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Bone Disease in Medullary Sponge Kidney and Effect of Potassium Citrate Treatment

Antonia Fabris^*, Patrizia Bernich^*, Cataldo Abaterusso^*, Nicola Marchionna^*, Chiara Canciani^*, Antonio Nouvenne, Mauro Zamboni, Antonio Lupo^*, and Giovanni Gambaro

Divisions of ^* Nephrology and Geriatrics, Department of Biomedical and Surgical Sciences, University Hospital of Verona, Verona, Italy; Department of Clinical Sciences, University of Parma, Parma, Italy; and Division of Nephrology and Dialysis, Columbus-Gemelli University Hospital, Catholic University, Rome, Italy

Correspondence: Prof. Giovanni Gambaro,Divisione di Nefrologia e Dialisi, Istituto di Medicina Interna e Geriatria, Università Cattolica del Sacro Cuore, Complesso Integrato Columbus-Policlinico Gemelli, Via Moscati 31-33, 00176 Roma, Italy. Phone: +39-06-3503434; Fax: +39-06-3054641; E-mail: giovanni.gambaro{at}rm.unicatt.it

Background and objectives: In medullary sponge kidney (MSK)—a common malformative renal condition in patients with calcium nephrolithiasis—hypercalciuria, incomplete distal renal tubular acidosis, and hypocitraturia are common. Clinical conditions with concomitant hypercalciuria and/or incomplete distal renal tubular acidosis are almost invariably associated with bone disease, making osteopathy highly likely in MSK, too. Patients with MSK have never been investigated for osteopathy; neither has the potential effect of potassium citrate administration (CA) on their urinary metabolic risk factors and on bone mineralization.

Design, setting, participants, & measurements: These issues were retrospectively analyzed in 75 patients with MSK and primary stone risk factor (PSRF; hypercalciuria, hypocitraturia, hyperuricosuria, and/or hyperoxaluria) on an outpatient basis; 65 received CA (2.9 ± 0.8 g/d), whereas 10 received only general "stone clinic" suggestions. The 24-h urinary excretion of calcium, phosphate, oxalate, uric acid, and citrate; morning urine pH; serum biochemistry; and bone mineral density were investigated at baseline and at the end of follow-up (78 ± 13 and 72 ± 15 mo in groups A and B, respectively).

Results: CA led to a significant rise in urinary pH and citrate and decreased urinary calcium and phosphate (all P < 0.001). Patients with MSK and PSRF had reduced bone density. Bone density improved significantly in the group that was treated with oral CA.

Conclusions: Bone disease is very frequent in patients with MSK and concomitant PSRF. Long-term CA improves bone density. The concurrent effects of treatment on PSRF suggest that the subtle acidosis plays a pivotal role in bone disease and hypercalciuria in patients with MSK.

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