Eight patients (6 women and 2 men) with
osteoporosis caused or aggravated by renal acidification defects are presented. Three of the female patients were premenopausal; the others were 9, 20 and 22 years postmenopausal, and two of them were on hormonal replacement
therapy. Two patients had
nephrolithiasis: one male with recurrent
calcium phosphate stones and a left sided
staghorn calculus, and one female with
nephrocalcinosis due to
medullary sponge kidney and
hypercalciuria (patients No. 1 and 2, respectively, Table 1). In the remaining subjects, clinical suspicion was based on: a) Hip fracture in a 44-yr-old premenopausal female without any risk factor (No. 3, Table 2). b) Several vertebral
compression fractures in a 45-yr-old male without
hypogonadism or other predisposing factors (No. 7, Table 2). c) Lack of response to antiosteoporotic
therapy in 3 women (patients No. 4, 6 and 8, Table 2). Serum
bicarbonate levels and urine acidification capacity were studied in all patients. Three had low serum
bicarbonate (two of whom showed high fractional excretion of
bicarbonate), four had a distal defect, and one had a mixed form. Serum
creatinine and
potassium, and venous blood pH were normal in all cases, suggesting incomplete
renal tubular acidosis. Bone mineral density in Z-score (means +/- s.e.m.) was - 1.75 +/- 0.08 in the lumbar spine (n = 8), and - 1.57 +/- 0.09 in the femoral neck (n = 4) [Tables 1 and 2; Figs 1 and 2]. Following one year treatment with oral
sodium bicarbonate and
potassium citrate, total skeletal
calcium increased by 3-10% in five of the patients. Whereas the high prevalence of renal acidification defects among renal stone formers with or without
hypercalciuria is well acknowledged,
renal tubular acidosis is not included in the list of entities causing secondary
osteoporosis. As shown in 6 patients of this series, incomplete RTA should be considered as another disease capable of causing
osteoporosis or worsening involutional bone loss.