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A Case Of Severe Hypokalaemia

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A Case Of Severe Hypokalaemia

  1. 1. A Case of Severe Hypokalaemia Sara Furness 25 th October 2004.
  2. 2. Mrs L.D <ul><li>23 Year Old Indian lady </li></ul><ul><li>Recently moved to the UK following her marriage </li></ul><ul><li>Presented acutely to the on call physicians with an episode of collapse. </li></ul><ul><li>Speaks no English, so gaining a full history extremely difficult. </li></ul>
  3. 3. Mrs. L.D <ul><li>Complained of muscle weakness </li></ul><ul><li>No obvious abnormalities on physical examination </li></ul><ul><li>Neurologically intact </li></ul><ul><li>ECG flattened T’s </li></ul><ul><li>CXR normal </li></ul><ul><li>Telemetry normal </li></ul><ul><li>Admission bloods: </li></ul><ul><li>Na + 140 </li></ul><ul><li>K + 1.5 </li></ul><ul><li>Ur 4.9 </li></ul><ul><li>Creat 73 </li></ul><ul><li>HCO 3 14 </li></ul><ul><li>CCa + 2.17 </li></ul><ul><li>PO 3 0.38 </li></ul>
  4. 4. Mrs L.D <ul><li>Treated as presumed hypokalaemic periodic paralysis </li></ul><ul><li>Potassium infusion given </li></ul><ul><li>Symptoms improved when K + normal </li></ul><ul><li>Discharged for clinic follow up. </li></ul><ul><li>Also noted to have microcytic anaemic </li></ul><ul><li>Fe deficient </li></ul><ul><li>B12 & Folate ok </li></ul><ul><li>Haemoglobinopathy screen negative. </li></ul><ul><li>Ferrous sulphate given. </li></ul>
  5. 5. Mrs L.D <ul><li>Clinic bloods: </li></ul><ul><li>Na + 138 </li></ul><ul><li>K + 2.6 </li></ul><ul><li>Urea 4.5 </li></ul><ul><li>Creat 85 </li></ul><ul><li>HCO 3 15 </li></ul><ul><li>Chloride 115 </li></ul><ul><li>CCa + 2.14 </li></ul><ul><li>PO 3 0.88 </li></ul><ul><li>Further investigations done………. </li></ul><ul><li>Urinary pH 7.2 </li></ul><ul><li>24hr pro 0.24g/dL </li></ul><ul><li>Urine Ca + excretion 2.8 [2.5- 7.5] </li></ul><ul><li>Urate exc . 2.5 [1.4-4.5] </li></ul><ul><li>Na + exc . 114 [50-200] </li></ul><ul><li>K + exc . 51.6 mmol/24hr </li></ul><ul><li>No urinary amino acids </li></ul><ul><li>Severe vit d deficiency </li></ul><ul><li>Referred to us…… </li></ul>
  6. 6. <ul><li>Hyperchloraemic Metabolic Acidosis: </li></ul><ul><li>Renal Tubular Acidosis </li></ul><ul><li>Diarrheoa </li></ul><ul><li>Urinary diversions </li></ul><ul><li>Chronic Renal Failure </li></ul><ul><li>Carbonic Anhydrase inhibitors </li></ul>
  7. 7. Renal Tubular Acidosis <ul><li>Hyperchloraemic metabolic acidosis due to an abnormality in renal acidification </li></ul><ul><li>3 major subgroups </li></ul><ul><li>type 1 (distal) </li></ul><ul><li>Type 2 (proximal) </li></ul><ul><li>Type 4 (hypoaldosteronism) </li></ul><ul><li>Type 3 is a rare Carbonic Anhydrase deficiency </li></ul><ul><li> </li></ul>
  8. 8. Bicarbonate handling <ul><li>Renal HCO 3 reabsorption mainly occurs in PCT via H + /Na + exchange </li></ul><ul><li>10% reabsorbed distally via H + ATPase </li></ul><ul><li>Virtually no HCO 3 is present in normal urine </li></ul><ul><li>Proximal RTA occurs when there is a failure to reabsorb the filtered HCO 3 in the proximal tubule. </li></ul><ul><li>When plasma HCO 3 drops low enough, HCO 3 can be reabsorbed so a steady state is achieved (12-15mmol) </li></ul><ul><li>HCO 3 loading increases urinary pH </li></ul>
  9. 9. Acid Excretion <ul><li>DCT excretes H + load with ammonia and PO 3 buffers </li></ul><ul><li>Ammonia freely diffuses across membrane, H + is actively transported. </li></ul><ul><li>Binds to H + and is trapped in collecting duct </li></ul><ul><li>Systemic acidosis stimulates distal ammonia production </li></ul><ul><li>Failure to produce ammonia leads to H + retention </li></ul><ul><li>Type 2 (distal) RTA 2 ry to impaired H + secretion into tubule </li></ul><ul><li>Type 4 (and acidosis of rneal impairment) due to impaired ammoniagenesis </li></ul><ul><li>Distal RTA associated with low K + </li></ul><ul><li>Type 4 with high K + (hypoaldosteronism) . </li></ul>
  10. 10. Renal Tubular acidosis Diabetes (hyporeninaemic hypoaldosteronism) <5.3 appropriate high >17 Type 4   Fanconi syndrome <5.3 in balance high if ↑ bicarb low 12-15 Type1 (proximal) Hypercalciuria nephrocalcinosis >5.5 inappropriate low Possible <10 Type 1(distal) Associations Urine pH Plasma K + Plasma HCO 3
  11. 11. Investigations <ul><li>Plasma electrolytes </li></ul><ul><li>Urine Electrolytes </li></ul><ul><li>Plasma Chloride and HCO 3 </li></ul><ul><li>Urine anion gap </li></ul><ul><li>[Na + + K + - Cl - ] (+ve = low Cl excretion) </li></ul><ul><li>Fractional Excretion HCO 3 (<5% = dRTA) </li></ul><ul><li>Happily, most of these are not available at Preston </li></ul><ul><li>Dynamic function testing : </li></ul><ul><li>Bicarbonate loading </li></ul><ul><li>Ammonium Chloride test </li></ul>
  12. 12. Back to Mrs L.D <ul><li>Bicarbonate loading test </li></ul><ul><li>Differentiates between type 1 & 2 </li></ul><ul><li>Response of urine pH when serum bicarbonate normalised </li></ul>
  13. 13. Mrs L.D <ul><li>Acid loading test </li></ul><ul><li>Given as ammonium chloride </li></ul><ul><li>Differentiates between normal and abnormal distal acidification of urine </li></ul>
  14. 14. So the diagnosis is……… <ul><li>Patient denies FH x of consanguineity </li></ul><ul><li>Patient denies family history of renal disease </li></ul><ul><li>No apparent symptoms auto immune disease </li></ul><ul><li>No previous drugs </li></ul><ul><li>Nil to suggest obstruction </li></ul><ul><li>Causes of dRTA </li></ul><ul><li>Idiopathic </li></ul><ul><li>Familial (AD, AR) </li></ul><ul><li>Sjogrens, SLE </li></ul><ul><li>Hypercalciuria </li></ul><ul><li>Rheumatoid Arthritis </li></ul><ul><li>Cirrhosis </li></ul><ul><li>Drugs (lithium, ifosfamide, amphoteracin </li></ul><ul><li>Renal transplant </li></ul><ul><li>Obstructive uropathy </li></ul><ul><li>Sickle cell anaemia </li></ul>Distal Renal Tubular acidosis
  15. 15. Mrs LD <ul><li>All autoantibodies negative except gastric parietal </li></ul><ul><li>No rheumatoid factor done!!! </li></ul><ul><li>IgG 29 (6-16) </li></ul><ul><li>IgA 9 (0.8-2.8) </li></ul><ul><li>IgM 1.31 (0.5-1.9) </li></ul><ul><li>Possible bands present </li></ul><ul><li>Sjogrens very rare in Indians, but possible </li></ul><ul><li>No clinical evidence of Rheumatoid </li></ul><ul><li>Due to come back for further treatment </li></ul><ul><li>For referral to rheumatologists ? Sjogrens </li></ul><ul><li>??? Any ideas??? </li></ul>

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