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Dr.S.Sethupathy,M.D.,Ph.D.,
Professor of Biochemistry,
Rajah Muthiah Medical College,
Annamali University
 Renal tubular acidosis (RTA) is due
either inherited or acquired kidney’s
inability to reabsorb bicarbonate or
secrete H+ secretion.
 It is characterized by normal anion gap
metabolic acidosis (Hyperchloremic)
 GFR will be normal or near normal.
 Classical form
 Inability to acidy urine maximum
 Distal defect – decreased H+ secretion
 Metabolic acidosis
 K+ secreted in stead of H+ - hypokalemia
 Urine pH > 5.5
 Hypercalciuria
 Renal stones
 Urinary loss of sodium causes volume contraction
 Increased aldosterone section
 Increased tubular secretion and decreased
reabsorption of potassium in proximal tubules
 Resulting in hypokalemia
 Chronic acidosis leads to decreased reabsorption
of Ca2+ -Hypercalciuria
 Acidosis and hypokalemia cause increased
reabsorption of citrate – hypocitraturia
 Hypercalciuria , hypocitraturia, alkaline urine –
leads to Calcium phosphate stone formation -
nephrocalcinosis
 Failure to thrive, growth
retardation
 Polyuria, polydipsia
 Nephrolithiasis
 Weakness, transient paralysis-
hypokalemia
 Bicarbonate administration – initially 2-3 meq/
Kg/day
 Then increased till serum bicarbonate level
becomes normal
 Usually maintenance dose will be 5-10
meq/kg/day
 Continued Life long
 Hypochloremic metabolic acidosis
 Decreased serum PO4
 Hypokalemia
 Proteinuria
 Urine anion gap = Na+ + K+ − Cl. where the
concentrations are expressed in units of
milliequivalents/liter (mEq/L).
 low urinary AG = GI loss of base
 no change in urinary AG = renal loss of base
 negative urinary AG = severe diarrhea
 positive urinary AG = altered urinary acidification
 The underlying defect is the impaired
cation exchange in the distal tubules with
reduced excretion of H+ and K+
 Hyperkalemic acidosis present
 Hypoaldosteronism or decreased
response to aldosterone
 Type 3 RTA no longer used.
 Hypoaldosteronism (low renin) -
Hyporeninemic hypoaldosteronism
(diabetes mellitus/mild renal impairment,
chronic interstitial nephritis, non-steroidal anti-
inflammatory drugs, beta-blockers)
 Hypoaldosteronism (high renin) –
Primary adrenal defect (congenital
hypoaldosteronism; Addison disease,
adrenalectomy, AIDS)
inhibition of aldosterone secretion (heparin,
ACE inhibitors, AT1 receptor blockers)
 Aldosterone resistance (drugs) -
Diuretics (amiloride, triamterene,
spironolactone),
calcineurin inhibitors (cyclosporine,
tacrolimus),
antibiotics (trimethoprim, pentamidine)
 Aldosterone resistance (genetic) -
Pseudohypoaldosteronism (PHA) types I
and II
Thank you

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Renal tubular acidosis

  • 1. Dr.S.Sethupathy,M.D.,Ph.D., Professor of Biochemistry, Rajah Muthiah Medical College, Annamali University
  • 2.  Renal tubular acidosis (RTA) is due either inherited or acquired kidney’s inability to reabsorb bicarbonate or secrete H+ secretion.  It is characterized by normal anion gap metabolic acidosis (Hyperchloremic)  GFR will be normal or near normal.
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  • 4.  Classical form  Inability to acidy urine maximum  Distal defect – decreased H+ secretion  Metabolic acidosis  K+ secreted in stead of H+ - hypokalemia  Urine pH > 5.5  Hypercalciuria  Renal stones
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  • 12.  Urinary loss of sodium causes volume contraction  Increased aldosterone section  Increased tubular secretion and decreased reabsorption of potassium in proximal tubules  Resulting in hypokalemia  Chronic acidosis leads to decreased reabsorption of Ca2+ -Hypercalciuria  Acidosis and hypokalemia cause increased reabsorption of citrate – hypocitraturia  Hypercalciuria , hypocitraturia, alkaline urine – leads to Calcium phosphate stone formation - nephrocalcinosis
  • 13.  Failure to thrive, growth retardation  Polyuria, polydipsia  Nephrolithiasis  Weakness, transient paralysis- hypokalemia
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  • 16.  Bicarbonate administration – initially 2-3 meq/ Kg/day  Then increased till serum bicarbonate level becomes normal  Usually maintenance dose will be 5-10 meq/kg/day  Continued Life long
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  • 32.  Hypochloremic metabolic acidosis  Decreased serum PO4  Hypokalemia  Proteinuria  Urine anion gap = Na+ + K+ − Cl. where the concentrations are expressed in units of milliequivalents/liter (mEq/L).  low urinary AG = GI loss of base  no change in urinary AG = renal loss of base  negative urinary AG = severe diarrhea  positive urinary AG = altered urinary acidification
  • 33.  The underlying defect is the impaired cation exchange in the distal tubules with reduced excretion of H+ and K+  Hyperkalemic acidosis present  Hypoaldosteronism or decreased response to aldosterone  Type 3 RTA no longer used.
  • 34.  Hypoaldosteronism (low renin) - Hyporeninemic hypoaldosteronism (diabetes mellitus/mild renal impairment, chronic interstitial nephritis, non-steroidal anti- inflammatory drugs, beta-blockers)  Hypoaldosteronism (high renin) – Primary adrenal defect (congenital hypoaldosteronism; Addison disease, adrenalectomy, AIDS) inhibition of aldosterone secretion (heparin, ACE inhibitors, AT1 receptor blockers)
  • 35.  Aldosterone resistance (drugs) - Diuretics (amiloride, triamterene, spironolactone), calcineurin inhibitors (cyclosporine, tacrolimus), antibiotics (trimethoprim, pentamidine)  Aldosterone resistance (genetic) - Pseudohypoaldosteronism (PHA) types I and II
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