Renal tubular acidosis and other causes of Normal anion gap Metabolic acidosis
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It discusses approach to a patient with normal anion gap metabolic acidosis with special emphasis on renal tubular acidosis and its types.
![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](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
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Renal tubular acidosis and other causes of Normal anion gap Metabolic acidosis
- 1. By Jagjit Khosla By Dr. 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 Normal Anion Gap By Dr. Jagjit Khosla
- 4. By Dr. Jagjit Khosla
- 5. Na+ + Unmeasured cations = 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 acid is added to blood Anion H+ Na+ HCO3 -+ Na Cl HCO3 UnHCO3 By Dr. Jagjit Khosla
- 7. Na Cl UnHCO3 Cl- Other Anion Normal Anion gap Metabolic Acidosis (Hyperchloremic) High Anion gap Metabolic Acidosis By Dr. Jagjit Khosla
- 8. By Dr. Jagjit Khosla
- 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 of HCO3 Ingestion Dilutional Post hypocapnia 1 2 3 4 Type II RTA5 By Dr. Jagjit Khosla
- 13. GI loss of HCO31 - Diarrhoea - Intestinal or pancreatic fistula - Ureteral diversion - Villous adenoma By Dr. Jagjit Khosla
- 14. GI loss of HCO31 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. Cl- Urea Ureter HCO3 - NH4 + Sigmoid Colon Urea-splitting organisms By Dr. Jagjit Khosla
- 16. GI loss of HCO3 Ingestion 1 2 - Acetazolamide - Sevelamer - Cholestyramine - Toluene By Dr. Jagjit Khosla
- 17. GI loss of HCO3 Ingestion Dilutional 1 2 3 - Due to rapid infusion of bicarbonate-free iv fluids By Dr. Jagjit Khosla
- 18. GI loss of HCO3 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 of HCO3 Ingestion Dilutional Post hypocapnia 1 2 3 4 Type II RTA5 By Dr. Jagjit Khosla
- 20. Type I RTA Type IV RTA 1 2 By Dr. Jagjit Khosla
- 21. By Dr. Jagjit Khosla
- 22. Definition Disorders affecting the overall 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 Reabsorption of 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 Cell Tubular 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 Cell Tubular 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 Potassium excretion 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 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
- 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 cell Lumen 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 cell Lumen 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 Familial Autosomal 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 Aldosterone production - Aldosterone resistance By Dr. Jagjit Khosla
- 41. Etiology Decreased aldosterone production Hyporeninemic hypoaldosteronism - Renal disease, 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 the epithelial 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. Jagjit Khosla
- 44. By Dr. Jagjit Khosla