Acid-base balance

Biochemistry was one subject which scared me a lot ,all those molecular level breakdown of carbohydrates,fats and protein with ultrastructure of DNA went above my head but i made my own peace with the subject in due course of time  so today i am taking a topic which reminds me of biochemistry and that is Acid-base balance,the question is , Define Base excess?How do kidneys compensate for acid-base balance?

Siggard and Anderson in 1948 developed a simpler measure of metabolic acid base activity and termed it "Base Excess/Deficit.
Defination
 This is defined as the amount of strong acid or base that is required to return the pH to 7.4 assuming that the PCo2 is 40 mm of Hg and the temperature is 38 deg centigrade.
this approach was modified and only serum base excess was taken into calculation instead of whole blood and the calculation was known as Standardised Base Excess(SBE).
Role of kidneys in compensation of acid base imbalance
 Kidneys mainly handle the sodium and chloride ions,because the dietary intake of both the ions is roughly equal the kidneys excrete a net chloride load using the ammonium a weak  cation to accompany chloride in the urine.
Renal compensation during acidosis
 the kidneys respond to acidemia by

• increased reabsorption of the filtered bicarbonate ions
• increased excretion of titratable acids 
• increased production of ammonia

1. Increased reabsorption of bicarbonate ions- Co2 within the renal tubular cells combines with H2O to form bicarbonic acid H2Co3 in the presence of enzyme carbonic anhydrase which rapidly dissociates into H+ and HCo3 ions of which most of the bicarbonate ions are reabsorbed to the blood stream and the H+ is secreted into the renal tubules where in the brush borders of luminal surface  the same reaction as above happens i.e H+ and some of the Bicarbonate that was filtered happens to result in H2O and Co2 of which the Co2 is diffused back into the renal tubular cells to replace that was consumed and hence the proximal tubules reabsorb 80 to 90% of the bicarbonate ions along with sodium ions whereas the distal tubules make up 10 to 20% and by this increased bicarbonate reabsorption maintain the acid base balance.
2. Increased Excretion of Titratable Acids:-  The H+ that are secreted into the tubular lumen can combine with monohydrogen phosphate( HPO4)2- to form dihydrogen phosphate( H2Po4)- this latter component is not readily reabsorbed because of its charge and is eliminated in the urine.this urinary( H2Po4 )-/(HPo4)2- buffer works ideally  at a pKa of 6.8 at further  lower pH the dihydrogen phosphate ion predominates and monohydrogen component is not available to bind with H+.This buffer works when all bicarbonate are reabsorbed to maintain balance of acid and base.
3. Increased Excretion of Ammonia:-  After complete reabsorption  of bicarbonate ions and consumption of the phosphate buffer the NH3/(NH4)+ pair  attains the most important urinary buffer status. Deamination of  glutamine within proximal tubular cells causes an increase in ammonia production which is also enhanced in states of increased acidosis,this ammonia combines with tubular fluid H+ to form (NH4)- which is unable to penetrate the luminal membrane and hence trapped in luminal cells  and has reduced H+ levels by binding with them  thus reducing acidemia.

Renal compensation during Alkalosis

 kidneys are prone to cause alkalosis with large amounts of( HCo3)- ions only in conditions of

• Sodium deficiency
• Mineralocorticoid excess

In sodium deficiency there is depletion of extracellular space and increased reabsorption of sodium ions Na+, which is accompanied with chloride ions (Cl)-, to maintain electrical neutrality and as urinary chloride ions are decreased the bicarbonate must be reabsorbed also there is increased secretion of  H+ ions with  increased Na+ ions which again augments bicarbonate reabsorption causing metabolic alkalosis while in mineralocorticoid excess there is aldosterone augmented sodium reabsorption in exchange for H+ secretion in distal tubules which in turn causes bicarbonate formation resulting in metabolic alkalosis.