Which of the following type of Renal tubular acidosis (RTA) is associated with hyperkalemia?
Ans. D. RTA type IV. (Ref H-17th/pg. 283, 1744t, 1805)Type IV Renal tubular acidosis (RTA) is associated with hyperkalemia.H17th/pg... 1805........." In primary distal RTA (dRTA), the kidneys are unable to acidify the urine to pH <5.5 in the presence of systemic metabolic acidosis or after acid loading as a result of impaired hydrogen ion secretion or bicarbonate reabsorption in the distal nephron. Other features are hypokalemia, hypocitraturia, hypercalciuria, nephrocalcinosis, and/ or nephrolithiasis".Disscussion: FindingType 1 RTAType 2 RTAType 4 RTAGI Bicarbonate Loss1Normal anion-gap acidosisYesYesYesYes2Minimum urine pH>5.5<5.5<5.55 to 63% Filtered bicarbonate excreted<10>15<10<104Serum potassiumLowLowHighLow5Fanconi syndromeNoYesNoNo6Stones/ nephrocalcinosisYesNoNoNo7Daily acid excretionLowNormalLowHigh8Urine anion gapPositiveNegativePositiveNegative9Daily bicarbonate replacement needs<4 mmol/kg>4 mmol/kg<4 mmol/kgVariableType 1 (Distal) RTA# In primary distal RTA (dRTA), the kidneys are unable to acidify the urine to pH <5.5 in the presence of systemic metabolic acidosis or after acid loading as a result of impaired hydrogen ion secretion or bicarbonate reabsorption in the distal nephron.# Other features are hypokalemia, hypocitraturia, hypercalciuria, nephrocalcinosis, and/or nephrolithiasis.# Chronic untreated acidosis may cause rickets or osteomalacia.# Inheritance of primary dRTA includes autosomal dominant and autosomal recessive forms with a broad spectrum of clinical expression.# RX: Early initiation of alkali replacement at doses equivalent to 1 - 3 mmol/kg/day of bicarbonate in divided doses will usually correct the acidosis, hypokalemia, and hypocitraturia, maintaining growth and preventing bone disease in early-onset dRTA.Type 2 (Proximal) RTA# Proximal RTA (pRTA) is the result of impaired bicarbonate reabsorption in the proximal tubular where the bulk of filtered bicarbonate is recovered.# It is most often secondary to various autoimmune, drug-induced, infiltrative, or other tubulopathies or a result of tubular injury from inherited diseases like Wilson's disease, cystinosis, tyrosinemia, galactosemia, hereditary fructose intolerance, glycogen storage disease type I, and Lowe's syndrome.# In this situation pRTA is but one of several abnormalities that constitute Fanconi syndrome.# Other features are hyperphosphaturia, hyperuricosuria, hypercalciuria, nonselective amino aciduria and glycosuria.In addition to hyperchloremic acidosis, rickets or osteomalacia are the predominant effects of Fanconi syndrome.# RX:of pRTA requires 5-15 mmol/kg/day of bicarbonate together with supplemental potassium and vit. D.Causes of normal anion-gap acidosisI. GI bicarbonate lossA. DiarrheaB. External pancreatic or small-bowel drainageC. Ureterosigmoidostomy, jejunal loop, ileal loopD. Drugs1. Calcium chloride (acidifying agent)2. Magnesium sulfate (diarrhea)3. Cholestyramine (bile acid diarrhea)II. Renal acidosisA. Hypokalemia21. Proximal RTA (type 2)2. Distal (classic) RTA (type l)2B. Hyperkalemia21. Generalized distal nephron dysfunction (type 4 RTA)2a. Mineralocorticoid deficiencyb. Mineralocorticoid resistance (autosomal dominant PHA I)c. Voltage defect (autosomal dominant PHA I and PHA II)d. Tubulointerstitial diseaseIII. Drug-induced hyperkalemia (with renal insufficiency)A. Potassium-sparing diuretics (amiloride, triamterene, spironolactone)B. TrimethoprimC. PentamidineD. ACE-Is and ARBsE. Nonsteroidal anti-inflammatory drugsF. Cyclosporine and tacrolimusIV. OtherA. Acid loads (ammonium chloride, hyperalimentation)B. Loss of potential bicarbonate: ketosis with ketone excretionC. Expansion acidosis (rapid saline administration)D. HippurateE. Cation exchange resins
RTA type I
RTA type I & II
RTA type II
RTA type IV
Kidney