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Renal Tubular Acidosis 8/12/10 PY Mindmaps - metabolic acidosis occurs in both chronic and acute renal failure - the anion gap may be elevated or normal - damage to glomeruli and tubules: high anion gap c/o failure of excretion of acid anions - damage to the tubules only: normal anion gap (RTA or hyperchloraemic type), GFR may be normal or only minimally affected. - causes are numerous - primary problem = inability to acidify the urine and excrete acid - may be incomplete and only develop in the presence of an acid load TYPE 1 RTA (distal) - ‘classic’ RTA - reduced secretion of H+ in distal tubule -> inability to maximally acidify the urine Causes (1) (2) (3) (4) (5) genetic autoimmune (Sjogrens, SLE, thyroiditis) disorders causing nephocalcinosis (primary hyperparathyroidism, vitamin D intoxification) drugs/toxins (amphotericin B, toluene inhalation) obstructive nephropathy Investigation - urine pH remains >5.5 despite severe acidaemia (HCO3 < 15mmol/L) may require an acid load test to see whether urinary pH remans > 5.5 hyperchloraemic acidosis + alkaline urine + renal stone formation secondary hyperaldosteronism -> increased K+ loss in urine Jeremy Fernando (2010) Treatment - NaHCO3 (corrects Na+ deficit, ECF volume and corrects hypokalaemia) - sodium and potassium citrate solutions can be useful if hypokalaemia persistent - citrate also binds Ca2+ in the urine and can help to prevent renal stones TYPE II RTA (proximal) - proximal because the main problem is impaired reabsorption of bicarbonate in the proximal tubule. - at normal plasma HCO3, 15% of filtered HCO3 is excreted in the urine -> in acidosis when HCO3 levels are low the urine can become HCO3 free. - symptoms take place when there is an increase in plasma HCO3 -> proximal tubule cannot reabsorb the increased filtered load -> delivered to distal tubule and is unable to be reabsorbed -> urinary loss of HCO3 - results = metabolic acidosis with an inappropriately high urinary pH + hyperchloraemia (Clreplaces HCO3 in circulation) - with increased distal tubular Na+ delivery -> hyperaldosteronism -> K+ wasting Causes - proximal tubular defects: affects reabsorption of glucose, phosphate and amino acids hereditary vitamin D deficiency cystinosis lead nephropathy amyloidosis medullary cystic disease Investigations - metabolic acidosis (usually not as severe as distal RTA) plasma HCO3 usually > 15mmol/L high urinary HCO3 (inappropriate) hypokalaemia during the NH4Cl loading test urinary pH drops < 5.5 Treatment - treat underlying disorder - NaHCO3 and K+ supplementation not always necessary (if required will require large doses) - thiazide diuretics (some patients respond to this which results in increased proximal HCO3 reabsorption) TYPE IV RTA - associated with renal failure caused by disorders affecting the renal interstitium and tubules. - GFR >20mL/min (unlike uraemic acidosis) - always associated with hyperkalaemia (unlike others) - defect in cation-exchange in the distal tubule with reduced secretion of both H+ and K+ - associated with: Addison’s disease or post bilateral adrenalectomy - acidosis not common unless there is associated renal damage affect the distal tubule. - the H+ pump in the tubule is not abnormal so that patients with this disorder are able to decrease their urinary pH to < 5.5 in response to the acidosis Jeremy Fernando (2010) URAEMIC ACIDOSIS - caused by failure to excrete acid anions (phosphate and sulphate) -> because of a decreased number of nephrons. - GRF < 20ml/min - low plasma HCO3 - patients often survive a long time and get chronic complications such as bone demineralisation. Jeremy Fernando (2010)