Lecture 45+46 Flashcards
(43 cards)
equation for filter load?
GFR x plasma concentration
equation for excretion
Urine volume x urinary concentration
Net filtration rate equation
FL - ER
\+ = net reabsorption - = net secretion 0 = no transport (net)
equation for renal blood flow?
RBF = RPF / (1 - HCT)
Proximal convoluted tubule and sodium uptake? how?
what enhances sodium intake?
2/3 of filtered sodium is reabsorbed here by
SGLT = sodium + glucose
NHE transporter = sodium in, H+ out
The basolateral Na/K pump creates the gradient for Na entry into the cell from the blood
catecholamines and Angiotension II stimulates Na uptake
PCT and water / electrolyte reabsorption?
the PCT has a high permeability to water
the water, K, and Cl follow Na (can occur through the tight junctions, paracellular, or go through the cell, transcellular
Cl goes into blood; anion goes out (formate)
BUN levels and kidney health?
Nitrogenous wastes are excreted from the body as urea, and, thus, plasma blood urea nitrogen (BUN) levels are a useful indicator of renal health and function
increased levels of BUN can lead to gout
moves paracellularly
PCT and glucose
All filtered glucose is reabsorbed in the PT via secondary active transport linked to sodium. Glucose
molecules are recovered from the early PCT by SGLT2 transporter and from the later PT by the SGLT1 transporter.
GLUT 1 and GLUT 2 transporters (facilitated diffusion) are also used
PCT and amino acids?
peptides enter the cell by the PepT1/T2 transporters
these transporters need H, as well. (H + AA)
these peptides are degraded in the cell by proteases and are transported in the blood as free AA
defects in this pathway lead to proteinuria
the concentration of glucose, AA should be zero leaving the PCT
can also go into cell by endocytosis and be released into blood by exocytosis
diabetes mellitus and the kidneys
reabsorption of glucose is proportional to plasma concentration until the Tm is meet
after the plasma glucose of 300mg is meet; glucose will be excreted due to saturation of transporters
will lead to polyuria + polydipsia
PCT- bicarbonate reabsorption
H+ is pumped into the tube by a Na/H exchanger
(H is out, Na in)
H+ combines with HCO3 to form H2CO3
Carbonic anhydrase converts H2CO3 to CO2 and H2O, then goes into cell
intracellular CA reforms H+ and HCO3
H+ is once again pumped out into tubule and HCO3 is returned to blood.
What stimulates the Na/H antiport in the PCT?
angiotensin II
In volume depleted states, the volume of HCO3 in the blood increases
what could happen due to defects in PCT?
metabolic acidosis
hypophosphatemia
osteopenia
How do diuretics work?
increase urine output by altering sodium handling
inhibit the reabsorption of Na, increase Na in the lumen, and thus more water remains in the lumen
more sodium excretion = more water excretion
used to reduce extracellular fluid volume (edema and hypertension)
Acetazolamide
This is a carbonic anhydrase inhibitor, thus a reduction in the reabsorption of HCO3 and reduction of activity of the Na/H antiport
sodium remains in lumen, thus more water in lumen
Used for altitude sickness
Loop of henle reabsorption?
Thin descending portion:
permeable to water
impermeable to solute
thin ascending portion:
impermeable to water
Thick ascending portion:
impermeable to water
solutes transported out of tubule
Loop of henle - thick ascending portion
Na/ K pump is very important because it leads to a deficiency of Na in the cell, thus allows for the action of the Na/Cl/K transporter
also allows for the Na/H antiporter to work (H out and Na in)
K will come into cell and then diffuse back into the lumen, thus the tubule is + in charge, thus this drives the movement of Mg and Ca into the blood via paracellular pathway
Loop diuretics?
Block the Na/K/Cl co-transporter
thus more Na/K/Cl in the urine, along with water and electrolytes!!
used for pulmonary edema
watch for hypocalcemia ( No K gradient)
Early distal tubule reabsorption
reabsorbs Na, Cl, and Ca
Na/K pump creates a low intracellular concentration, thus NaCl crosses into cell by the Na/Cl symporter
Cl diffuses into blood
this segment is impermeable to water! Osmolarity decreases (lowest osmolarity)
Ca reabsorption in the EDT?
Ca enters the cell passively by PTH
is put into the circulation by the 3Na/Ca antiporter
calbindin facilitates reabsorption of Ca
Gitelman’s syndrome
mutation of the Na-Cl cotransporter
leads to ‘salt wasting’ due to excretion of Na and Cl
may lead to low blood Ca levels
Thiazide diuretics
Inhibit the Na/Cl symporter of the DT
used to treat hypertension and heart failure
can lead to hypercalcemia!!
inhibiting Na leads to hyperpolarization which drives Ca into the blood
Role of principle cells in the DT and collecting duct
role of aldosterone?
reabsorb sodium and secrete potassium
influenced by aldosterone
- increases ENaC channels
- increase ENaC opening time
- stimulates Na/K ATPase
ADH and principle cells in the DT/CD?
principle cells express aquaporins that are regulated by ADH
ADH acts on the V2 receptors which increases water reabsorption
low ADH = low water reabsorption
