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Chronic kidney disease.

In the USA, the proportion of the population with chronic kidney disease (CKD) reached 15% by 2017. [1] In South Africa (SA), this figure may well be higher. CKD management in the developed world aims at the apex of the triangle, e.g. improvements in dialysis and transplantation, as well as the mid-triangle area, i.e. strategies in slowing the progression to end-stage renal disease. In SA, however, the huge costs of dialysis and transplantation dictate that our CKD management should first and foremost be aimed at prevention and, secondly, at renoprotection. The review presented in the CME section of SAMJ [2] highlights recent information relating to the use of metformin in the management of diabetes in patients with CKD, the essential and early treatment of CKD acidosis (i.e. estimated glomerular filtration rate (eGFR) [less than or equal to] 59 mL/min), early dietary therapy, early lowering of serum uric acid and the introduction of adequate and ongoing exercise--all aimed at slowing the progression of CKD. Furthermore, the use of high-dose statins in preventing cyst growth and eventual renal failure in patients with autosomal-dominant polycystic disease is explained.

One development not mentioned in the review, is the pivotal importance of vitamin D metabolism and secondary hyperparathyroidism (sHPT) in renoprotection. Effective treatment of sHPT significantly reduces the risk of myocardial infarction, stroke and heart failure; therefore, correct management is essential. This is discussed in an article by Friedl and Zitt [3] on vitamin D pro-hormone in the treatment of sHPT in patients with CKD. Early in CKD (stage 2), the osteocyte begins to produce increased levels of fibroblast growth factor 23 (FGF23), and by CKD stages 3a and 3b the levels are >1 000 times increased. With every decrement of the GFR, phosphate retention would tend to occur, but is offset by an even higher secretion of FGF23. Given the inexorable fall in GFR, sooner or later the serum phosphate will be permanently increased. A reduction in dietary phosphate ingestion is mandatory for all patients with CKD stage 3 and onwards.

Sunlight converts epidermal vitamin [D.sub.2] into inactive vitamin D3 (calciferol), which is stored in the liver. However, large quantities are also stored in adipose tissue of obese persons. Low levels of circulating vitamin D3 are commonly found in CKD stage 3a onwards, especially in overweight patients. FGF23 inhibition of the reabsorption of tubular phosphate results in intermittent hypophosphataemia, which occurs early on in CKD. Moreover, the increased FGF23 markedly inhibits the action of the proximal tubular 1a-hydroxylase enzyme responsible for the conversion of calciferol to calcitriol (1,25[(OH).sub.2][D.sub.3]). Low levels of active vitamin D3 result in a marked decrease in the absorption of dietary calcium, resulting in intermittent hypocalcaemia and sHPT. Prevention of sHPT should start early, when the eGFR is [less than or equal to] 60 mL/min. Early administration of calcitriol has resulted in accelerated coronary and carotid artery calcification. However, the administration of relatively large doses of calciferol (20 000-30 000 IU weekly) on a permanent basis is safe, and will not lead to hypercalcaemia or metastatic vascular calcification. The extent to which this strategy is effective in preventing sHPT is still a matter of debate, but does form part of the most recent recommendations. [4] Calcitriol in a dose of 0.25 [micro]g/day should be introduced only when the eGFR has decreased to <20 mL/min.

Finally, it is in the hands of our general practitioners and primary healthcare workers to diagnose CKD early and to either introduce adequate therapy or to refer early. Future government support for a prevention programme is also absolutely essential, but is currently not provided for.

A M Meyers

National Kidney Foundation of South Africa, Johannesburg; School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg; Faculty Practice Centre, Donald Gordon Medical Centre, Johannesburg; and Renal Dialysis Unit, Klerksdorp Hospital, South Africa nkfsa@mweb.co.za

DOI:10.7196/SAMJ.2017.v107i9.12785

[1.] Henriques C. New CDC infographic shows 1 in 7 Americans now have chronic kidney disease. https://ckdnews/2017/06/07/chronic-kidney-diseases-now-affects-1in-7-us-adults-according-to-cdcinfopraphic/ (accessed 8 August 2017).

[2.] Meyers AM, Davies M. Recent important strategies in the management of chronic kidney diseases. S Afr Med J 2017;107(9):730-733. https://doi.org/10.7196/SAMJ.2017.v107i9.12366

[3.] Friedl C, Zitt E. Vitamin D prohormone in the treatment of secondary hyperparathyroidism in patients with chronic kidney disease. Int J Nephrol Renovasc Dis 2017;10:109-122. https://doi.org/10.2147/IJNRD. S97637

[4.] Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int 2013;(Suppl 3):1-150. https://doi.org/10.1038/kisup.2012.76
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Title Annotation:GUEST EDITORIAL
Author:Meyers, A.M.
Publication:South African Medical Journal
Article Type:Editorial
Geographic Code:6SOUT
Date:Sep 1, 2017
Words:797
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