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2011 | 6 | 6 | 804-806

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Diagnosis, treatment and follow-up in a patient with Nephrocalcinosis due to distal renal tubular acidosis


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Ten years ago, a 73 year-old patient presented at our unit with a right nephritic colic and elevated serum creatinine (2.1 mg/dl). This was the first time that the patient had consulted for a urology workup. An abdominal X-ray was performed in which we observed a severe bilateral nephrocalcinosis with right ureteral lithiasis. One of the causes of nephrocalcinosis is distal renal tubular acidosis (dRTA), in that sense the patient presented metabolic acidosis (pH 7.25) together with normopotassaemia (4.4 meq/L) and normochlorine (105 mEq/L). A 24-hour urine test detected citrate (55 mg/dl), calcium (12 mg/dl) and pH of 6.5. A diuretic renogram showed the right relative renal function as 91.2% and left relative renal function as 8.8%. A test with bicarbonate and acetazolamide was performed, confirming a diagnosis of dRTA because the urinary CO2 pressure was 32 mmHg (normal, greater than 70 mmHg). Treatment with potassium citrate and increased intake of liquids was prescribed. Consequently, the patient’s serum creatinine normalized, her blood pH rose to 7.35 and urinary citrate increased to 154 mg/dl. After 10 years of treatment with potassium citrate the patient remains stable. We believe that in these patients it is crucial to carry out an alkalizing treatment: patients with dRTA cannot acidify the urine because a defect in the permeability of the tubule membrane prevents secretion of H+. It is important to administer potassium citrate continuously to improve blood pH, increase urinary citrate and reduce the risk of calcium phosphate crystallization.










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1 - 12 - 2011
8 - 10 - 2011


  • San Cecilio University Hospital, Granada, Spain
  • San Cecilio University Hospital, Granada, Spain
  • San Cecilio University Hospital, Granada, Spain
  • San Cecilio University Hospital, Granada, Spain


  • [1] Fauci AS, Braunwald E, Kasper DK, Hauser SL, Longo DL, Jameson JL. Ed Harrison: Principios de medicina interna. 17 ed. Madrid: Interamericana; 1994
  • [2] Bouzidi H, Daudon M, Najjar MF. Primary distal renal tubular acidosis. Ann Biol Clin. 2009; 67:135–140 [WoS]
  • [3] Saito T, Hayashi D, Shibata S, Jogamoto M, Kamoda T. Novel compound heterozygotus ATP6V0A4 mutations in an infant with distal renal tubular acidosis. Eur J Pediatr. 2010; 169: 1271–1273 http://dx.doi.org/10.1007/s00431-010-1184-9[WoS]
  • [4] Chemli J, Missaoui N, Selmi H, Miled H, Doggi M, Essoussi AS et al. Complete primary distal renal tubular acidosis in children: 11 cases. TunisMed. 2008; 86: 629–635
  • [5] Sharma AP, Sharma RK, Kapoor R, Kornecki A, Sural S, Filler G. Incomplete distal renal tubular acidosis affects growth in children. Nephrol Dial Transplant. 2007; 22: 2879–2885 http://dx.doi.org/10.1093/ndt/gfm307[Crossref]
  • [6] Merino-Salas S, Arrabal-Polo MA, Arrabal-Martin M, Lopez-Leon V, Lahoz-García C, Miján-Ortiz JL et al. La acidosis tubular renal distal y la litiasis. Nuevo enfoque diagnóstico-terapéutico. Actual Med. 2011; 96: 25–31
  • [7] Sakamoto H, Tomizawa T, Tamura T, Fujita K, Sato K, Tamura J. Bilateral nephrocalcinosis associated with distal renal tubular acidosis. Intern Med. 2005; 44: 81–82 http://dx.doi.org/10.2169/internalmedicine.44.81[Crossref]
  • [8] Arrabal Polo MA, Arrabal Martín M, Jiménez Pacheco A, Zuluaga Gómez A. Nephrocalcinosis in patient with distal tubular renal acidosis: a case report. Med Clin (Barc). 2009; 133: 604–605 http://dx.doi.org/10.1016/j.medcli.2008.10.024[WoS][Crossref]
  • [9] Arrabal-Polo MA, Arrabal-Martin M, Zuluaga-Gomez A. Nephrocalcinosis in a patient with complete distal renal tubular acidosis. Acta Clin Belg. 2010; 65: 281 [WoS]
  • [10] Walsh SB, Shirley DG, Wrong OM, Unwin RJ. Urinary acidification assessed by simultaneous furosemide and fludrocortisone treatment: an alternative to ammonium chloride. Kidney Int. 2007; 71: 1310–1316 http://dx.doi.org/10.1038/sj.ki.5002220[WoS][Crossref]
  • [11] Alvarado LC, Voyer LE, Bortolazzo G, Costa MA. Urinary acidification by furosemide test. Medicina (B Aires). 1991; 51: 338–342
  • [12] Luiten I, Kellertas I, Voyer LE. Evaluation of hydrogen excretion by the distal tubule using the alkaline overload test. Medicina (B Aires). 1979; 39: 639–644
  • [13] Kerbl K; Clayman RV. Endourologic treatment of nephrocalcinosis. Urology. 2000. 26: 508 http://dx.doi.org/10.1016/S0090-4295(00)00675-0[Crossref]

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