Renal Tubular Acidosis (RTA)
                        ============================
þ RTA as dyspnea
 - [Bomann JS, Peckler BF. Type IV renal tubular acidosis presenting as dyspne
   in two older patients taking angiontensin-converting enzyme inhibitors. Ann
   Emerg Med 2002;39(1): 73-6.]
 - IF: hyperchloremic (non-anion-gap) acidosis without diarrhea:
  + if hyperkalemia: Type IV RTA
  + if hypokalemia: check urine pH.
   - Urine pH less than 5.5, volume contraction, no renal calculi: Type II RTA
   - Urine pH more than 5.5, renal calculi: Type I RTA

5. Renal Tubular Acidosis.
   i. Comparison Table
                        Proximal  (II)       Distal (I)         CRF
      ===============================================================
      Tubular defects   + (Fanconi synd.)    rare               rare
      Stone Formation   rare                 common (Ca++)      rare
      Bicarb and pH     low                  low                low
      Anion Gap         -                    -                  +
      Chloride          up                   up                 low
      K+                low                  low                high
      BUN               normal               normal             high
      Urine pH          usually < 6          never < 5.5        <=6.0
   ii. Type II (proximal)
      a. Normal tubular functions:
         1. H+ excretion -> HCO3- reabsorbtion
         2. NH3 excretion to accept H+ and turn to NH4+
         3. H+ excretion -> PO4--  ("titratable acid")
         4. Carbonic anhydrase to facilitate HCO3-- reabsorbtion
      b. Normally, 80% of HCO3- is reabsorbed in proximal tubule;
         failure of this mechanism leads to Proximal (Type II) RTA (e.g.
         Wilson's disease, lupus kidney)
      c. Fanconi Syndrome is Proximal RTA (failure of HCO3-
         reabsorption proximally) with failure to reabsorb other ions
         as well (e.g. outdated TCN pills, congenital, myeloma) proximal
         defects: protein, glucose, amino acids, urate, phosphate.
      d. Results of RTA:  volume depletion ->  renin ->  aldo ->  K+
         & Cl- & nl. ion gap acidosis BUT urine still acidic (because
         can still secrete H+ distally).
      e. Diagnosis:  check fractional excretion of HCO3- (give HCO3- to
         serum level of 23 prior to checking) or check total urine HCO3-
      f. Treatment:  bicarb & KCl & HCTZ.
      g. Patients have  Ca citrate reabsorbtion from bone but have no
         Ca++ stones because of increased citrate loss in urine.
   iii. Type I (distal) (most common)
      a. Mechanism:  deficiency of carbonic anhyudrase in distal
         tubule, although H+ can still be secreted.
      b. Causes:  sickle cell disease or trait, obstructive uropathy,
         interstitial disease.
      c. Mechanisms
         1.  H+ pump:  (caused by local tubule damage and/or  aldo
            effect [via an aldo effect NOT blocked by aldactone]).
         2. electric:  Cl- leak and  Na+ pumping (e.g. from  aldo).
         3. H+ backleak  (e.g. Ampho B toxicity).
         4.  H+ acceptors  (e.g.  NH3 or PO4-- delivery).
      d. Serum bicarb is higher than with proximal RTA (type II), but
         still have hyperchloremic acidosis and urine pH >= 6 (can't
         acidify).
      e. May get Ca++ stones because they do NOT have citrate loss in
         the urine like proximal RTA (type II).
      f. Dx:  give Florinef to make sure the voltage gradient is OK.
         Next day, give Na2SO4 (SO4-- not reabsorbed even by normal
         tubules).  If urine pH still > 5.0 it's Type I RTA.
  iv. Type IV (Type I + Type II/hyporenin-hypoaldo/aldo resistance)
      a. Dx:  once Type I RTA diagnosed, give Lasix and have pt. walk
         for a couple of hours, then check renin and aldo levels to see
         if they are appropriately stimulated.
      b. Rx:  bicarb.
   v. Type III (Type I + Type II) (although some say Type IV includes
      this and no Type III exists)