Renal Regulation of

Na+, K, Mg, Ca
 ECF ICF
Na 142 10
K 4 140
Ca 2.4 0.0001
Mg 1.2 58
 Regulation of K
 98%of total body K is in cell
 2% in ECF
 Hypokalemia:- Loss of K from ECF cause
Hypokalemia
 Distribution of K between ECF and ICF play
important role in K Homeostasis
Factors that can alter K Distribution
Between ECF and ICF
Factor that shift K+in to cell Factors that shift K+ out of cell
(Decrease Extracellular (Increase Extracellular K+
K+)
2. Insulin 1 Insulin Deficiency
3. Aldosterone
4. Beta-Adrenergic 2 Aldosterone Deficiency
stimulation
5. Alkalosis 3 Beta-Adrenergic Blockage

4 Acidosis
5 Cell Lysis
6 Strenuous Exercise
Aldosterone
 Excess aldosterone secretion is associated with
hypokalemia due to movement of extracellular k+ in
to the cell
 Patient with Deficient Aldosteron Production often
have Hyperkalemia due to accumulation of k+
Beta-Adrenergic Stimulation
 Increase secretion of Catecholamines ,especially Epi-
nephrine cause movenment of K+ from ECF to ICF
by Activation of Beta 2 adrenergic receptor
Acid-Base Abnormalities
 Metabolic acidosis increases loss of K from
the cell
 Metabolic alkalosis decreases ECF K
concentration
Cell Lysis
 If cells are destroyed k+ are released to the

Extracellular compartment ,causing

Hyperkalemia
 Eg.RBC lysis ,severe muscle Injury
 Renal Absorption of K+
 K+ is Reabsorbed in PCT and
Ascending loop of Henle ,where it is
actively co-transported along with Na
and Chloride
 Renal K Secretion
 K is Secreted in to Late distal Tubule and collecting
Ducts
 In DCT Principle cells and intercalated cells helps
in secretion
Principle cells:-
Factors that control K secretion by the
principle cells are
5. The activities of Na,k ATPase Pump
6. Electro chemical gradient for K secretion
7. Permeability of the luminal membrane of K
 In circumstances associated with severe K
Depletion ,there is a net Reabsorption of k in
the Late distal and collecting tubule .This
reabsorption occurs through the intercalated
cells
 For this Hydrogen-potassium ATPase act in
the luminal membrane
 This transporter reabsorb K in exchange for
hydrogen ion secreted in the tubular lumen
 Secretion of potassium from the blood
into Lumen occur in two step
 Uptake of K from interstitium by Sodium-
Potassium ATPase acting on the basolateral
side.This pump moves Na out of the cell and the
same time moves potassiun to the interior of the cell
 This creats a high-intracellular K concentration which
provides the driving force for passive difussion of K from
cell to the tubular lumen
 The luminal membrane of the principle cell is
highly permeable to potassium
 Once reason for the permeability is that there
are special channels that are specifically
permeable to potassium ions
 Factors That Regulate K+
Secretion
 The most important factors that stimulate k+
secretion by the principle cell include
 1.Increased extracellular fluid k+
concentration.
 2.Increased aldosterone
 3.Increased sodium tubular flow.
 Another factor that decrease k+ secretion is:
 Increased H+ concentration[Acidosis].
ALDOSTERONE STIMULATES K+ SECREATION
 1.Aldosterone stimulates active reabsorption
of Na+ by the principle cell of the late DCT
and Collecting Duct.
 2.At the same time it pumps K+ into the cell.
 3.A second effect of aldosterone is to Increase
the permeability of Luminal membrane for K+.
 CONTROL OF RENAL CALCIUM.

 Calcium is stored in bone.

 1.Hypocalcemia: when calcium ion decrease into low level.
Due to this the excitability of nerve and muscle cells increase.
 2.Hypercalcemia depresses s neuromuscular excitability and
can lead to cardiac arrhythmias.
 3.50%of total calcium in plasma the plasma exist in ionized
form.
 4.The rest is bound to plasma protein or complexed in non
ionized form.
 5.Plasma H+ concentration can influence the degree of
calcium binding to plasma protein.
 6.with acidosis calcium is bound to the plasma
protein.
 7.Therefore patient alkalosis are more susceptible to
hypocalcemic tetany.
 8.one of the most important regulators of bone uptake
and release of calcium is PTH.
 9.when extracellular calcium concentration falls
below normal the parathyroid glands are directly
stimulated by the low calcium levels promote
secreation of PTH.It act directly on the bone causing
the release of large amount of calcium into ECF.
 10.Thus PTH regulatesplasma calcium
concentration through 3 main effects:
 By stimulating bone reabsorption
 By stimulating activation of vit.D,which then
increases intestinal reabsorption of calcium
 By directly increasing renal tubular calcium
reabsorption.
 Control of Ca Excretion By the
Kidney
 Renal Ca Excretion =Calcium Filtered-calcium Reabsorbed
 99% of the Ca is Reabsorbed
 65% is Reabsorbed in PCT
 25-30% Is reabsorbed in loop of Henle
 4-9% are re-absorbed in DCT and Collecting Tubule
 With increase levels of PTH there is increase Ca reabsorption
in the thick ascending loop of Henle and DCT
 In PCT Ca reabsorption usually Parallels Na and Water
Reabsorption
 With Decreased Blood Pressure Ca excretion Decreased
Because of Increased Reabsorption in PCT
 Increase In Plasma Phosphate stimulates PTH
 Factors affecting Renal calcium
Excretion
 Decrease Ca Excretion  Increased Ca Excretion
2. Increase PTH 2. Decreased PTH
3. Decreased ECF 3. Increased ECF volume
Volume 4. Increase Blood
4. Decreased Blood Pressure
Pressure 5. Decreased Plasma
5. Increase Plasma Phosphate
Phosphate 6. MetabolicAlkalosis
6. Metabolic Acidosis
 Control of Renal Mg
 More than Half of Body’s Mg is stored in
Bone
 Mg is involved in many Bio-chemical process
including activation of many enzyme
 PCT Reabsorbed only 25% of Filtered Mg
 Primary site of Reabsorption is Loop of Henle
where 65% is Reabsorbed
 Less than 5% is Reabsorbed in DCT and
Collecting Duct
 Increase In Mg Excretion Caused by:-
2. Increase ECF Mg concentration
3. Extra cellular volume expansion
4. Increased ECF Ca concentration
 CONTROL OF RENAL SODIUM

 Excretion= Glomerular Filtration-Tubular

Reabsorption.
 If the kidneys become greatly vasodilated and GFR
increases this raises sodium chloride delivery to the
tubules which in turn leads to
 i.Increased tubular reabsorption of much of the extra
sodium chloride filtered called Glomerulotubular
balance
 ii.Macula Densa Feedback in which increased sodium
chloride delivery to DCt causes Afferent arteriolar
constriction.
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