1. Human Physiology Renal Physiology
by Talib F. Abbas

2. Role of Urea in ECF
Urea contributes to the establishment of the osmotic gradient in the medullary pyramids and to the ability to form a concentrated urine in the collecting ducts. Urea transport is mediated by urea transporters, presumably by facilitated diffusion. There are at least four isoforms of the transport protein UT-A in the kidneys (UT-A1 to UT-A4); UT-B is found in erythrocytes.
a high-protein diet increases the ability of the kidneys to concentrate the urine.

4. Water diuresis
The osmotic gradient in the medullary pyramids would not last long if the Na+ and urea in the interstitial spaces were removed by the circulation. These solutes remain in the pyramids primarily because the vasa recta operate as countercurrent exchangers.
the solutes tend to recirculate in the medulla and water tends to bypass it, so that hypertonicity is maintained. The water removed from the collecting ducts in the pyramids is also removed by the vasa recta and enters the general circulation.
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5. Osmotic diuresis
The presence of large quantities of unreabsorbed solutes in the renal tubules causes an increase in urine volume called osmotic diuresis.
Therefore, they “hold water in the tubules.” In addition, the concentration gradient against which Na+ can be pumped out of the proximal tubules is limited. Osmotic diuresis is produced by the administration of compounds such as mannitol and related polysaccharides that are filtered but not reabsorbed.
For example, in diabetes mellitus, if blood glucose is high, glucose in the glomerular filtrate is high, thus the glucose will remain in the tubules causing polyuria. Osmotic diuresis can also be produced by the infusion of large amounts of sodium chloride or urea.

6. Free water clearance
In order to quantitate the gain or loss of water by excretion of a concentrated or dilute urine, the "free water clearance"(CH2O) is sometimes calculated. This is the difference between the urine volume and the clearance of osmoles (COsm):
where V• is the urine flow rate and UOsm and POsm the urine and plasma osmolality, respectively. COsm is the amount of water necessary to excrete the osmotic load in a urine that is isotonic with plasma. Therefore, CH2O is negative when the urine is hypertonic and positive when the urine is hypotonic.
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7. Renal Hydrogen secretion
The cells of the proximal and distal tubules secrete hydrogen ions.
Acidification also occurs in the collecting ducts. The reaction that is primarily responsible for H+ secretion in the proximal tubules is Na–H exchange. This is an example of secondary active transport; extrusion of Na+ from the cells into the interstitium by Na, K ATPase lowers intracellular Na+, and this causes Na+ to enter the cell from the tubular lumen, with coupled extrusion of H+. The H+ comes from intracellular dissociation of H2CO3, and the HCO3– that is formed diffuses into the interstitial fluid. Thus, for each H+ ion secreted, one Na+ ion and one HCO3– ion enter the interstitial fluid.

8. Carbonic anhydrase
catalyzes the formation of H2CO3, and drugs that inhibit carbonic anhydrase depress both secretion of acid by the proximal tubules and the reactions which depend on it.

9. Ammonia secretion
Reactions in the renal tubular cells produce NH4+ and HCO3–. NH4+ is in equilibrium with NH3 and H+ in the cells. Because the pK' of this reaction is 9.0, the ratio of NH3 to NH4+ at pH 7.0 is 1:100. However, NH3 is lipid- soluble and diffuses across the cell membranes down its concentration gradient into the interstitial fluid and tubular urine. In the urine it reacts with H+ to form NH4+, and the NH4+ remains in the urine.

10. Ammonia secreation
The principal reaction producing NH4+ in cells is conversion of glutamine to glutamate. This reaction is catalyzed by the enzyme glutaminase, which is abundant in renal tubular cells. Glutamic dehydrogenase catalyzes the conversion of glutamate to α-ketoglutarate, with the production of more NH4+. Subsequent metabolism of α-ketoglutarate utilizes 2H+, freeing 2HCO3–.

11. Ammonia secreation

13. Factors effecting acid secretion
Renal acid secretion is altered by changes in the intracellular PCO2, K+ concentration, carbonic anhydrase level, and adrenocortical hormone concentration. When the PCO2 is high (respiratory acidosis), more intracellular H2CO3 is available to buffer the hydroxyl ions and acid secretion is enhanced, whereas the reverse is true when the PCO2 falls. K+ depletion enhances secretion, apparently because the loss of K+ causes intracellular acidosis even though the plasma pH may be elevated. Conversely, K+ excess in the cells inhibits acid secretion. When carbonic anhydrase is inhibited, acid secretion is inhibited because the formation of H2CO3 is decreased. Aldosterone and the other adrenocortical steroids that enhance tubular reabsorption of Na+ also increase the secretion of H+ and K+.

15. Bicarbonate excretion
Although the process of HCO3– reabsorption does not actually involve transport of this ion into the tubular cells, HCO3– reabsorption is proportional to the amount filtered over a relatively wide range.
When the plasma HCO3– concentration is low, all the filtered HCO3– is reabsorbed; but when the plasma HCO3– concentration is high; that is, above 26 to 28 mEq/L (the renal threshold for HCO3–), HCO3– appears in the urine and the urine becomes alkaline.

16. Bicarbonate excreation
when the plasma HCO3– falls below about 26 mEq/L, the value at which all the secreted H+ is being used to reabsorb HCO3–, more H+ becomes available to combine with other buffer anions.
Therefore, the lower the plasma HCO3– concentration drops, the more acidic the urine becomes and the greater its NH4+ content.

17. Defense of Hydrogen concentration
Defense of H+ concentration: The mystique that envelopes the subject of acid–base balance makes it necessary to point out that the core of the problem is not “buffer base” or “fixed cation” or the like, but simply the maintenance of the H+ concentration of the ECF.

18. Amino acid metabolism and Urea

19. Renin-Angiotensin system
The rise in blood pressure produced by injection of kidney extracts is due to renin, an acid protease secreted by the kidneys into the bloodstream.
This enzyme acts in concert with angiotensin- converting enzyme to form angiotensin II.
plasma renin concentration (PRC): exogenous angiotensinogen is often added, Deficiency of angiotensinogen as well as renin can cause low plasma renin activity (PRA) .
The plasma angiotensin II concentration in such subjects is about 25 pg/mL (approximately 25 pmol/L).

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22. The Juxtaglomerular Apparatus TV
The renin in kidney extracts and the bloodstream is produced by the juxtaglomerular cells (JG cells). These epitheloid cells are located in the media of the afferent arterioles as they enter the glomeruli.
The membrane-lined secretory granules in them have been shown to contain renin.
Renin is also found in agranular lacis cells that are located in the junction between the afferent and efferent arterioles, but its significance in this location is unknown.
The lacis cells, the JG cells, and the macula densa constitute the juxtaglomerular apparatus.

23. Renin Regulation Factors
intrarenal baroreceptor mechanism that causes renin secretion to decrease when arteriolar pressure at the level of the JG cells increases.
Renin secretion is inversely proportional to the amount of Na+ and Cl– entering the distal renal tubules from the loop of Henle.
NO and K+ level effect the Renin secreation.
Angiotensin II feeds back to inhibit renin secretion by a direct action on the JG cells.
Vassopressin inhibit renin.
increased activity of the sympathetic nervous system increases renin secretion
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