave
Na/K/2Cl symporter (luminal side) => electroneutral transport (inhibitor: furosemide) -> water + salt loss => diuresis
TAL impermeable to water => lumen = hypoosmotic
- Distal convoluted tubule: Na/Cl symport absorbs further 5% of the filtered Na (inhibitor: thiazide derives => diuresis)
Cl carried by K/Cl cotransported
Ca transport directed by the calcium saving effect of PTH.
Hormonal + Pharmacological effects
- Distal convoluted tubule: PTH: Ca reabsorption, calcitonin: Ca excretion, both: P excretion
- Proximal + Distal convoluted tubules + collecting ducts: carbonic anhydrase inhibitors
- Thick ascending limb: furosamide
- Distal convoluted tubule: thiazide
Transport in the distal connective tubule + collecting tubule
Formation of the hormonally regulated final urine:
- CNT, CCT = mineralocorticoid Na dependent reasorption
- CCT = ADH-dependent water reabsorption
- MCT = ADH-dependent water + urea reabsorption
- ANP-dependent Na excretion
▪️Mineralocorticoid dependent Na/K transport: Na/K pump (basolateral side), Na and K channels (luminal side). Aldosterone dependent. Transport of K is passive in both directions + determined by aldosterone []. If K in excess => more aldosterone => more channels
▪️Active water transport: water flow is directed by osmotic forces. In CCT + CNT / MCT sections: water transport is hormonally regulated: aquaporin-2.
▪️Acid-base balance: CCT + CNT. K secretion + hydrocarbonate reabsorption. Alkalosis: independent hydrocarbonate prod + secr
- Defense against acidosis: H (water) -> lumen by ATPase, the carbonic anhydrase unites CO2 + OH => HCO3, which is transported to the blood by Cl/HCO3 antiporter.
- Defense against alkalosis: dissociation of water => H -> interstitium by H/K ATPase pump. HCO3 -> lumen via HCO3/Cl antiporter.
▪️K transport: [K] is regulated by the organism, as its [] change affects all irritable tissues. CCT principal cells: reabsorption of Na + mineralocorticoid dependent secretion of K, CCT intercalary cells: reabsorption with H/K exchange.
Transport- proximal tubule
70% of the filtrate is reabsorbed here.
Actively -> interstitium
Passively -> peritubular capillaries
- Na: Na -> interstitium, K -> cell (Na/K-ATPase pump)
- H: Na => H secretion. Inhibited by amiloride
- Bicarbonate: cell is impermeable to it. CO2 diffused -> cell, H with the help of carbonic anhydrase => HCO3 (indirect)
- Cl: prerequisite: lower pH in lumen than in cell. Cl-acidic anion antiporter: Cl -> cell + acidic anion -> lumen. Cl binds H => free acid (diffuses back) then dissociates
- Water: increased peritubular oncotic P => water migrates from lumen -> interstitium. Aquaporin-1
- Glucose, aa: 100% withdrawn from prox tubule. They have their own specific carriers + inhibitors
- Urea: half = passively reabsorbed, the rest stays in the interstitium => special osmotic layering in the kidney
- Proteins: some -> lumen, majority -> back to the tubular cells by pinocytosis
Osmoregulation
Maintain osmotic homeostasis, because a shift may destroy important physiological processes.
Salt deficiency/ excess, shortage/ excess of water => feedback.
Fast restoration is carried out on the expense of a shift of the isovolaemia.
Hyperosmosis
Due to mannit + glucose, Na. EC + IC are getting osmotic equalized => hyperosmotic isovolaemia.
- Hypothalamic osmoreceptor activity + ADH level: increase
- Expression of AQP-2: increases, water clearance: decreases
- > direction of isosmotic hypovolemia