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Acidification of Urine

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Acidification of urine

Renal control of Acid – Base


balance
• By excreting either acidic or basic
urine by 3 mechanisms
1. Secretion of H+
2. Reabsorption of filtered
HCO3-
3. Production of new HCO3-
H+ ion secretion
• all parts of tubule except descending
and ascending thin limb of LOH
Late DCT and CD -Intercalated cells
• H+ Secretion in Late DCT and CD is
responsible for forming maximally
acidic urine though only 5% of H+ is
secreted .H+ concentration ↑ as
much as 900-fold
• In PT, H+ concentration↑ only about
3-4fold although large amounts of H+
are secreted
Limiting pH
• The maximal H+ gradient against
which the transport mechanisms can
secrete H+
• pH 4.5 is thus the limiting pH
corresponds to H+ concentration in
the urine that is 1000 times the
concentration in plasma
• If no buffers that "tied up“ free
H+ in the urine, limiting pH
+
reached rapidly, and H secretion
stops
pH Changes Along the
Nephron
Proximal Tubule Distal TUBULE
• More H+ sec • Only 5% H+sec
• H+ con can be ↑ • H+ con can be ↑
to only 3-4 fold 900 fold
pH Changes Along the
Nephron
Proximal Tubule Distal TUBULE
• Not much • pH ↓to 4.5 –
change in maximally acidic
luminal pH as urine
sec H+ reacts
with HCO3_ to
form H2CO3
which breaks to
Bicarbonate reabsorption
Reabsorption of filtered bicarbonate-

• Coupled to H+ ion secretion


• 80-90% occurs in PCT
• For each HCO3- reabsorbed from
lumen, one HCO3- diffuses in to
blood, though this is not the one that
is reabsorbed from the tubule.
Production of New HCO3-

• Reaction with phosphate buffer-


H+ excreted as titrable acid.
+
• Ammonia buffer- H excreted as
NH4 +
Phosphate Buffer-
Phosphate Buffer
• Consist of H2PO4 - and HPO42_
• in DT & CD---bcoz phosphate which
escapes proximal reabsorption is
greatly concentrated by the
reabsorption of water.
Titrable acidity
• Measure of acid excreted in urine by
kidney
• amount of NaH2PO4 present in urine
determine titrable acidity of urine
• As a result pH of urine is ↓
Ammonia Buffer –
PT,AscLOH,EarlyDT
Ammonia Buffer-CD
Diffusion trapping
• NH3 is lipid-soluble and diffuses into
CD lumen reacts with H+ to form
NH4+
• This lipid insoluble NH4+ is cannot
pass into cell & stay back in tubular
fluid
• Trapping of NH4+ in tubular lumen of
CD & is excreted in urine
Non ionic Diffusion
• Some weak acids & bases soluble in cell
membrane in undissociated form & cross
with difficulty in ionic form.
• CD cells not permeable to NH4+ but
permeable to NH3
• Process by which NH3 secreted into urine
& changed into NH4+ maintaining a
concentration gradient for NH3 diffusion
is called nonionic diffusion
Regulation of H+ secretion
• Most important stimuli for H+
secretion is
• ↑ Pco2 of ECF
• ↑ H+ or a ↓ in HCO3-
Aldosterone
• stimulate Intercalated cells increase
H+ secretion.
• Conn,s syndrome- increased H+
secretion-- increased HCO3
reabsorption--- Alkalosis
↓ECF volume
• stimulates H+ secretion & HCO3- and
Na+ reabsorption by
1. ↑Angiotensin II, which stimulates
Na+- H+ exchanger
2. ↑ Aldosterone levels
ECF volume depletion causes Alkalosis
K+
• Hypokalemia- increased H+
secretion, increased HCO3
reabsorption Alkalosis
• Hyperkalemia  decreased H+
secretion, decreased HCO3
reabsorption  Acidosis
Acute renal failure Chronic renal
• Onset – failure
Sudden over • Gradual over
days /weeks months or
• Reversible years
• Cause – • Irreversible
Prerenal/postre • Renal/extraren
nal al
• Oliguria/anuria • Polyuria &
nocturia
Acute renal failure Chronic renalfailure
Characteristic • Edema,
features – Proteinuria,
small sized
• Sudden ↓ GFR
kidneys
• Rapid ↑ BP,
Anaemia,
urea
Acidosis,hyperk
&creatinine
alemia,
level
hypertension,
osteomalacia
Treatment
Acute renal failure Chronic
• Dialysis – short renalfailure
period • Chronic
Maintenance
dialysis
• Renal
transplantation
Nephrotic syndrome

• Glomerular permeability affected

proteinuria---Hypoproteinemia

Edema

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