The kidney controls acid-base balance through 3 main mechanisms: 1) secretion of hydrogen ions, 2) reabsorption of filtered bicarbonate, and 3) production of new bicarbonate. Hydrogen ion secretion occurs along most of the nephron except the descending and ascending thin limbs of the loop of Henle. The late distal convoluted tubule and collecting duct are responsible for maximal acidification of urine through hydrogen ion secretion, lowering pH to as low as 4.5. Bicarbonate reabsorption is coupled to hydrogen ion secretion, with 80-90% occurring in the proximal convoluted tubule. New bicarbonate is produced through phosphate and ammonia buffers.
The kidney controls acid-base balance through 3 main mechanisms: 1) secretion of hydrogen ions, 2) reabsorption of filtered bicarbonate, and 3) production of new bicarbonate. Hydrogen ion secretion occurs along most of the nephron except the descending and ascending thin limbs of the loop of Henle. The late distal convoluted tubule and collecting duct are responsible for maximal acidification of urine through hydrogen ion secretion, lowering pH to as low as 4.5. Bicarbonate reabsorption is coupled to hydrogen ion secretion, with 80-90% occurring in the proximal convoluted tubule. New bicarbonate is produced through phosphate and ammonia buffers.
The kidney controls acid-base balance through 3 main mechanisms: 1) secretion of hydrogen ions, 2) reabsorption of filtered bicarbonate, and 3) production of new bicarbonate. Hydrogen ion secretion occurs along most of the nephron except the descending and ascending thin limbs of the loop of Henle. The late distal convoluted tubule and collecting duct are responsible for maximal acidification of urine through hydrogen ion secretion, lowering pH to as low as 4.5. Bicarbonate reabsorption is coupled to hydrogen ion secretion, with 80-90% occurring in the proximal convoluted tubule. New bicarbonate is produced through phosphate and ammonia buffers.
The kidney controls acid-base balance through 3 main mechanisms: 1) secretion of hydrogen ions, 2) reabsorption of filtered bicarbonate, and 3) production of new bicarbonate. Hydrogen ion secretion occurs along most of the nephron except the descending and ascending thin limbs of the loop of Henle. The late distal convoluted tubule and collecting duct are responsible for maximal acidification of urine through hydrogen ion secretion, lowering pH to as low as 4.5. Bicarbonate reabsorption is coupled to hydrogen ion secretion, with 80-90% occurring in the proximal convoluted tubule. New bicarbonate is produced through phosphate and ammonia buffers.
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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