The pH of urine is variable depending on H⁺
ions secreted.
Urine has a pH of approx 6
This implies kidneys contribute to the
acidification because it is formed from
plasma pH=7
The H⁺ generated in the body is eliminated by
acidified urine.
Renal mechanism tries to provide a
permanent solution to the acid – base
disturbance where as that provided by blood
and respiratory system is temporary.
As end product of metabolism
Protein rich diet
Renal tubular generation of H⁺
Sources of non-carbonic acids
The major site of acidification of urine is DCT
& CT
There is no significant contribution of H⁺
from the glomerular filtrate. The H⁺ is from
tubular secretion.
Formation of carbonic acid
Dissociation of carbonic acid
Secretion of H⁺ into lumen occurs through
Na⁺-H⁺ ATPase
The H⁺ combines with HCO3⁻ and helps in its
absorption
Therefore this process doesn’t result in net
excretion of H⁺
The HCO3⁻ formed in the cell diffuses into IF
PCT
In DCT & CD the H⁺ secretion is independent
of Na⁺
Secretion occurs by 2 mechanism by the
intercalated cells
ATP driven proton pump( H⁺ ATP ase)
H⁺ K⁺ ATPase
DCT
The secretion of H⁺ can occur only if the pH is
immediately buffered in the luminal fluid.
The tubular cells can secrete H⁺ upto luminal
fluid pH about 4.5
In the absence of buffering of H⁺ the limiting
pH would reach very fast stopping further H⁺
secretion.
In the PCT the H⁺ is buffered by filtered
HCO3⁻
In the DCT and CD it is buffered by Na2HPO4
& ammonia ( phosphates and ammonium
buffer) acidification
Three buffers are present in the kidney
1.HCO3⁻ buffer
[Link] phosphate buffers
[Link] buffers
HCO3⁻ reabsorption if required for prevention
of its loss from kidney and maintain acid base
balance.
Under normal condition almost all the HCO3⁻
is reabsorbed by different segment.
In the PCT- 80% of filtered HCO3⁻ is
reabsorbed
In the LOH -15% of filtered HCO3⁻ is
reabsorbed
In the DCT & CD -5% which escapes PCT is
reabsorbed.
Mechanism- the H⁺ secreted combines with
filtered HCO3⁻ to form H2CO3. This splits into
H2O and CO2 which diffuse into tubular cells.
75% of the filtered HPO4⁻ is reabsorbed
Only 25% is available for buffering
Exchange of Na⁺ for H⁺ converts dibasic
sodium phosphate to monobasic dihydrogen
phosphate which is excreted in urine as
titratable acid.
PHOSPHATES BUFFERS
Ammonium enters the tubular lumen not by
filtration but by synthesis and secretion
mainly confined to DCT and CT
Source of NH4⁺ in renal tubules
60% produced by deamination of AA
glutamine
Glutamine + H2O Glutaminase glutamic acid
+ NH4⁺
30% from deamination of glutamic acid
Glutamic acid Glutamic dehydrogenase ἀ keto
glutamic acid + NH4⁺
10% is produced by deamination of other AA-
asparagine, glycine, alanine.
Some NH3 directly enter from arterial blood.
NH3 is lipid permeable and easily move out of the cell.
The renal contribution of newly synthesized
HCO3⁻ is accompanied by the excretion of an
equivalent amount of acid in the urine in the
form of Titratable Acid, NH4⁺ or both.
Net quantity of free hydrogen ion in
association with a buffer system in the urine
measured by the amt of alkali needed for
returning acid urine to pH 7.4 this is called
titratable acidity.
H⁺ excretion is measured by sum of titratable
acidity and ammonium excreted.
Acid base 1º pH pCO2 HCO3⁻ H⁺
abnormality disturbance 7.4 40mmHg 24meq/l 40meq/l
Respiratory ↑pCO2 ↓ ↑↑ ↑ ↑
acidosis
Metabolic ↓HCO3⁻ ↓ ↓ ↓↓ ↑
acidosis
Respiratory ↓ pCO2 ↑ ↓↓ ↓ ↓
alkalosis
Metabolic ↑ HCO3 ↑ ↑ ↑↑ ↓
alkalosis
