Chronic Kidney Disease in Children Medication

  • Author: Sanjeev Gulati, MBBS, MD, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada); Chief Editor: Craig B Langman, MD   more...
 
Updated: Apr 23, 2012
 

Medication Summary

Some medications (eg, nonsteroidal anti-inflammatory drugs [NSAIDs]) and radiocontrast agents are contraindicated in children with chronic kidney disease (CKD) because of the risk of deterioration of kidney function. Dose modification is required for a wide variety of drugs belonging to different categories.

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Iron salts

Class Summary

Iron salts are used to replenish iron stores. The body stores iron in compounds called ferritin and hemosiderin for future use in the production of hemoglobin. Iron absorption is a variable of the existing body iron stores, the form and quantity in foods, and the combination of foods in the diet. The ferrous form of inorganic iron is more readily absorbed.

Ferrous sulfate (Feosol, MyKidz Iron, Fer-Iron)

 

Ferrous sulfate is a source of iron for hemoglobin synthesis in the treatment of anemia of chronic renal failure. This agent is used with erythropoietin to prevent iron stores depletion. Oral solutions and chewable tablet formulations of ferrous iron salts are available for use in pediatric populations.

Sodium ferric gluconate complex (Ferrlecit, Nulecit)

 

Sodium ferric gluconate complex is used to treat microcytic hypochromic anemia due to iron deficiency when oral administration is unfeasible or ineffective as well as to replenish iron stores in individuals on erythropoietin therapy who cannot take or tolerate oral iron supplementation.

Iron sucrose (Venofer)

 

Iron sucrose is a polynuclear iron (III) hydroxide in sucrose for intravenous use. This agent contains no preservatives or dextran polysaccharides. Iron sucrose is used to treat microcytic hypochromic anemia due to iron deficiency when oral administration is unfeasible or ineffective as well as to replenish iron stores in individuals on erythropoietin therapy who cannot take or tolerate oral iron supplementation.

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Colony Stimulating Factors

Class Summary

Colony-stimulating factors are used to stimulate blood cell production. Endogenous erythropoietin stimulates red blood cell (RBC) hematopoiesis. Recombinant human erythropoietin (epoetin alfa) and darbepoetin stimulate erythropoiesis in anemic conditions.

Epoetin alfa (Epogen, Procrit)

 

Epoetin alfa stimulates the division and differentiation of committed erythroid progenitor cells and induces the release of reticulocytes from the bone marrow into the blood stream.

Darbepoetin alfa (Aranesp)

 

Darbepoetin alfa stimulates the division and differentiation of committed erythroid progenitor cells and induces the release of reticulocytes from the bone marrow into the blood stream.

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Phosphate binders

Class Summary

Phosphate binding agents are indicated if phosphate elevation is uncontrolled by dietary phosphate restriction. Calcium phosphate binders are typically the initial therapy for hyperphosphatemia. Calcium supplements and calcitriol may also possibly be used for hypocalcemia.

Calcium acetate (Eliphos, PhosLo)

 

Calcium acetate is indicated for the treatment of hyperphosphatemia secondary to chronic renal failure. This agent combines with dietary phosphorus to form insoluble calcium phosphate, which is excreted in feces. One caplet or tablet of calcium acetate 667 mg is equivalent to 169-mg elemental calcium (ie, 1 g calcium acetate equivalent to 250-mg of elemental calcium).

Calcium carbonate (Caltrate, Tums, Alcalak)

 

Calcium carbonate is used to treat hyperphosphatemia in chronic renal failure. This agent combines with dietary phosphorus to form insoluble calcium phosphate, which is excreted in feces. Calcium carbonate is also indicated for hypocalcemia. Calcium carbonate 1 g is equivalent to 400 mg of elemental calcium.

Sevelamer (Renagel, Renvela)

 

Sevelamer is indicated to reduce serum phosphorous in patients with end-stage renal disease (ESRD). This agent binds dietary phosphate in the intestine, thus inhibiting its absorption as well as reduces the incidence of hypercalcemic episodes in patients on hemodialysis compared with patients receiving calcium acetate treatment.

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Vitamin D Analogues

Class Summary

Hyperparathyroidism is treated with calcitriol or other active vitamin D analogues. These drugs may also be used to treat hypocalcemia.

Calcitriol (Rocaltrol, Calcijex, Vectical)

 

Calcitriol is a primary active metabolite of vitamin D-3. This agent increases calcium levels in serum by promoting absorption of calcium in the intestines and retention in the kidneys. Calcitriol decreases excessive serum phosphatase levels and parathyroid levels as well as decreases bone resorption.

Calcitriol should be used in patients with renal failure who are unable to convert the inactive prohormone forms to the active metabolite. This agent is available in oral and parenteral formulations. This active form of vitamin D is used in cases of proximal renal tubular acidosis (pRTA) as multitherapy with large quantities of alkali and potassium supplementation and is also used to suppress parathyroid production and secretion in secondary hyperparathyroidism and for treatment of hypocalcemia in chronic renal failure by increasing intestinal calcium absorption.

Paricalcitol (Zemplar)

 

Paricalcitol, an active form of vitamin D, is formed through the removal of the 19th carbon group and modifications to the side chain of calcitriol, thus reducing the calcemic effect. This agent has been reported to suppress parathyroid hormone (PTH) without significant impact on calcium, phosphorus, or calcium-phosphorus product. Paricalcitol increases calcium levels in serum by promoting absorption of calcium in intestines and retention in kidneys, decreases excessive serum phosphatase levels and PTH levels, and decreases bone resorption.

This agent should be used in patients with renal failure who are unable to convert the inactive prohormone forms to the active metabolite. It is also used to suppress parathyroid production and secretion in secondary hyperparathyroidism and for treatment of hypocalcemia in chronic renal failure by increasing intestinal calcium absorption. Paricalcitol is available in oral and parenteral formulations.

Doxercalciferol (Hectorol)

 

Doxercalciferol is a vitamin D analogue (1-alpha-hydroxyergocalciferol) that does not require activation by the kidneys but does require hydroxylation in the liver to be converted to an active vitamin D metabolite. This agent controls intestinal absorption of dietary calcium, tubular reabsorption of calcium by the kidneys, and in conjunction with parathyroid hormone, the mobilization of calcium from skeleton. Doxercalciferol is indicated for the treatment of secondary hyperparathyroidism in end-stage renal disease (ESRD).

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Growth hormones

Class Summary

These agents are used pharmacologically as a growth-promoting agent to help optimize growth in developing children with chronic kidney disease (CKD).

Growth hormone (Nutropin, Saizen, Genotropin)

 

Growth hormone is a human growth hormone (hGH) produced by recombinant DNA technology and whose use results in stimulation of linear growth. This agent stimulates erythropoietin, which increases red blood cell mass.

Growth hormone is currently widely available in subcutaneous (SC) injection form. Adjust the dose gradually based on clinical and biochemical responses assessed at monthly intervals, including body weight, waist circumference, serum insulinlike growth factor-1 (IGF-1), insulinlike growth factor binding protein-3 (IGFBP-3), serum glucose, lipids, thyroid function, and whole body dual-energy x-ray absorptiometry (DEXA). In children, assess treatment response based on height and growth velocity. Continue treatment until the child's final height or epiphysial closure or both have been recorded.

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Calcimimetic Agent

Class Summary

Calcimimetic agents reduce parathyroid hormone (PTH) levels. A small clinical trial with cinacalcet by Muscheites et al in children with secondary hyperparathyroidism showed an 80% decrease in serum PTH levels.[21]

Cinacalcet (Sensipar)

 

Cinacalcet directly lowers intact parathyroid hormone (iPTH) levels by increasing the sensitivity of the calcium-sensing receptor on chief cell of the parathyroid gland to extracellular calcium. This process also results in concomitant serum calcium decrease. Cinacalcet is indicated for secondary hyperparathyroidism in patients with chronic kidney disease on dialysis.

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Contributor Information and Disclosures
Author

Sanjeev Gulati, MBBS, MD, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada)  Additional Professor, Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences; Senior Consultant in Pediatric Nephrology and Additional Director, Department of Nephrology and Transplant Medicine, Fortis Institute of Renal Sciences Transplantation, India

Sanjeev Gulati, MBBS, MD, DNB(Peds), DM, DNB(Neph), FIPN(Australia), FICN, FRCPC(Canada) is a member of the following medical societies: American Society of Pediatric Nephrology, Indian Academy of Pediatrics, International Society of Nephrology, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Laurence Finberg, MD  Clinical Professor, Department of Pediatrics, University of California, San Francisco, School of Medicine and Stanford University School of Medicine

Laurence Finberg, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Frederick J Kaskel, MD, PhD  Director of the Division and Training Program in Pediatric Nephrology, Vice Chair, Department of Pediatrics, Montefiore Medical Center and Albert Einstein School of Medicine

Frederick J Kaskel, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American Pediatric Society, American Physiological Society, American Society of Nephrology, American Society of Pediatric Nephrology, American Society of Transplantation, Eastern Society for Pediatric Research, Federation of American Societies for Experimental Biology, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Renal Physicians Association, Sigma Xi, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD  The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, Children's Memorial Hospital

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, and International Society of Nephrology

Disclosure: NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

References
  1. US Renal Data System (USRDS). 2010 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States. Bethesda, Md: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2010. Available at http://www.usrds.org/adr.htm. Accessed June 13, 2011.

  2. [Guideline] Kopple JD. National kidney foundation K/DOQI clinical practice guidelines for nutrition in chronic renal failure. Am J Kidney Dis. Jan 2001;37(1 Suppl 2):S66-70. [Medline].

  3. [Guideline] National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis. Feb 2002;39(2 Suppl 1):S1-266. [Medline].

  4. [Guideline] KDOQI. KDOQI Clinical Practice Guideline for Nutrition in Children with CKD: 2008 update. Executive summary. Am J Kidney Dis. Mar 2009;53(3 Suppl 2):S11-104. [Medline].

  5. Seikaly MG, Ho PL, Emmett L, et al. Chronic renal insufficiency in children: the 2001 Annual Report of the NAPRTCS. Pediatr Nephrol. Aug 2003;18(8):796-804. [Medline].

  6. Gulati S, Mittal S, Sharma RK, Gupta A. Etiology and outcome of chronic renal failure in Indian children. Pediatr Nephrol. Sep 1999;13(7):594-6. [Medline].

  7. Ardissino G, Dacco V, Testa S, et al. Epidemiology of chronic renal failure in children: data from the ItalKid project. Pediatrics. Apr 2003;111(4 Pt 1):e382-7. [Medline].

  8. [Best Evidence] Choi AI, Rodriguez RA, Bacchetti P, Bertenthal D, Hernandez GT, O'Hare AM. White/black racial differences in risk of end-stage renal disease and death. Am J Med. Jul 2009;122(7):672-8. [Medline].

  9. Craven AM, Hawley CM, McDonald SP, et al. Predictors of renal recovery in Australian and New Zealand end-stage renal failure patients treated with peritoneal dialysis. Perit Dial Int. Mar-Apr 2007;27(2):184-91. [Medline].

  10. [Guideline] Hogg RJ, Furth S, Lemley KV, et al. National Kidney Foundation's Kidney Disease Outcomes Quality Initiative clinical practice guidelines for chronic kidney disease in children and adolescents: evaluation, classification, and stratification. Pediatrics. Jun 2003;111(6 Pt 1):1416-21. [Medline].

  11. Eknoyan G. The importance of early treatment of the anaemia of chronic kidney disease. Nephrol Dial Transplant. 2001;16 Suppl 5:45-9. [Medline].

  12. Sanchez CP. Secondary hyperparathyroidism in children with chronic renal failure: pathogenesis and treatment. Paediatr Drugs. 2003;5(11):763-76. [Medline].

  13. [Guideline] Noordzij M, Korevaar JC, Boeschoten EW, Dekker FW, Bos WJ, Krediet RT. The Kidney Disease Outcomes Quality Initiative (K/DOQI) Guideline for Bone Metabolism and Disease in CKD: association with mortality in dialysis patients. Am J Kidney Dis. Nov 2005;46(5):925-32. [Medline].

  14. Seeherunvong W, Abitbol CL, Chandar J, Zilleruelo G, Freundlich M. Vitamin D insufficiency and deficiency in children with early chronic kidney disease. J Pediatr. Jun 2009;154(6):906-11.e1. [Medline].

  15. Salusky IB. A new era in phosphate binder therapy: what are the options?. Kidney Int Suppl. Dec 2006;(105):S10-5. [Medline].

  16. Saland JM, Ginsberg H, Fisher EA. Dyslipidemia in pediatric renal disease: epidemiology, pathophysiology, and management. Curr Opin Pediatr. Apr 2002;14(2):197-204. [Medline].

  17. Soergel M, Schaefer F. Effect of hypertension on the progression of chronic renal failure in children. Am J Hypertens. Feb 2002;15(2 Pt 2):53S-56S. [Medline].

  18. Swinford RD, Portman RJ. Measurement and treatment of elevated blood pressure in the pediatric patient with chronic kidney disease. Adv Chronic Kidney Dis. Apr 2004;11(2):143-61. [Medline].

  19. Haffner D, Schaefer F, Nissel R, et al. Effect of growth hormone treatment on the adult height of children with chronic renal failure. German Study Group for Growth Hormone Treatment in Chronic Renal Failure. N Engl J Med. Sep 28 2000;343(13):923-30. [Medline].

  20. Hodson EM, Willis NS, Craig JC. Growth hormone for children with chronic kidney disease. Cochrane Database of Systematic Reviews. 2012.

  21. Muscheites J, Wigger M, Drueckler E, Fischer DC, Kundt G, Haffner D. Cinacalcet for secondary hyperparathyroidism in children with end-stage renal disease. Pediatr Nephrol. Oct 2008;23(10):1823-9. [Medline].

  22. Fogo AB. Mechanisms of progression of chronic kidney disease. Pediatr Nephrol. Jul 24 2007;[Medline].

  23. Mak RH. Chronic kidney disease in children: state of the art. Pediatr Nephrol. Oct 2007;22(10):1687-8. [Medline].

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Major clinical predictors to be used for the perioperative management of a patient with chronic renal failure. CHF = congestive heart failure.
Intermediate clinical predictors to be used for the perioperative management of a patient with chronic renal failure. CHF = congestive heart failure; METs = metabolic equivalents of task; MI = myocardial infarction.
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Hands of a transfusion-dependent patient on long-term hemodialysis. Several uremia-related cutaneous disorders are visible. The pigmentary alteration results from retained urochromes and hemosiderin deposition. The large bullae are consistent with either porphyria cutanea tarda or the bullous disease of dialysis. All nails show the distal brown-red and proximal white coloring of half-and-half nails.
 
 
 
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