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Flashcards in Pathophys of CKD Deck (19)
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Say you have 2 twin brothers. One has healthy kidneys, one has CKD. They eat the same diet. Which, if any, solutes will be excreted in larger/smaller quantities by the brother with CKD?

None - the brother with CKD will have higher BUN, Cr, etc. but he will have reached a new steady state and excrete the amount he ingests.


What's the key concept about how kidneys with CKD handle electrolytes?

They behave as if there's simply a smaller number of normally functioning nephrons.
They keep up until extremes of kidney failure...


3 theories about why GFR progressively declines in CKD?

Hyperfiltration theory. (remaining glomeruli have increased filtration / flow... which leads to disease progression)
Podocyte destruction theory.
Interstitial fibrosis theory.


If a substance is only excreted via filtration, how will GFR affect the serum concentration of that substance?

The serum concentration will increase to a level such that the new, reduced GFR will filter the substance at a rate matching production/intake.


There were experiments with an animal with 1 CKD-modeling kidney and 1 normal kidney, each with its ureter contents analyzed. What did these experiments tell us about the solute handling of the diseased kidney?

When factored for GFR, the diseased kidney functioned exactly the same as the normal kidney. (as long as GFR is about 25% of normal)


What does "kidneys with CKD keeping up solute handling despite reduced GFR" look like in the real world?

Fractional excretions will be higher - eg. for sodium, if half as much is filtered, twice as much of what is filtered must be eliminated.
Nephrons must "work harder".


Do patients with CKD have tolerance for changes in Na+ intake?

Yes. It only becomes a problem at extremes of Na+ intake levels / reduced GFR.


Why are people with CKD unable to tolerate extremely low Na+ diets?

High levels of urea cause an osmotic diuresis that prevents optimum Na+ retention.


K+ handling is also okay in CKD. Why is low K+ more tolerable in CKD than is low Na+?

K+ reabsorption doesn't depend on the loop of Henle, so high levels of urea isn't going to affect it as much.


Why do people often get hyperkalemia in very advanced CKD?

Hypoaldosteronism and drug effects.


Take home points about water handling (response to ADH or lack thereof) in CKD?

At high solute concentrations, can't dilute or concentrate urine (even with exogenous AVP).
Urine osmolality approaches that of plasma.


Bottom line for water handling in CKD?

No special modifications of water intake need to be made - thirst is an okay guide.


How is acid/base handling impaired in CKD?

Ammoniagenesis is often impaired, which impairs acid excretion.


Why are Ca++ and phosphate levels maintained in CKD? (assuming unrestricted phosphate intake)

Secondary hyperPTH.


Vitamin D deficiency... keeps Ca++ and phosphate from getting too high in CKD. What are 2 reasons for decreased calcitriol in CKD?

Decreased functioning kidney mass?
"Phosphate retention"


What's the "phosphate retention" theory for why calcitriol is reduced in CKD?

Reduced GFR -> increased phosphate -> increased FGF-23 and Klotho -> reduced Vit D activation.


What drives the hyperPTH in CKD?

Low calcitriol.


High phosphate is bad. Why?

It can lead to calcium phosphate deposition in tissues.
Secondary hyperPTH -> bone loss and hypocalcemia.


4 therapies for Ca++ and phosphate imbalance in CKD?

Reduce phosphate intake / phosphate binders.
Calcimimetics - agonize CaSR.