Marc E. De Broe

Calcium Balance in Renal Failure Patients with CKD 3 ~ 5 and in Dialysis Patients

The external calcium balance between gastrointestinal uptake and urinary excretion, as well as the internal balance between the extracellular fluid, the rapid exchangeable pool and the bone calcium are all maintained by the actions of the various calciotropic hormones (PTH, vitamin D3 and calcitonin). Patients with CKD 3 ~ 5 not in dialysis have a tendency to develop a negative calcium balance, (vitamin D deficiency) certainly when on a normal to low calcium diet (500 mg/day) and they all have secondary hyperparathyroidism if not treated with vitamin D and or calcium-containing phosphate binders. There are several reasons why patients in dialysis develop in contrast to patients with CKD 3 ~ 5, not in dialysis, a positive calcium balance: • No renal function, black box, deposition in bone and vessels, soft tissues. • Administration of vitamin D, increasing calcium absorption. • Use of calcium containing-phosphate binders (1,000 ~ 2,500 mg/day). • Use of non-calcium containing phosphate binders. • Calcium load through dialysate (if ＞ 1.50 mmol/L of calcium). • Peritoneal dialysis (calcium: 2.5 ~ 3.0 mEq/L; serum iCa: 1.8 ~ 2.5 mEq/L = + balance). • Diet. This positive calcium balance may explain to a certain extend the high incidence of vascular calcifications in dialysis patients compared to patients with severe renal failure not yet in dialysis.

Aluminium Iron: Implications for Alzheimer’s Disease

Summary There is no doubt that aluminium may cause neurotoxic effects. In dialysis patients the elements role in the development of the so-called aluminium-related dialysis dementia is now well recognized. The role of the element in the aetiopathogenesis of Alzheimers disease however, remains controversial. In contrast to aluminium, iron is essential for neurological function because of its role in oxidative metabolism and because it is a co-factor in the synthesis of neurotransmitters and myelin. Nevertheless, abnormal iron accumulation in diseased brain areas, including Alzheimers disease, has been reported. There is strong evidence for iron-mediated oxidative damage as a primary contributor to cell death in these disorders. Since aluminium and iron display a number of similar physicochemical characteristics, interactions between both elements in the development of neurotoxic effects may reasonably be suggested.

5-Aminosalicylic acid and chronic interstitial nephritis

For decades, sulphasalazine, an azo-compound derived from sulphapyridine and 5-aminosalicylic acid (5-ASA) (Fig. 1), has been the only valuable non-cortico-steroid drug in the treatment of inflammatory bowel disease. Azad Kahn et al. [1] showed that the pharmacologically active moiety in sulphasalazine for the treatment of these diseases was 5-ASA. Moreover, it has been shown that the metabolite sulphapyridine was largely responsible for the side-effects of sulphasalazine. Consequently, this resulted in a number of new 5-ASA formulations (mesalazine, olsalazine, balsalazine) for topical and oral use. 5-ASA is partially resorbed, particularly in the acetylated form and eliminated as such in the urine. The colon is the predilected place for this acetylation since in the small bowel there is a lack of the responsible bacterial flora. Hence, 5-ASA is readily absorbed as such in the small bowel. How far this may form a rationale for a possible difference in nephrotoxicity for the different preparations reamins to be determined.