In the present study, risk factors for PTX were female gender, age 40–55 years, and non-diabetic cause of renal disease. In the adjusted model, having had a functioning renal graft for less than one year was also associated with increased risk of PTX, whereas having had a functioning renal graft for more than one year was associated with decreased risk, compared with zero time with functioning graft.
The increased risk of PTX in women, patients in younger middle age and non-diabetics is congruent with results from previous studies [1–4]. The regional distribution of PTX was heterogeneous with the lowest rate in the Northern region. We believe, as was also suggested by previous authors, that lower access to specialist nephrology might account for these regional differences . Having had a functioning renal transplant for more than a year was associated with a decreased risk of PTX in the adjusted analysis. This is to be expected, given that renal transplantation usually ameliorates sHPT .
In the present study the overall unadjusted PTX rate was 8.8 (95% CI, 8.1-9.4) per 1000 person-years, which is in line with previous investigations, reporting an incidence between 4.3 and 15.2/1000 person-years [1–5, 12].
We found no significant differences in the PTX incidence during the period 1993 to 2000 in comparison with the reference year 2000. However, from 2001 to 2004 the rate increased significantly, even after adjusting for patient characteristics, and showed a tendency to decrease from 2005 onwards. Our results are similar to the most recent study reporting change over time of PTX in sHPT by Li et. al. They found that the adjusted PTX rate increased in 1998, peaked in 2002 and decreased through 2005 with a new increase in 2006 and 2007 . Malberti et. al showed a relatively constant PTX rate throughout the study period of 1983 and 1996 . Kestenbaum et. al reported a slight rise in adjusted PTX rates between 1990 and 1995 with a subsequent decline of 30% in 1999 . Foley et. al reported a progressive decline from 1992 to 1998 with an increase in 2002 .
There are several possible explanations for this reported diversity in PTX rates. Firstly, the studies cover a large span of time from 1971 to 2007 with different observational and comparison periods. Secondly, the patient cohorts studied are heterogenous, often comprising subgroups of RRT patients [1–4].
Our study comprises all RRT patients in Sweden and covers the period before and after key publications on the consequences of sHPT on mortality and cardiovascular risk [13–16] and after the publication of the KDOQI guidelines for PTX . The increase in PTX rates after 2000 might be a consequence of these reports. After 2005 the PTX rate fell and remained lower throughout the study period. This decrease was associated in time with the introduction of paracalcitol in December 2004 and calcimimetics in 2005 in Sweden. Changes in PTX rates coincided with changes in the aggregate sale of cinacalcet during this period (Figure 2).
A limitation of the present study is the lack of biochemical data, such as levels of parathyroid hormone, and of information on medical treatment. Strengths include the high quality of the Swedish Renal Registry, with an almost 100% nation wide coverage and a data reporting incidence of 95% . In addition, our follow-up period comprises different eras of treatment availability and modality. The fact that this study is based on an entire population with a wide geographical distribution within the country is to our knowledge a unique situation. We also believe that external validity was increased by including all patients on RRT, irrespective of treatment modality. The linkage of three nation-wide registries with broad and accurate coverage further adds to the validity of the present results.