Foreword

In this edition of Nephrology, the revised CARI (Caring for Australasians with Renal Impairment) guidelines, for a range of important biochemical targets are published. All of these targets take on great significance in the day-to-day care of the chronic kidney disease (CKD) patient but as the underlying evidence summaries indicate, there is still considerable controversy as to how to achieve those targets. A particular area of that controversy surrounds bone and mineral metabolism, where in the past decade there has been a substantial paradigm shift in both the understanding of bone and mineral metabolism in patients with CKD and also in the recognition of the critical relationship between mineral metabolism and vascular calcification. In the same period, a range of new therapeutic options have also been developed including new phosphate binders such as lanthanum and sevelamer, new Vitamin D analogues and more recently, calcimimetics such as Sensipar®. Concurrently, the advancement of imaging techniques, parathyroid hormone (PTH) assays and other techniques to examine vascular health such as Pulse Wave Velocity have helped to identify those CKD patients at increased risk of cardiovascular disease (CVD) events. This is clearly critical if we are to improve patient outcomes, as CVD events remain the major cause of premature death and morbidity in all stages of CKD. In 2003, the US National Kidney Foundation organised a consensus conference called Controversies in Mineral Metabolism and Bone Disease. The participating experts developed a series of suggested education initiatives aimed at the wider dissemination and reinforcement of guideline initiatives to control biochemical parameters of bone and mineral metabolism and to heighten awareness of the importance of medial and intimal vascular calcification. A further Controversies Conference called: Definition, Evaluation, and Classification of Renal Osteodystrophy, organised by the KD: IGO (Kidney Disease: Improving Global Outcomes) group was recently held in Madrid. The deliberations of this meeting are to be published soon but importantly, in reaching consensus on the Definition, Evaluation, and Classification of Osteodystrophy, a relationship between the bone histology, imaging techniques and serum biomarkers, and calcific vascular disease was seen to be pivotal. The clinician may need to remember that Clinical Practice Guidelines are essentially tools to critically review the summary of the evidence base that underpins the range of therapeutic options offered to patients. In the case of bone and mineral metabolism and associated vascular disease, the implementation of current target guidelines is problematical. The range of therapies is potentially wide but in Australia and New Zealand not all agents are readily available. In addition, finding the right prioritisation of the targets (e.g. phosphorous versus calcium × phosphorus product versus PTH) is not easy to achieve in practice. It is hoped that this current set of revised CARI Guidelines, which have been designed primarily for Australians and New Zealanders, will help a little in that therapeutic decisionmaking process. All of us involved in the CARI process remain indebted to the two CARI sponsors, Amgen and Janssen-Cilag, without whose generous support these CARI Guidelines would not exist. The Working Party Convenors and Members involved in the current publication should be congratulated for their effort in producing these excellent guidelines and to all the Working Groups for their continuing support of CARI. Those in the CARI Office, under the leadership of Denise Campbell, deserve special praise as well for their tirelessness and professionalism.