Download Renal Tubular Acidosis

Renal Tubular Acidosis
8/12/10
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- 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)