k regulation

hyprkalemia

urinary excretion of k exactly=  intake on the diet

* from 1-100% of the filtered load

• *depends on :
•  dietary k intake 
• aldosterone levels 
• acid base status

filtrated freely across the glomerular capillary 

TF/P(K) in bowmans space is 1 

reabsorbs 67% of the filtered K ,along with Na and  H2O

• 1.reabsorbs 20% 
• 2. re-absorption is from the Na-k-2Cl cotransporter in the lumenal surface of the cells in thick ascending limb 

• The side of the tissue facing the lumen is the apical surface of the epithelial tissue

• reabsorbs or secretes k
• depending on dietary intake

1.H,K ATPase in the apical membarance of the INTERCALATED CELLS A .

• 2.OCCURS ONLY on LOW K diet -k depletion
• low intracellula k so that is driving force for k secretion decrease , the A intercalated cells are stimulated to reabsorb k by H-K-ATPase
• 3.can be very low 1% of filtered load  because kidney conserves as much k as possible

occurs in in principal cell

variable and accounts for the wide range of urinary k exrition 

• depends on
• 1.dietary k
• 2.aldosterone levels 
• 3.acid base status
• 4.urinary flow

• 1.basolateral membrane , k is actively transported  into the cell by: Na-k pump
• this mechanism maintains a high intracellular k concentration 
• 2.lumenal membrane  , k is passively transported into the lumen  (flow rate dependent ) through k channels 
• the magnitude of the passive secretion is determined by the electrical and chemical driving forces on k across the luminal membrane 
•  maneuvers which increase the intracellular k cc or decrease the luminal k cc will increase secretion by increasing the driving force

1. at high k diet (in which intracellular k increases) increase secretion 

• 2.aldosterone ---> increase k secrition by 
• increase # of luminal membrane k channels
• (tfser bldftr ljded)

• 3. acid base:isohydria and k homeostasis are coupled
• effectively H/K antiport across the basolateral cell membrane 
• alkalosis increases k secretion , blood contains too little H+ 
• ACIDOSIS  DECREASE K SECRETION , blood cont. excess of H+

• 4. thiazide and loop diuretics ---> increase K secretion 
• diuretics increase flow rate through distal tubule (thiazidediuretics,loop diuretics) cause dilution of the luminal k concentration so increase k secretion. 
• (leads to hyperkalemia)

• 5.k spearing diuretics 
• increase k secretion 
• if used alone cause hyperkalemia 
•  
• 6.luminal anions: 
• excess anions in the lumen cause an increae in k secretion by increasing the negativity of the lumen , which favors k secretion 

• 1.high k diet
• 2.hyperaldesteron
• 3.luminal anions
• 4.loop diuretics
• 5.thiazide diuretics 
• 6.alkalosis

• 1.low k diet
• 2.hypoaldesteron
• 3.acidosis
• 4.k sparing diuretica

1.ALDOSTERON 

• 2.insulin:
• *direct stimulation of NA-K PUMP
• *STIMULATION OF NA-H antiporter in liver muscle and left tissue 

3.katecholamines direct stimulation of Na-K pum

• regulation includes the function of
• 1.parathyroid gland
• 2.bones
• 3.gastrointestenal glands 
• 4.kidney

1 kg

700 g

Ca2+ intake: 200-1000 mg/day, 5-25 mmol/day   40 - 50 % of the plasma Ca2+ content (2,2 - 2,6 mmol/L) is protein-bound.

• This bound protein is not filtrating in the glomeruli,
• The non-protein bound Ca2+ is freely filtrating
• 97-99% of the filtrated Ca2+ is reabsorbed in the tubular system.

The daily excretion is 2,5 - 7,5 mmol Ca2+.

200-1000 mg/day

5-25 mmol/day

2.2-2.6 mmol/L

2.5-7.5 mmol

1. 70 % of the filtrated Ca2+is reabsorbed in the proximal tubule

2. 20-25% of the filtrated Ca2+is reabsorbed in the Henle-loop

3. A 5-10 % of the filtrated Ca2+is reabsorbed by an ACTIVE PROCESS in the distal nephron 

causes increased urinary Ca excretion 

because Ca reabsorption is linked with Na reabSorption in LOOP OF HENLE

• 1.PTH - in distal tubule by activating adenylate cyclase
• 2. thiazide diuretics in distal tubule so decrease Ca excretion

85-95 % of the filtrated phosphate is reabsorbed in the proximal tubuli. by      Na-phosphate  cotransport

due to the fact that the distal nephron does not reabsorb phosphate --> 15%of the remaining PHOSPHATE IS EXCRETED

This reabsorption is coupled to Na+ reabsorption, thus it has a Tm value .

Regulation of phosphate excretion is achieved by parathyroid hormone- PTH that inhibits the phosphate reabsorption in the proximal tubuli.by ACTIVATING Adenylate Cyclase, generating cyclic AMP 

High plasma level of PTH  may yield the excretion of 40 % of the filtrated amount (hyperphosphaturia).

Low plasma level of PTH is associated with the excretion of less than the 5% of the filtrated amount (hypophosaturia).

PTH acts through these mechanisms on the plasma Ca++ level. PTH acts through specific receptors on the baso-lateral surface through specific receptors through the route described at Ca++- ions.

urinary buffer for the H excretion of h2po4

• 1.proximal tubule
• 2.thick ascending limb
• 3.distal tubule

Mg and Ca compete for reabsorption in the thick ascending limb 

hypercalemia-->increase in Mg excretion (by inhebiting Mg reabsorption)

hypermagnesemia-> causes increase in Ca excretion (by ihebiting Ca reabsorption)

calciotrop hormons:

• 1.PTH-PARATHYROID GLAND
• 2.CALCITONIN-thyroid gland
• 3.VITAMIN D-CALCITORIOL

• regulate [CA]SERUM
• synthesized and secreted by the CHIEF CELLS of parathyroid glands
• 48 amino acids
• prephormon (145 amino acids)

regulated by the SERUM [Ca] binding to Ca sensing receptors in parathyroid ell membrane

PTH 1.binds to PTH receptors 2.increase adenilate cyclase and phospholipase C activity

PTH effect is executed by contribution of IP3 and cAMP

• PTH INCREASE when  [Ca] decreased

CAMP

INCREASE PTH secretion

• 1.in kidney and bone DIRECT EFFECT
• 2.small intestine indirect effect through calcitriol

• 1.increase Ca reabsorption in thick ascending limb  and the distal nephron
• 2.phosphate excretion