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Watch Prof. Goldsmith's NUE 2019 talk: current concepts in treating SHPT

19 August 2020

What do we know about the optimal management of SHPT in ND-CKD patients?

Professor David Goldsmith* explores this question in a presentation given at Nephro Update Europe (NUE) 2019. A link to the full presentation is provided at the end of this article.

CKD–MBD is a complicated syndrome1

There are many questions concerning the optimal management of secondary hyperparathyroidism (SHPT) in non-dialysis chronic kidney disease (ND-CKD) patients. In this 25-minute presentation, entitled ‘Current concepts in the management of SHPT in ND-CKD patients’, Professor Goldsmith summarises the latest developments and highlights the questions for which we still don’t have answers.

Professor Goldsmith begins his presentation by exploring the complexities of chronic kidney disease–mineral and bone disorder (CKD–MBD), the syndrome that encompasses SHPT.1 He explains that, as kidney function declines, several blood parameters lose homeostasis,1,2 and no one knows exactly how they affect each other.

The “four brightly burning questions” regarding SHPT management

After exploring the association between SHPT, cardiovascular disease, bone disease and mortality,3 Professor Goldsmith lists four questions regarding the management of SHPT that he thinks haven’t been fully answered despite being out in the open since the late 1980s. The questions are:

  1. In CKD, what concentration of serum 25-hydroxyvitamin D (25D) is needed to maintain adequate levels of serum 1,25-dihydroxyvitamin D (1,25D)?
  2. What concentration of serum 25D is needed to prevent SHPT in stages 3 and 4 CKD?
  3. When treating SHPT with vitamin D formulations, what is the optimal PTH concentration to target?
  4. In CKD, is SHPT always maladaptive or is it an appropriate physiological response that is necessary to prevent adynamic bone disease?

While discussing these questions, Professor Goldsmith provides his reasoning as to why normalising PTH is rarely a good idea and why relatively high levels of 25D may be needed to control PTH in ND-CKD patients.4

“To D or not to D, that is the question”

“Should we D or should we not D?” – that is, should vitamin D formulations be used to control PTH levels in CKD patients?

After going over the complexities of vitamin D metabolism and the prevalence of vitamin D deficiency in different populations, Professor Goldsmith looks at the guidelines on the treatment of SHPT in both dialysis and non-dialysis patients as provided by Kidney Disease: Improving Global Outcomes (KDIGO). He explains why he agrees with KDIGO that active vitamin D (AVD) and AVD analogues should not be routinely used in patients with stage 3 or 4 CKD, the reason being that they significantly increase the risk of hypercalcaemia.5 He then highlights the limitations of nutritional vitamin D in the treatment of SHPT in the same patient population, pointing out that, although NVD can increase 25D, it fails to consistently and reliably reduce PTH.6 

Thus, targeting SHPT early is challenging for two reasons:

  1. The optimal PTH level is unknown5
  2. No treatment is currently available in Europe that can reliably reduce PTH to the required level without negatively impacting
    other key CKD–MBD parameters6,7

Professor Goldsmith concludes with a look at the pros and cons of using different formulations of 25D, with emphasis on promising
results yielded by a new formulation.8

You can watch the full presentation by Professor Goldsmith on the Streamed-up website.

 

Footnotes and references

*Emeritus consultant nephrologist at Guy’s and St Thomas’ NHS Foundation Trust; London, UK.

 

1. Moe S et al. Kidney Int. 2006;69:1945–53.

2. Kuro-o M et al. Bone. 2017;100:4–18.

3. Geng G et al. Osteoporos Int. 2019;30:2019–25.

4. Ennis JL et al. J Nephrol. 2016;29:63–70.

5. Kidney Disease: Improving Global Outcomes (KDIGO) Work Group. Kidney Int Suppl. 2017;7:1⁠–⁠59.

6. Gunnarsson J et al. Poster presented at: 57th ERA–EDTA Congress; 2020 June 6–9; virtual.

7. Cunningham J et al. Clin J Am Soc Nephrol. 2011;6:913–21.

8. Sprague SM et al. Am J Nephrol. 2016;44:316–25.