AB0808 Incomplete Distal Renal Tubular Acidosis in Patients with Osteo-Porosis/Osteopenia – Prevalence and Treatment
Authors: J.J. Sromicki, S. Matter, K. Sitzmann, B. Hess
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Impaired renal H<sup>+</sup> ion secretion causes acid retention which is known to promote bone dissolution <h3>Objectives</h3> To prospectively assess the prevalence of distal renal tubular acidosis (dRTA) in low bone mass patients (LBM) and the effects of alkali treatment. <h3>Methods</h3> Between January 1, 2006, and December 31, 2010, we screened all LBM referred for metabolic evaluation of T-Scores ≤ -1.0 at lumbar spine and/or hip (measured by Hologic or Lunar) for dRTA. Calcium intake (mineral waters and dairy products) was assessed by food content tables. In fasting venous blood, Ca<sup>++</sup>, venous bicarbonate (VenBic) and creatinine (Crea) were measured by blood gas analyzer, 25-OH-vitamin D (25-OH-D) by immunoassay. LBM with hypercalcemic disorders were excluded. In fasting urines, calcium (Ca), citrate (Cit) and Crea were measured, and renal calcium reabsorption (CaR) was calculated as filtered calcium (Ca<sup>++</sup>) - excreted calcium (CaE). In all 182 LBM (156 F, 26 M, age 17-86 ys.), pH was measured (Metrohm pH-meter) in 2nd morning urines (U-pH) after 12 hrs. of fasting. If U-pH remained &gt;5.80, LBM underwent 1-day acid loading by ammonium chloride (NH<sub>4</sub>Cl, 50 mg/kg BW in 3 oral doses), and U-pH and venous blood were remeasured the next morning. Normal values for acid loading were obtained from 21 healthy controls (C, 11 F, 10 M, age 25-80 yrs.). The acidifying effect of NH<sub>4</sub>Cl was assessed by measuring urine Ca, Cit and Crea in 17 C and 35 LBM. All LBM with dRTA were recommended alkali citrate (K-Cit), and follow-up DXAs were obtained until 1/2014. Paired and unpaired t-tests were used for statistics, values are mean±SD. <h3>Results</h3> 84 LBM with U-pH &gt;5.80 underwent NH<sub>4</sub>Cl loading; this caused U-pH to drop from 6.64±0.54 to 5.62±0.69 (p&lt;0.0001) vs. from 5.71±0.55 to 5.09±0.17 in C (p&lt;0.001). The fall in U-Cit/Crea (p&lt;0.0001 in all subjects) proved the systemic effects of NH<sub>4</sub>Cl. If U-pH remained &gt;5.44 (mean + 2 SDs of C) after NH<sub>4</sub>Cl, dRTA was diagnosed; this was found in 42 LBM (39 F, 3 M), i.e. 23.1%. Since VenBic was normal, all cases had <i>incomplete</i> dRTA (idRTA) by definition. Daily calcium intake and 25-OH-D were not different between subgroups. At baseline, CaR (mmol/l) was reduced in idRTA (1.17±0.04 vs. 1.22 + 0.03 in C, p=0.005). NH<sub>4</sub>Cl lowered VenBic (mEq/l) by 1.35±1.75 in C (p&lt;0.005) and 1.44±2.60 in Non-RTA (p&lt;0.05), but only by 0.71±2.59 in idRTA (NS). After NH<sub>4</sub>Cl, urine CaE rose insignificantly and equally in all subgroups, whereas blood Ca<sup>++</sup> (mmol/l) increased only in idRTA (0.023±0.057, p=0.042), suggesting enhanced Ca release from bone. Baseline bone mineral densities were equal in Non-RTA and idRTA. Among idRTA, 15 were lost for follow-up. In idRTA adherent to K-Cit for 1.6-7 years (n=19), T-scores rose from -2.14±0.81 to -1.72±0.88 (p&lt;0.001) at lumbar spine, but did not change at total hip and femoral neck. In idRTA not taking K-Cit (n=7), T-scores at all sites were unchanged. <h3>Conclusions</h3> 1) The prevalence of idRTA in LBM is surprisingly high, i.e. 23%; 2) Upon acid loading, idRTA do not lower VenBic and U-pH normally, but rise blood Ca<sup>++</sup>, suggesting reduced extra-, but increased <i>intra</i>cellular acid buffering by bone tissue. 3) Additional K-Cit treatment helps to further improve bone mass at lumbar spine in idRTA. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3481