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How does increased extracellular pCO2 affect renal hydrogen extretion?

- Tubular cells respond directly
- Respiratory acidosis
- Increase rate of H+ secretion
- Hyperventilation


How does a loss in ECF affect renal hydrogen excretion?

- Stimulates sodium reabsorption, increases H+ secretion, increases HCO3- reabsorption
- Increase angiotensin II, directly stimulate activity of Na+/H+ exchange
- Increase aldosterone levels, stimulate H+ secretion by cortical collecting tubules
- Alkalosis due to excess H+ secretion and HC)3- reabsorption


Explain the effect of hypokalaemia on renal hydrogen excretion

- Stimulates H+ secretion in proximal tubule
- Increased H+ concentration in renal tubular cells
- Increasig H+ secretion and HCO3- reabsorption
- Tends to cause alkalosis


Explain the effect of hyperkalaemia on renal hydrogen excretion

- Inhibitis H+ secretion in proximal tubule
- Decreases H+ secretion and HCO3- reabsorption and tends to cause acidosis


Explain the effect of hypochloraemia on renal hydrogen excretion

- Secretion and HCO3- reabsorption
- Na+ must be absorbed in exchange for H+ and K+ secretion
- Paradoxical aciduria


Explain how lungs and kidney work together to control plasma pH

- Lungs open system, release CO2 to atmostphere
- CO2 rises, drop in pH, raise H+, increase resp to remove more CO2 and bring back to normal
- In kidney: excretion of NH4+ to remove H+ ions, reabsorption of HCO3-
- Degree of this controlled by pH


What may be an effect of dehydration?

- High urine creatinine, urea and albumin
- Also reduced flow rate through nephrons


What is renal insufficiency?

Renal function impairment not severe enough to cause azotaemia, but sufficient to cause loss of renal reserve. May have reduced ability to compensate for dehydration
- Urine concentrating ability may be diminished


Define renal disease

Damage or functional impairment of the kidneys. Can var yin severity from very mild, to severe enough to cause uraemia


Define renal failure

Renal functional impairment sufficient to cause azotaemia. Urine concentrating ability usually impaired.


How can diet be modified to limit progression of renal failure?

- Low protein diet (reduces production and thus build up of urea)
- Low sodium diet
- Low phosphorous diet


How does renal failure cause high blood pressure?

- Decreased perfusion of kidney (likely due to initial damage from hypertension)
- Increases release of renin
- Activates angiotensin II = constriction of blood vessels


Why is a low phosphorous diet important in renal disease?

- Can lead to secondary renal hyperparathyroidism
- Calcification of body tissues in high phos (block up nephrons)


How is anaemia caused in renal disease?

- Erythropoeitin produced in kidney
- Damaged kidney produces less EPO


What is azotaemia?

The build up of creatinine and urea in the blood (nitrogen compounds)


Outline the ocular manifestations of hypertension in the cat

- Blindness
- High BP leads to thickening of walls of blood vessles to retina, restricts blood flow and leads to retina detaching


Outline appropriate therapy for cats with hypertension

- Low protein, sodium adn phosphorous diet
- ACE inhibitors, vasodilators (to reduce BP)
- Fluids not useful as unable to concentrate urine
- Exogenous EPO to manage anaemia


What is the function of intracellular potassium?

- Maintaining intracellular volume
- Cell growth (needed for enzyme function)


Why is potassium regulation important?

- Cellular depolarisation
- Threshold potential (point at which sodium influx exceeds potassium efflux)
- Heart most affected when K goes wrong


What is the effect of hyperkalaemia on cells?

- Makes cells hyperexcitable (increased K opens some voltage gated Na channels, charge closer to AP threshold)
- Slow repolarisation


What may cause hypokalaemia?

- Decreased intake
- Translocation from ECF to ICF
- Increased loss (Gi, urinary, drugs, mineralocorticoid xs)


What may cause hyperkalaemia?

- Pseudohyperkalaemia (poor blood sampling technique leading to haemolysis)
- Increaed intake
- Translocation ICF to ECF (insulin defic, tumour lysis syndrome, acidosis etc)
- Decreased urinary excretion (renal failure, rupture, obstruction, Addison's)


Describe Addison's disease

- Hypoaldosteronism
- Low aldosterone = low Na, high K
- Weakness, lethargy, collapse
- Severe bradycardia


What are the main points for treating Addison's disease?

- Rehydration/support
- Glucose infusion (or insulin) if bradycardic
- Corticosteroids


What are the main sources of potassium?

- Gastrointestinal (passive diffusion in small intestine, active transport in colon)
- Cellular breakdown (haemolysis, tissue damage)


What is teh primary control of K+ and why?

- Excretion
- Most is intracellular


Why is the control of flux between intra/extracellular compartments important?

- Can serve asrapid source of more K+ (in cases of hypokalaemia)
- Or as overflow site (in cases of hyperkalaemia)


How is uptake of K+ into liver and muscle promoted?

- Hormones (insulin and adrenaline, affect beta 2Rc)
- Increase activity of Na+/K+ ATPase


Briefly describe renal control of plasma potassium concentrations

- K+ freely filtered at glomerulus
- 70% proximal tubule (cellular and paracellular, mainly passive)
- 10-20% in AL of LoH
- Net reabsorption or secretion in dista nephron


How is potassium reabsorbed in the early proximal tubule?

- No active transport
- With water by solvent drag
- Transepithelial potential difference is lumen negative


How is potassium reasborbed later in the proximal tubule?

- Transepithelial potential difference becomes lumen positive
- K+ reabsorbed by transcellular route
- K channel in luminal and basolateral membrane
- K/Cl cotrasnproter in basolateral membrane


How is potassium reabsorbed in the thick ascending loop of Henle?

- Transepithelial potential difference strongly lumen positive
- Most K+ reabsorption by transcellular route
- K+ channels in luminal membrane for paracellular
- Transcellular route is lumina NaK2Cl cotransporter, K channels, K/Cl cotransporter in basolateral membrane


Describe ion (Na, Cl, K) movements in the distal convoluted tubule

- Na/Cl cotransporter (thiazine sensitive)
- K/Cl transporter
- Secretion of K, reabsorption of Na, Cl recycled across luminal membrane
- Basolateral Na/K ATPase maintains low intracellular Na and high intracellular K (facilitating secretion of K+)


Describe the movement of ions in the connecting tubule and collecting duct

- K secretion (Na/K ATPase)
- High intracellular K to facilitate K secretion down gradient


Describe the role of the principle cells in potassium secretion

- Found in connecting tubule
- Electrogenic Na channel
- Makes transepithelial potential difference negative
- Promote secretion of K through luminal K channels


What are the 2 types of intercalated cells and where are they found?

- Distal nephron
- Alpha: collecting duct, cortical collecting duct, outer medullar collecting duct
- Beta: only in cortical collecting duct


How do the alpha-intercalated cells carry out their function?

- H+ ATPase, K-ATPase, Cl/HC)3- counter transporter
- CL and K channels in basolateral membrane


How do the beta-intercalated cells carry out their function?

Secrete HCO3- ions as their polarity is reversed


Where in the nephron is potassium reabsorbed?

- Proximal tubule
- Thick ascending loop of Henle
- Inner and outer medullar collecting duct (even though TEPD is negative)


Where in the nephron is potassium secreted?

- Distal convoluted tubule
- Connecting tubule
- Collecting duct


List the factors that influence renal potassium excretion

- Sodium
- Potassium
- Aldosterone
- Hydrogen


Explain how sodium influences renal potassium excretion

- High sodium leads to increased K+ excretion
- Increased Na+ into cells causes increased Na+/K+ ATPase to pump Na+ into peri-tubular renal interstitium
- Increased cellular uptake of K+, K+ moves down electrochemical gradient into nephron


Explain how potassium influences renal potassium excretion

- High K+ = more K+ excretion
- INcreased aldosterone, increased activity of Na/K ATPase, increased secreton of K+ by tubular cells


What is the effect of hydrogen on potassium excretion?

- High H+ (acidosis) decreases K+ excretion
- Low H+ (alkalosis) increased K+ excretion


What is the role of aldosterone in potassium regulation?

Increases potassium excretion


Describe the mechanism by which aldosterone regulates potassium

- Binds to cytoplasmic receptors in principle cells of DT
- Synthesis of proteins for apical Na+ channel and Na+/K+ ATPase
- Membrane permeability increased, sodium pump activity increased, NaCl cotransporter increased, ENaC increased
- K+ secretion is result


In what endocrine condition can potassim rise to dangerously high levels due to lack of aldosterone?

Addison's disease


What stimulates secretion of aldosterone?

- Angiotensin II (RAAS)
- K+


What inhibits secretion of aldosterone?

Atrial natriuretic peptide (ANP)


Under what circumstances is ANP released?

- Sodium and or water loading
- Inhibits aldosterone secretion (which would act to retain sodium as well as secrete potassium)


How is the regulation of potassium and hydrogen linked?

- Alkalaemia stimulates increased uptake K+ into cells (ECF to ICF)
- Acidosis: K+ from ICF to ECF
- K+ exchanged for H+ i.e. in hypokalaemia K+ to ECF, H+ to ICF, increased H+ secretion = alkalosis


What stimualtes uptake of K+ into cells?

- Insulin
- Aldosterone
- beta-adrenergic receptor stimulation
- Alkalaemia


What causes movement of K+ out of cells?

- Insulin deficiency
- Aldosterone deficiency
- beta-adrenergic blockage
- Acidemia
- Cell lysis
- exercise
- Increased ECF osmolarity


Explain how increased tubular flow rate can reduce K+ excretion

- Volume expansion, high sodium and diuretic increase tubular flow rate and K secretion
- Tubular K increases, reduces gradient for diffusion across luminal membrane
- Therefore flushed down tubule
- Helps preserve normal K excretion during high sodium intake
- decreases aldosterone, decreasing K excretion


What are the 3 main pathways by which nitrogenous waste can be excreted

- The urea cycle
- The uric acid pathway
- As ammonia


Describe the removal of nitrogenous waste as ammonia

- Binds to hydrogen to give ammonia
- Toxic
- Excreted directly by some animals e.g. fish
- Need lots of water


Which animals use ammonia for removal of nitrogenous waste?

Fish, amphibians


Which animals use the uric acid pathway for removal of nitrogenous waste?

Birds, reptiles


Which animals use the urea cycle for removal of nitrgenous waste?



Rank the nitrogenous waste removal pathways by the amount of water needed for excretion (high to low)

- Ammonia: most water
- Urea: middle amount
- Uric acid: least water


Rank the nitrogenous waste removal pathways by the amount of energy needed for excretion (high to low)

- Uric acid (most energy required)
- Urea (medium)
- Ammonia (low amount of energy


Describe the excretion of urea (or uric acid) by the kidney

- Urea produced in liver, via plasma to kidney
- Freely filtered through glomerulus
- In edullary collecting duct some urea reabsorbed into interstitium
- Into vasa recta
- Back to lumen of LoH for excretion


Describe the process of urea recycling

- Urea transported into interstitium in medullary collectin gduct
- Urea enters vasa recta at distal end of hairpin loop of LoH
- Passes near descending limb of nearby nephrons
- Urea transporters return urea to lumen for excretion
- Small amount enters systemic circulation


What is the function of urea recycling?

Enables urea to be excreted, but also to contribute to hypertonicity at bottom of LoH
- Contributes to ~50% of medullary concentration gradient


What will increase urea?

- Decreased GFR
- Increased nitrogen intake
- Poor blood flow


How does a decreased GFR increase blood urea?

- Slower filtration
- Increased urea reabsorption


How does poor blood flow lead to increased blood urea?

- Less put back into descending loop from vasa recta
- More in blood


What may cause a decreased GFR?

- Poor renal perfusio (deydration, hypovolaemia, decreased cardiac out put)
- Too few function nephrons
- Urinary tract obstruction/rupture
- I.e. pre-renal, renal, post-renal


Why can urea be used as a marker of renal function?

- More affected by poor perfusion than creatinine
- Due to slow flow rate
- Creatinine unchanged through tube, urea reabsorbed fom collecting duct (so high urea means low reabsorption)
- Slow flow rate leads to less in urine
- Early sign of kidney disease


What are the limitations of using urea as an indicator of renal clearance in horses?

- Colonic secretion of urea
- Metabolised by GI bacteria
- Use nitrgoen to make proteins and energy
- Product of this is ammonia
- Taken up into portal circulation where it is turned into urea again
- i.e. is constantly cycled round


What are the limitations of using urea as an indicator of renal clearance in birds?

- Mostly use uric acid for nitrogen excretion
- Low urea in blood
- Urea reabsorption at low flow rates very high


What are the limitations of using urea as an indicator of renal clearance in reptiles

- Do not synthesise urea
- uric acid secreted by proximal convoluted tubule and affected by post-prandial (high protein food leads to increase), pre-renal (dehydration leads to increase), renal and body temperature


What happens to the urine that is produced during hibernation?

- Almost all ultrafiltrate reabsorbed
- Able to reabsorb urine from bladder
- Do not develop azotaemia


Describe protein metabolism during hibernation

- Protein turnover continues at low level
- Protein synthesis maintained
- Protein degradation reduced
- I.e. high synthesis and low degradation = conservation of limited supply


Describe urea recycling in bears

- AA degradation leads to production of ammonium (but little taking place)
- In bears, urease expressing gut bacteria hydrolyse urea to free N which is used to form new AAs to maintain muscle mass


Explain how urea recylcing is linked to the generation of fatty intermediates in hibernation

- To reincorporate N into body protein need some carbon
- Non-protein source of carbon is glycerol
- Lipolysis -> glycerol -> TCA cycle -> pyruvate -> alanine
- Also produces water


Define oliguria

Production of abnormally small amounts of urine


Define anuria

No urination


Why is the tonicity of urine in chronic renal disease and why?

- Isosthenuric
- Lost ability to modify (reabsorb or secrete) the ultrafiltrate


What is the effect of renal failure on urine volume?

- Polyuria
- Inability to retain water thus dehydration and increased thirst, furthering increased urination


List the laboratory methods used to assess renal function and identify renal failure

- Renal clearnace
- Creatinine/urea clearance
- Electrolyte/fractional clearance
- Acid-base balance
- Urinalysis
- Haematology


How can glomerular function be assessed in the laboratory?

- Urinalysis
- Look for protein in urine (although can be caused by things at all levls of urinary tract)
- Protein:creatinine ratio


Why is protein:creatinnie ratio used rather than protein alone to assess glomerular function?

- Protein can come from all levels of UT (inflammation)
- Creatinine should be excreted in consistent way and should match creatinine production
- By comparing can quantify importance of protein in urine


What can be used to assess renal tubular function?

- Electrolyte/fractional clearance
- Acid-base balance
- Urinalysis
- Assessment for presence of casts


What is the function of the proximal tubule and how does it carry out this function?

- Regulates pH of filtrate (exchanges H+ in interstitium for HCO3- in filtrate)
- Secretion of organic acids
- Reabsorption to peritubular capillaries
- Na/K ATPase in basolateral memrbane driving reabsorption


What is renal fractional clearance?

- the ratio of electrolyte clearance to creatine clearance
- I.e. the volume of plasma that would have been cleared of the substance to give the amount of that substance found in the urine in the given time period


What is suggested by low fractional electrolyte clearance?

- Net conservation
- More reabsorption than secretion
- e.g. volume depletion, sodium retained, FC of sodium very low (less is being cleared)


What would be expected of the fractional clearance in renal damage?

- High FC
- Reabsorption has been decreased, more secretion
- Except phosphate, poorly secreted in damaged situation


How can urinalysis be used to asses renal tubular function?

- Urea and creatinine
- Assess pH, protein, glucose


What is likely to happen to urea:creatinine in renal damage?

- Increased
- Reduction in ability to reabsorb urea


What is likely to happen to USG in chronic renal failure?

- Isosthenuric urine
- Loss of concentrating ability


What is the significance of the presence of casts in urinalysis?

- Should be non in urine
- Formed in lumen of tubules
- Suggestive of disease/damage
- Cahnge in type according to duration of urine in tubule
- Caused by slow flow


What are the different types of casts that may be seen in urinalysis?

- Cellular
- Granular
- Waxy
- Hyaline


What is likely to be seen on haematology in renal damage?

- Chronic renal disease leads to loss of renal tissue, reduced EPO
- EPO deficiency
- Non-regenerative anaemia
- Inflammation


Under what conditions is the clearance equal to GFR?

- If teh substance is filtered, not reabsorbed and not secreted
- e.g. creatinine


Experimentally, GFR can be measured using the clearance of what?

- Inulin
- Creatinine
- Plasma clearance markers


What may lead to low creatinine levels?

Low muscle mass, not as much production of creatinine possible


What (other than renal causes) may lead to high urea levels?

- High protein in diet
- Haemorrhage (leading to high protein in gut from blood digestion)


What different types of renal damage are there?

- Glomerular (affecting filtration)
- Tubular (affecting secretion and reabsorption)
- Interstitial (affecting concentrating ability)
- Mixed (most cases)


What are the non-excretory roles of the kidney?

- Maintain water and composition of plasma
- Water, ion, pH level regulation
- Nutrient retention
- Endocrine function (EPO, calcitriol, renin)