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

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Arrabal-Polo M., Arrabal-Martin M., Jiménez-Pacheco A., Merino-Salas S.
Open Medicine
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2011
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vol. 6
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issue 6
804-806
EN
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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Alendronate in patients with calcium nephrolithiasis and loss of bone mass

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Arrabal-Polo M., Arrabal-Martin M., Arias-Santiago S., Zuluaga-Gomez A.
Open Medicine
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2012
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vol. 7
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issue 4
429-434
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