To the Editor: The recent report by Jamal et al.1 should further raise awareness that some women with osteoporosis have chronic kidney disease (CKD). However, their manuscript has misinterpreted the Kidney Diseases Outcome Quality Initiative (K/DOQI) classification. In their paper, they state that “severe” disease is defined as an estimated glomerular filtration rate (eGFR) of <45 ml/min (estimated with a method using bone densitometric measurements of lean body weight, without a reference given about validation of this technique). This could cause misunderstanding in the care of patients with osteoporosis and CKD, because the term was intended for use only in CKD stages 4 and 5. As kidney function and muscle mass decrease with aging, a “normal” serum creatinine frequently is found in elderly patients with stages 3 and 4 CKD [The K/DOQI of the National Kidney Foundation has proposed a classification of CKDs2 that is gaining international acceptance. This important initiative has improved communication about the stages of kidney diseases between physicians, investigators, and patients. The details of the scheme can be found on the Kidney Foundation website (http://www.kidney.org/professionals/KDOQI/guidelines_ckd/toc.htm). The stages are based on the eGFR, derived from the modification of diet in renal disease (MDRD) formula as follows: stage 1 = eGFR > 90 ml/min/1.73 m2 but with other manifestations of kidney disease such as proteinuria; stage 2 = eGFR between 60 and 89 ml/min/1.73 m2; stage 3 = eGFR between 30 and 59 ml/min/1.73 m2; stage 4 = eGFR between 15 and 29 ml/min/1.73 m2; stage 5 = eGFR < 15 ml/min/1.73 m2. The term “severe” can be used for stages 4 and 5.] Thus, many patients with postmenopausal osteoporosis also have early stages of CKD. It is essential that physicians recognize that kidney disease may complicate some of the bone disease in their patients. In the FIT trial, the upper limit of serum creatinine was 144 μM3; about one half of the women had stage 2 CKD, ∼45% had stage 3 CKD, but <20 women had stage 4 CKD. Furthermore, women were excluded from the osteoporosis trial if they had evidence of increased serum PTH levels or alkaline phosphatase activity, which are frequently manifestations of the bone disease seen in stage 4 CKD.4 Therefore, the results of their study do not show that alendronate is safe or effective in “severe” kidney disease. Rather, the study was not able to detect any decrease in effectiveness or safety in women with stage 3 CKD who had an eGFR < 45 ml/min. The effectiveness or safety of chronic bisphosphonate therapy in stages 4 or 5 CKD is currently unknown. Miller et al.5 analyzed the use of risedronate in clinical osteoporosis trials, which included a group of women with eGFR < 30 ml/min, in whom risedronate reduced vertebral fracture rate but did not increase femoral neck BMD. In this group, the median eGFR was 27 ml/min (although the formula for eGFR determination differed from that used in the K/DOQI classification system), and none had elevations of PTH, so the findings may not apply to all patients with stage 4 CKD. A recent abstract presented by Amerling et al.6 found that there was a 100% incidence of low turnover bone disease with absent tetracycline uptake in patients with stages 2–5 CKD who were taking oral alendronate. Lu et al.7 reported increased PTH levels with pamidronate use in dialysis patients. Further research into methods of treating bone disease in patients with CKD stages 4 and 5 is clearly needed.