REGULATION OF K,Ca, PHOSPHATE & MAGNISIUM Potassium K regulation 4.2+/- 0.3 mEq/L Mainly intracellular 2% extracellular Excreted mainly by the kidney and 5-10% of the intake by GI

Factors shift K inside the cell decrease outside: After meal most of the ingested K moves into the cells until the kid can eliminate the excess. A-Insulin B-Aldosteron C-Beta adrenergic receptors stimulation as increase epinephrine D-Alkalosis

Factors shift K outside the cell A-Decrease insulin B-Decrease aldosteron C-Beta blockers D-Acidosis E-Cell lysis (muscle injury and RBC lysis) F-Sever exercise G-Increase extracellular osmolarity

K filtrate, absorbed, secreted and excreted 65% of K Reabsorption in the proximal tubule And 25-30% reabsorbed in the thick ascending part of loop of Henle as active co- transport along with Na and Cl

-Variation in K excretion caused by changes of K secretion in late distal and cortical collecting tubules by principal cell. K in these segments can be absorbed or secreted depend on needs of the body. -During K reduction in the body , intercalated A cells also can reabsorb K(H). Intercalated B cells can also secrete K.

FACTORS REGULATE K SECRETION 1- Increase K Concentration in ECF 2-Increase aldosteron:Stimulate active reabsorption of Na through Na-K ATPase 3-Increase K in ECF stimulate aldosterone secretion 4-Increase tubular flow rate as with high salt intake which decrease aldosterone and increase flow rate which counterbalance each other so little change in K excretion and vice versa

5-H ion concentration(Acidosis) in ECF : acute cause decrease K excretion, chronic cause increase K Loss by: dec proximal tubule Na,Cl,H2O absorption and which increase distal vol delivery. Population diet high in K and low in Na do not develop age related hypertension and CV diseases.

CONTROLL OF Ca++ EXCRETION AND ECF Ca ion CONCENTRATION 99% in the bone 1% Intracellular 0.1% extracellular fluid Total Ca in the plasma 5mEq/L: 50% ionized form 40% Bound with plasma protein 10% Complexed with Phosphate &citrate

Hypocalcemia ^ nerve and muscle excitability and can cause tetany Hypercalcemia depress excitability and can cause arrhythmia. With acidosis less Ca bound to plasma protein and alkalosis can cause hypocalcemic tetany. Main Ca excretion in feces

PTH is the most important regulator of bone uptake and release of Ca (Endocrine) by: 1-Stimulate bone resorption 2-Activation of vit D which ^ Ca absorption from GIT 3-^ directly renal tubular Ca reabsorption.

Control of Ca excretion by the Kid: 99% of filtrated Ca is reabsobed same patern as for Na : 65% in the proximal tubule:Para & transcellular 25-30% in loop of Henle:Thick ascending limb, para & transcellular stimulated by PTH 4-9% in the distal & collecting tubules (Active)

Control of Ca absorption 1-PTH increase Ca absorption in distal & collecting tubules. 2-Ca absorption ^ with ^ plasma phosphate concentration and metabolic acidosis

Decrease renal Ca excretion with 1-^ PTH 2-Decrease extracellular fluid 3-Decrease BP 4-^ Phosphate 5-Metabolic alkalosis 6-Vit D

RENAL PHOSPHATE REGULATION Renal Phosphate regulation :It has transport maximum about 0.1mmol/min. Threshold about 0.8mM/L 75-80% absorbed in proximal tubule, distal tub 10% and 10% excreted. Phosphate concentration about 1mM/L ^PTH decrease tubular phosphate absorption & ^ excretion (more with endocrine).

MAGNESIUM Control of renal Magnesium : 50% in the bone Rest within the cell Less than 1% in the extracellular fluid. Total plasma Mg concentration is 1.8 mEq/L & 50% of this bound to plasma protein, only 0.8mEq/L freely ionized Mg . Kidney excrete 10-15% of filtrated Mg

Mg absorption: 1-25% in the proximal tubule 2-65% in the loop of Henle 3-5% distal & collecting tubules. Mg excretion ?? ^ with 1-^Mg concentration in ECF 2-^ ECF vol 3-^ ECF Ca concentration.

INTEGRATION OF RENAL MECHANISM FOR CONTROL OF ECF 1-ADH & Thirst mechanisms 2-Na absorption and excretion (steady state condition) 3-Na Excretion is control by change GF or tubular reabsorption rate 4-Pressure natriuresis & Pressure diuresis as in case of increase fluid and salt intake and B.P. regulation

5-Sympathetic stimulation A-Constriction of renal arterioles and dec GFR B-^absorption of salt and water C-Increase of Angiotensin II & aldosteron 6-Role of Angiotensin II in control renal excretion (The most powerful controller of Na excretion) 7-Role of aldosterone:Retain Na & H2O & excrt K 8-Role of atrial natriuretic peptide: Small changes

Increase Na intake in normal person can cause slight increase in ECF volume and this triggers the followings mechanisms 1-Actvate low pressure receptor reflex to inhibit symp activity 2- Suppress angiotensin II formation 3-Stimulate natriuretic system ANP. If high Na intake continuo for months or years, kid damage may develop which can lead to hypertension

Increase Blood volume and Extracellular fluid: 1-Congestive heart failure 2-Pregnancy increase capacitance of circulation 3-Large varicose veins : Increase capacity

Increase extracellular fluid with normal blood volume: 1-Nephrotic syndrome :Proteinuria decrease colloid osmotic pressure and incr cap permeability to fluid and increase absorption of Na and H2O by the kid cause edema 2-Liver cirrhosis : Decrease formation of protein and similar events occur as in nephrotic syndrome.