<prompt> Which of the following type of Renal tubular acidosis RTA is associated with hyperkalemia?RTA type IRTA type I IIRTA type IIRTA type IV  <response>: Ans. D. RTA type IV. Ref H-17thpg. 283, 1744t, 1805Type IV Renal tubular acidosis RTA is associated with hyperkalemia.H17thpg... 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 pH5.55.55.55 to 63 Filtered bicarbonate excreted101510104Serum potassiumLowLowHighLow5Fanconi syndromeNoYesNoNo6Stones nephrocalcinosisYesNoNoNo7Daily acid excretionLowNormalLowHigh8Urine anion gapPositiveNegativePositiveNegative9Daily bicarbonate replacement needs4 mmolkg4 mmolkg4 mmolkgVariableType 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, andor 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 mmolkgday 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 Wilsons disease, cystinosis, tyrosinemia, galactosemia, hereditary fructose intolerance, glycogen storage disease type I, and Lowes 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 mmolkgday 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 agent2. Magnesium sulfate diarrhea3. Cholestyramine bile acid diarrheaII. Renal acidosisA. Hypokalemia21. Proximal RTA type 22. Distal classic RTA type l2B. Hyperkalemia21. Generalized distal nephron dysfunction type 4 RTA2a. Mineralocorticoid deficiencyb. Mineralocorticoid resistance autosomal dominant PHA Ic. Voltage defect autosomal dominant PHA I and PHA IId. Tubulointerstitial diseaseIII. Drug-induced hyperkalemia with renal insufficiencyA. Potassium-sparing diuretics amiloride, triamterene, spironolactoneB. TrimethoprimC. PentamidineD. ACE-Is and ARBsE. Nonsteroidal anti-inflammatory drugsF. Cyclosporine and tacrolimusIV. OtherA. Acid loads ammonium chloride, hyperalimentationB. Loss of potential bicarbonate: ketosis with ketone excretionC. Expansion acidosis rapid saline administrationD. HippurateE. Cation exchange resins 