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![Definition
- Blood pH <7.35 (Acidemia)
- [HCO3
-]
- [PaCO2]
(1.2 mm Hg fall in [PaCO2] for every 1 meq/L reduction in [HCO3
-])
By Dr. Jagjit Khosla](https://image.slidesharecdn.com/rta-150721181157-lva1-app6891/75/Renal-tubular-acidosis-and-other-causes-of-Normal-anion-gap-Metabolic-acidosis-2-2048.jpg)
![Features
• U. HCO3- (FeHCO3 > 15%)
• U. pH <5.5,
• S. [HCO3
-] 12-20
• U. Na+
• U. K+ - Hypokalemia
Mechanism of enhanced K+ excretion
- Increased distal Na+ delivery
- Sodium wasting induced secondary hyperaldosteronism
By Dr. Jagjit Khosla](https://image.slidesharecdn.com/rta-150721181157-lva1-app6891/75/Renal-tubular-acidosis-and-other-causes-of-Normal-anion-gap-Metabolic-acidosis-30-2048.jpg)
![Effect on Potassium excretion
With alkali therapy
Increased S. [HCO3
-]
Increased filtered load above proximal reabsorptive capacity
Increased distal sodium and water delivery
Enhanced distal potassium excretion
Note : Alkali therapy in proximal RTA should be accompanied with potassium
to prevent hypokalemia
By Dr. Jagjit Khosla](https://image.slidesharecdn.com/rta-150721181157-lva1-app6891/75/Renal-tubular-acidosis-and-other-causes-of-Normal-anion-gap-Metabolic-acidosis-32-2048.jpg)
Uploaded byJagjit Khosla
Renal tubular acidosis and other causes of Normal anion gap Metabolic acidosis
The document discusses metabolic acidosis, detailing definitions, types (high and normal anion gap), and underlying causes such as renal tubule disorders and gastrointestinal losses. It elaborates on anion gap equations, urine anion gap implications, and the mechanisms of renal acid-base regulation, including renal tubular acidosis (RTA) types. The document further explores the intricacies of bicarbonate reabsorption and potassium excretion related to proximal and distal tubular functions.
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Renal tubular acidosis and other causes of Normal anion gap Metabolic acidosis
- 1. By Jagjit Khosla ByDr. Jagjit Khosla
- 2. Definition - Blood pH<7.35 (Acidemia) - [HCO3 -] - [PaCO2] (1.2 mm Hg fall in [PaCO2] for every 1 meq/L reduction in [HCO3 -]) By Dr. Jagjit Khosla
- 3. Metabolic Acidosis High Anion Gap NormalAnion Gap By Dr. Jagjit Khosla
- 4. By Dr. JagjitKhosla
- 5. Na+ + Unmeasuredcations = Cl- + HCO3 - + Unmeasured anions Or, Unmeasured anions – Unmeasured cations = Na+ - (Cl- + HCO3 -) Anion Gap = Na+ - (Cl- + HCO3 -) Definition Anion gap is Quantity of anions not balanced by cations - usually due to the NEGATIVELY CHARGED PLASMA PROTEINS as the charges of the other unmeasured cations and anions tend to balance out. Na Cl HCO3 Un Normal Anion Gap (10 – 12 mM/L) Note : - Adjust for HypoalbuminemiaBy Dr. Jagjit Khosla
- 6. If an acidis added to blood Anion H+ Na+ HCO3 -+ Na Cl HCO3 UnHCO3 By Dr. Jagjit Khosla
- 7. Na Cl UnHCO3 Cl- OtherAnion Normal Anion gap Metabolic Acidosis (Hyperchloremic) High Anion gap Metabolic Acidosis By Dr. Jagjit Khosla
- 8. By Dr. JagjitKhosla
- 9. Normal Anion Gap Metabolic Acidosis (+)Urine Anion Gap (-) Urine Anion Gap By Dr. Jagjit Khosla
- 10. Cl UNa+ + UK++ Unmeasured cations = UCl- + Unmeasured anions Or, Unmeasured anions – Unmeasured cations = (UNa+ + UK+) - UCl- Urine Anion Gap (UAG) = (UNa+ + UK+) - UCl- - NH4 + is the primary unmeasured cation which is not balanced by anions. - UAG as indirect assay for renal NH4+ excretion Na K NH4 + By Dr. Jagjit Khosla
- 11. Negative Positive Increased renal NH4+excretion (Response to acidemia) Failure of Kidneys to secrete NH4 + By Dr. Jagjit Khosla
- 12. GI loss ofHCO3 Ingestion Dilutional Post hypocapnia 1 2 3 4 Type II RTA5 By Dr. Jagjit Khosla
- 13. GI loss ofHCO31 - Diarrhoea - Intestinal or pancreatic fistula - Ureteral diversion - Villous adenoma By Dr. Jagjit Khosla
- 14. GI loss ofHCO31 Pancreas Ileum Colon Pancreas Ileum Colon HCO3 - HCO3 - Cl- HCO3 - Cl- K+ HCO3 - Normal Diarrhea Cl- Flooding the colon with HCO3 - instead of Cl- drives K+ secretion By Dr. Jagjit Khosla
- 15.
- 16. GI loss ofHCO3 Ingestion 1 2 - Acetazolamide - Sevelamer - Cholestyramine - Toluene By Dr. Jagjit Khosla
- 17. GI loss ofHCO3 Ingestion Dilutional 1 2 3 - Due to rapid infusion of bicarbonate-free iv fluids By Dr. Jagjit Khosla
- 18. GI loss ofHCO3 Ingestion Dilutional Post hypocapnia 1 2 3 4 - Rapid correction of respiratory alkalosis by renal wasting of HCO3 - leading to transient acidosis By Dr. Jagjit Khosla
- 19. GI loss ofHCO3 Ingestion Dilutional Post hypocapnia 1 2 3 4 Type II RTA5 By Dr. Jagjit Khosla
- 20. Type I RTA TypeIV RTA 1 2 By Dr. Jagjit Khosla
- 21. By Dr. JagjitKhosla
- 22. Definition Disorders affecting theoverall ability of the renal tubules either to secrete hydrogen ions or to retain bicarbonate ions Types - Type I (Distal) - Type II (Proximal) - Type IV (Hypoaldosteronism) By Dr. Jagjit Khosla
- 23. - Proximal Acidification Reabsorptionof HCO3 - in Proximal tubule - Distal Acidification H+ secretion in Collecting tubule Type II RTA Type I & Type IV RTA By Dr. Jagjit Khosla
- 24. Proximal Tubule CellTubular Lumen Na+ H+ H20 CO2 3HCO3 - Na+ CA II 3Na+ 2K+ Na+K+ ATPase H+ HCO3 - + H2CO3 CO2 H2O+ Carbonic Anhydrase IV + H+HCO3 - + H2CO3 Na+H+ Exchanger Na+ HCO3 - Cotransporter Na+ Blood By Dr. Jagjit Khosla
- 25. Proximal Tubule CellTubular Lumen Na+ H+ H20 CO2 3HCO3 - Na+ CA II 3Na+ 2K+ H+ HCO3 - + H2CO3 CO2 H2O+ Carbonic Anhydrase IV + H+HCO3 - + H2CO3 Na+H+ Exchanger Na+ HCO3 - Cotransporter Na+ 1 2 5 6 3 4 Na+K+ ATPase Blood By Dr. Jagjit Khosla
- 26. • Fanconi’s syndrome- Loss of Glucose, Calcium, phosphate, citrate, uric acid, lysozymes, light chain immunoglobins, and amino acids. • Isolated HCO3 wasting is rarely identified. Isolated HCO3 wasting Generalised Proximal tubular dysfunction By Dr. Jagjit Khosla
- 27. Primary disorders • Idiopathic,sporadic • Familial disorders – Cystinosis – Tyrosinemia – Hereditary fructose intolerance – Galactosemia – Glycogen storage disease(Type I) – Wilson’s disease – Lowe’s syndrome – Carbonic Anhydrase deficiency Secondary disorders • Multiple myeloma • Drugs – Tenofovir – Carbonic anhydrase inhibitors – Ifosfamide • Amyloidosis • Heavy metals poisoning (Lead, Cadmium, Hg, Cu) • Vitamin D deficiency • Renal transplantation • Paroxysmal nocturnal hemoglobinuria By Dr. Jagjit Khosla
- 28. 80% reabsorbed 15% reabsorbed 5%excreted HCO3 HCO3 HCO3 HCO3 100% By Dr. Jagjit Khosla
- 29. 60% reabsorbed 15% reabsorbed 25%excreted HCO3 HCO3 HCO3 HCO3 100% Decreased Proximal tubule reabsorption Cl- K+ By Dr. Jagjit Khosla
- 30. Features • U. HCO3-(FeHCO3 > 15%) • U. pH <5.5, • S. [HCO3 -] 12-20 • U. Na+ • U. K+ - Hypokalemia Mechanism of enhanced K+ excretion - Increased distal Na+ delivery - Sodium wasting induced secondary hyperaldosteronism By Dr. Jagjit Khosla
- 31. Effect on Potassiumexcretion Without alkali therapy Principal Cell LumenBlood Na+ K+ Na+ Channel K+ Channel 3Na+ 2K+ Na+K+ ATPase Na+ -+ K+ Aldosterone By Dr. Jagjit Khosla
- 32. Effect on Potassiumexcretion With alkali therapy Increased S. [HCO3 -] Increased filtered load above proximal reabsorptive capacity Increased distal sodium and water delivery Enhanced distal potassium excretion Note : Alkali therapy in proximal RTA should be accompanied with potassium to prevent hypokalemia By Dr. Jagjit Khosla
- 33. • Collecting tubule(CT) is the major site of H+ secretion • Made up of : – Cortical Collecting tubule – H+ secretion coupled with Na+ reabsorption – Medullary Collecting tubule – H+ secretion independent of Na+ reabsorption • Alpha-intercalated cells are main cells involved in H+ secretion By Dr. Jagjit Khosla
- 34. Alpha Intercalated cellLumen K+ H+ H2CO3 H20CO2 + HCO3 - CA II Cl- H+ Blood 3Na+ 2K+ Na+K+ ATPase H+ ATPase H+ K+ ATPase H+ HPO4 2- NH3 H2PO4 - NH4 + Anion Exchanger By Dr. Jagjit Khosla
- 35. Principal Cell LumenBlood Na+ K+ Na+Channel K+ Channel 3Na+ 2K+ Na+K+ ATPase Na+ -+ K+ H+ By Dr. Jagjit Khosla
- 36. Alpha Intercalated cellLumen K+ H+ H2CO3 H20CO2 + HCO3 - CA II Cl- H+ Blood 3Na+ 2K+ Na+K+ ATPase H+ ATPase H+ K+ ATPase H+ HPO4 2- NH3 H2PO4 - NH4 + Anion Exchanger 1 2 3 By Dr. Jagjit Khosla
- 37. Principal Cell LumenBlood Na+ K+ Na+Channel K+ Channel 3Na+ 2K+ Na+K+ ATPase Na+ -+ K+ H+ 4 By Dr. Jagjit Khosla
- 38. Mechanisms - Defective H+-K+ATPase (Classic Hypokalemic dRTA) - Defective H+ ATPase (Normokalemic dRTA) - Gradient defect (Backleak of secreted H+ e.g. Amphotericin B) - Voltage depended defect (Hyperkalemic dRTA) - Abnormal Anion Exchange By Dr. Jagjit Khosla
- 39. Etiology Primary Idiopathic, Sporadic FamilialAutosomal dominant or recessive Secondary Sjogren’s syndrome Hypercalciuria Rheumatoid Arthritis Hyperglobulinemia Ifosfamide Amphotericin B Cirrhosis SLE Sickle Cell Anemia Obstructive Uropathy Lithium Renal transplantation By Dr. Jagjit Khosla
- 40. Mechanisms - Reduced Aldosteroneproduction - Aldosterone resistance By Dr. Jagjit Khosla
- 41. Etiology Decreased aldosterone production Hyporeninemic hypoaldosteronism - Renaldisease, most often diabetic nephropathy - Nonsteroidal anti-inflammatory drugs - Calcineurin inhibitors - Volume expansion, as in acute glomerulonephritis Medications - ACE inhibitors, angiotensin II receptor blockers, and direct renin inhibitors Heparin Primary adrenal insufficiency Severe illness Inherited disorders Congenital isolated hypoaldosteronism Pseudohypoaldosteronism type 2 (Gordon's syndrome) By Dr. Jagjit Khosla
- 42. Etiology Aldosterone resistance Inhibition of theepithelial sodium channel - Potassium-sparing diuretics, such as spironolactone, eplerenone, amiloride, and triamterine - Antibiotics, trimethoprim and pentamidine Pseudohypoaldosteronism type 1 By Dr. Jagjit Khosla
- 43. By Dr. JagjitKhosla
- 44. By Dr. JagjitKhosla