Issue 2

Kidney

Newsletter

Keeping you up to date with the latest exciting advances and discussions in nephrology

Clinical challenges in kidney disease management

The majority of patients with CKD have mineral and bone disorders.1

This presents as abnormalities in the following parameters:2

SHPT is a progressive disease that manifests frequently in patients with stage 3–4 CKD and from as early as stage 2 CKD2,3

The images are not of real patients

~40–55% of stage 3b CKD patients are affected by SHPT4

Rising to ~70–85% in stage 4 CKD4

SHPT and/or high PTH is associated with an increased risk of:

Cardiovascular
events5,6 regardless
of CKD stage7

Fractures5,8

Progression to dialysis5,7

Therapeutic resistance9

Death5,8
You can explore shpt, its treatment challenges, and more here Explore SHPT

Hyperphosphatemia is particularly common in patients on dialysis (affecting ~40% of these patients)4

Uncontrolled serum phosphorus levels
(>5.2 mg/dL)10 are associated with:

Increased all-cause mortality10

Serum phosphorus levels
>6.0 mg/dL11 are associated with:

Increased CV mortality11

What are the barriers to optimizing clinical care across the ckd continuum?

Despite the availability of global and regional guideline recommendations,
there remain a number of challenges for the clinical management of CKD-MBD1

In pre-dialysis patients with SHPT…  

Adherence to CKD-MBD monitoring recommendations is sub-optimal12,13

A growing body of evidence suggests
 that vitamin D levels should be
higher than current guideline targets
in order to effectively control SHPT
in pre-dialysis CKD15,16

Unclear targets for PTH and vitamin D levels14
delay the initiation of effective vitamin D-based treatment

The KDIGO guidelines state that
“In patients with CKD G3a–G5 not on
dialysis, the optimal PTH level is
not known”14

Few therapeutic agents are licensed for use in the pre-dialysis CKD/SHPT setting17

Nutritional vitamin D
  • Increases vitamin D levels to a certain extent, while the potential to reliably reduce PTH levels is limited in pre-dialysis CKD patients with SHPT18
  • KDIGO states that studies with sufficient duration were lacking and thus this therapy remains unproven14
 Active vitamin D/analogs
  • Can effectively suppress PTH levels but are associated with an increased risk of hypercalcemia and hyperphosphatemia in pre-dialysis CKD17,19
  • KDIGO guidelines state calcitriol and active vitamin D analogs should not be routinely used in pre-dialysis CKD patients14
Dietary restriction of phosphate is a recommended management strategy for hyperphosphatemia in CKD stage 3–5D20

Dietary phosphate restriction is associated with severe consequences

  • Hypoalbuminuria and protein-energy wasting are associated with increased mortality, hospitalizations and a reduced quality of life21–25
Prescription of a simplified phosphate binder regimen could improve patient adherence and perhaps improve serum phosphorus and PTH levels26

The use of phosphate binders in patients on dialysis can:26–28

  • Reduce phosphorus levels
  • Allow an increase in protein intake
You can explore shpt, its treatment challenges, and more here Explore SHPT
References and footnotes

FOOTNOTES

Ca, calcium; CKD, chronic kidney disease; CV, cardiovascular; FGF-23, fibroblast growth factor 23; G, grade, KDIGO, Kidney Disease: Improving Global Outcomes; MBD, mineral and bone disorder; P, phosphorus; PTH, parathyroid hormone;
SHPT, secondary hyperparathyroidism.

 

 

REFERENCES

  1. Waziri B, et al. Int J Nephrol Renovasc Dis 2019;12:263–76;
  2. Cunningham J, et al. Clin J Am Soc Nephrol 2011;6:913–21;
  3. Wolf M. J Am Soc Nephrol 2010;21:1427–35;
  4. Levin A, et al. Kidney Int 2007;71:31–8;
  5. Xu Y, et al. Clin Kidney J 2021;sfab006;
  6. Arase H, et al. Circ J 2020;84:1105–11;
  7. Bermudez-Lopez M, et al. ERA-EDTA 2020: Abstract PO878;
  8. Geng S, et al. Osteoporos Int 2019;30:2019–25;
  9. Tabibzadeh N, et al. Nephrol Dial Transplant 2021;36:160–9;
  10. Fernandez-Martin J, et al. Nephrol Dial Transplant 2015;30:1542–51;
  11. Tentori F, et al. Am J Kidney Dis 2008;52:519–30;
  12. Roetker N, et al. Am J Nephrol 2019;49:225–32;
  13. Wetmore J, et al. Kidney Rep 2021;6:1141–50;
  14. KDIGO. Kidney Int Suppl 2017;7:1–59;
  15. Strugnell SA, et al. Am J Nephrol 2019;49:284–93;
  16. Ennis JL, et al. J Nephrol 2016;29:63–70;
  17. Cozzolino M, Ketteler M. Expert Opin Pharmacother 2019;20:2081–93;
  18. Bover J, et al. Clin Kidney J 2021;sfab035;
  19. Cozzolino M, et al. Clin Kidney J 2021. doi.org/10.1093/ckj/sfab091;
  20. KDIGO. Kidney Int Suppl 2009:S1–130;
  21. Eriguchi R, et al. Clin J Am Soc Nephrol 2017;12:1109–17;
  22. Kalantar-Zadeh K, et al. Clin J Am Soc Nephrol 2010;5:519–30;
  23. Shinaberger C, et al. Am J Clin Nutr 2008;88:1511–8;
  24. Sarav M, Kovesdy C. Clin J Am Soc Nephrol 2018;13:1558–60;
  25. Jadeja Y, Kher V. Indian J Endocrinol Metab 2012;16:246–51;
  26. Fissel R, et al. Hemodial Int 2016;20:38–49;
  27. Gutekunst L. J Ren Nutr 2016;26:209–18;
  28. Coyne D, et al. Clin Nephrol 2017;88:59–67.

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