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A Case Of Severe Hypokalaemia
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A Case Of Severe Hypokalaemia

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