Renal 3 Case 1: acidic patient

Basic concept: H filtrate: increase

Increase amount of flow of filtrate, increases H in PCT: not reabsorbed

excretion.
Increase amount in plasma, increases the Na in PCT: highly reabsorbed to release H
amount in the urine.
Excrete: high H, decreased Na..
SODIUM major EXtracellular cation
Case 2: hypernatremic patient
Hypervolemia=expansion
Na filtrate: increase filtration
Hypovolemia=contraction
K filtrate: normal
Important sodium channels:
Na PCT: not reabsorbed
1. Na/K antipor
2. Na/H antiport K PCT: reabsorbed, normal
3. Na?Ca symport
Na excretion: increased
4. Na/HCO3
5. Na glucose, AA, PO4, lactic acid symport K excrete: normal
6. One way channeling
PCT: Order of reabsorbed from high to low..from
Osmotic gradient early segment to late segment
1. Na with water 1. Glucose, AA (HIGH Tm)
2. Na with Cl 2. Na
3. K
Regulation:
4. HCO3 as CO2 bicarbonate is largely
1. Rennin- reabsorbed as CO2
a. local vasoconstrictor 5. Ca
b. release is stimulated by decrease 6. PO4
volume and increased osmolarity 7. Mg at the thin descending loop or late PCT
(majorly affected by Na) in the ECF.
Potassium - major INtracellular cation
c. Releases angiotensin II and III-
generalized vasoconstriction. It - Role in acid base
decreases the RBF thus low GFR. - Modified by aldosterone, hyperkalemia,
d. Inhibited by ANGII and ADH alkalosis
2. Reabsorption (Majority in the PT, proximal - Channels: K/H, K/Na
convoluted and straight tubule)
Case 3: cushings
Interstitial space tubule
K filtrate: normal filtration

K in PCT: normally reabsorbed

K
Na K in DCT: increased, high secretion
H
Urine volume: decrease, to compensate high
Na osmolarity

Na/K and Na/H is active transport. Case 4: hyperkalemia

Osmotic gradient for Na with Cl, H2O K filtrate: increased filtration

Macula densa- stimulated by decrease volume in the K PCT: not reabsorbed

ECF, stimulated JG to release renin.
Na PCT: normally reabsorbed

K excrete: normal
 Phosphate

ACID BASE Vit D calcitonin

Alkalosis Diet blood Bone

In ICF: HCO3 stays, H stays, K moves out PTH, Vit D

IN ECF: HCO3 stays, H moves in the cell, K stays Kidney

Acidosis Inhibit excretion: Calcitonin

In ICF: HCO3 stays, H leaves the cell, K stays Promote secretion: PTH, VIt D

In ECF: HCO3 moves in the cell, H stays, K moves Urine

in
Ammonia NH3
Case 4: Alkalosis
-permeable to tubular epithelium with Urea
K filtrate: normal
- pathway: glutamine->NH3->secreted by tubular
HCO3 filtrate: increase filtration epi.->NH3 binds with H-> produces NH4-> NH4
binds with Cl-> NH4Cl is excreted in urine
K PCT: normal reabsorb
Case 5: Acidosis
HCO3: not reabsorbed
Glutamine level: decreased
K DCT: normal to increase due to H being
reabsorbed Cl in blood: decreased, transient hypochloremia

HCO3 DCT: increased, intercalated cells does not

reabsorb HCO3

Calcium pathway

Vit D calcitonin

Diet blood Bone

PTH, Vit D

Kidney

Inhibit excretion: PTH, VItD,

Calcitonin

Urine

Substance not reabsorbed in DCT/CD: PO4,

Glucose, AA, Mg