eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Pseudohypoaldosteronism: Differential Diagnoses & Workup

Author: Robert J Ferry Jr, MD, Chief, Division of Pediatric Endocrinology and Diabetes, Le Bonheur Children's Medical Center, University of Tennessee Health Science Center at Memphis and St Jude Children's Research Hospital; Lieutenant Colonel (Medical Corps), 162nd Area Support Medical Company, Army National Guard
Coauthor(s): Jose F Pascual-y-Baralt, MD, Chief, Division of Pediatric Nephrology, San Antonio Military Pediatric Center; Clinical Professor, Department of Pediatrics, University of Texas Health Science Campus
Contributor Information and Disclosures

Updated: Jul 11, 2008

Differential Diagnoses

17-Hydroxylase Deficiency Syndrome
Chronic Kidney Disease
3-Beta-Hydroxysteroid Dehydrogenase Deficiency
Cystic Fibrosis
Acute Tubular Necrosis
Dehydration
Adrenal Glands
Failure to Thrive
Adrenal Hypoplasia
Adrenal Insufficiency
Cerebral Salt-Wasting Syndrome

Other Problems to Be Considered

Addison disease
Chronic renal failure
Isolated hypoaldosteronism
Nephronophthisis
Obstructive uropathy
Salt-wasting nephropathies

Workup

Laboratory Studies

  • Renal pseudohypoaldosteronism type I
    • The clinical characteristics of pseudohypoaldosteronism type I (PHA-I) are those of hypoaldosteronism (ie, hyponatremia, hyperkalemic metabolic acidosis, hyper-reninemia, and renal salt wasting).
    • Diagnosis is made by demonstrating inappropriately high urinary sodium losses in the presence of hyponatremia, decreased urinary potassium excretion, normal GFR, normal adrenal function, and increased levels of aldosterone and renin.
    • Hyponatremia is usually present but may be masked by hemoconcentration.
    • Hyperkalemia and metabolic acidosis are typically present despite a normal GFR. Plasma potassium concentration varies from moderately to greatly increased values.
    • Occasionally, hypercalciuria and nephrocalcinosis have also been described.
    • The only biochemical abnormality in patients with early childhood hyperkalemia is the presence of hyperkalemia and hyperchloremic (nonanion gap) metabolic acidosis. Azotemia and sodium chloride wasting are notably absent.
  • Multiple target organ defects pseudohypoaldosteronism type I
    • Urinary salt wastage, as in renal PHA-I, is characteristic of multiple target organ defects (MTOD) PHA-I.
    • Salt wastage can occur from the salivary glands, sweat glands, and colon.
    • A variant of MTOD PHA-I has been described in the literature with salt wastage limited to sweat and salivary glands without associated renal salt wasting.
  • Pseudohypoaldosteronism type II
    • Hyperkalemia, hyperchloremic metabolic acidosis, and normal GFR are present with low aldosterone and renin levels.
    • Sodium wasting is absent, in contrast to renal PHA-I and mineralocorticoid deficient states.
    • Patients with PHA have hyperkalemia and decreased renal potassium excretion in the absence of glomerular insufficiency. Children with the chloride shunt syndrome (Spitzer-Weinstein syndrome) are typically hyperkalemic at presentation. Potassium excretion responds to sodium sulfate infusion but not to sodium chloride infusion.
    • Serum bicarbonate concentration is typically low, but this is a more variable finding in children and is observed in only one half of cases.
    • Hypercalciuria has usually been overlooked as a biochemical feature of this disorder, although its presence has been recognized occasionally.
    • Nephrolithiasis is unusual.
  • Secondary pseudohypoaldosteronism: The clinical presentation in children is that of renal tubular resistance to aldosterone (ie, hyponatremia, hyperkalemia, and metabolic acidosis).

Imaging Studies

  • Chest radiography may reveal an increased volume of liquid in the airways in patients with MTOD PHA-I, secondary to failure to absorb liquid from airway surfaces. These findings mimic cystic fibrosis
  • Renal ultrasonography may show nephrocalcinosis in patients with PHA-I and nephrolithiasis in patients with PHA-II.

Other Tests

  • Renal pseudohypoaldosteronism type I
    • Overall renal function is normal.
    • Plasma aldosterone concentration, urinary aldosterone excretion, and PRA are usually elevated.
    • Plasma deoxycorticosterone and corticosterone concentrations are within the reference range.
    • The ratio of plasma 18-hydroxycorticosterone to aldosterone is within the reference range.
    • The ratio of urinary excretion of tetrahydroaldosterone to 18-hydroxytetrahydro-compound A is within the reference range in contrast to primary hypoaldosteronism.
    • Sweat and salivary sodium and chloride determinations are characteristically normal.
    • Children with the early childhood hyperkalemia variant of renal PHA-I have consistently normal or elevated PRA and 24-hour urinary aldosterone excretion. Functional evaluation reveals a normal ability to acidify the urine, low ammonium and potassium excretion, and a mild defect in bicarbonate reabsorption (ie, functional markers of type IV RTA). Renal bicarbonate wasting can be observed with high-dose alkali therapy, but, in contrast to type II proximal RTA, associated kaluria is not observed. In contrast to type I and II RTA, this subtype has no hypercalciuria but, rather, a relative hyper-reabsorption of calcium and a high urinary citrate excretion; thus, nephrocalcinosis is absent.
  • Multiple target organ defects pseudohypoaldosteronism type I
    • Urinary sodium is typically elevated.
    • Sweat and salivary sodium concentrations are elevated, and active sodium transport in the rectal mucosa is impaired.
  • Pseudohypoaldosteronism type II
    • Renin and aldosterone levels are low to normal; renin and aldosterone levels increase if volume expansion is corrected by diuretics or salt restriction. Although aldosterone levels may be within the reference range in some cases, they are probably not appropriately elevated for the degree of hyperkalemia.
    • Renal concentration and dilution are normal.
    • Fractional excretion of bicarbonate (FE HCO3) is normal.
    • Urinary acidification after an ammonium chloride load is normal; however, most patients have a marked reduction in urinary acid excretion and in net acid excretion.
  • Secondary pseudohypoaldosteronism: Plasma aldosterone concentration is elevated, and fractional sodium excretion may be inappropriately high.

Histologic Findings

  • Renal biopsy findings in PHA-I are usually normal; however, hypertrophy of the juxtaglomerular apparatus has been occasionally reported.

More on Pseudohypoaldosteronism

Overview: Pseudohypoaldosteronism
Differential Diagnoses & Workup: Pseudohypoaldosteronism
Treatment & Medication: Pseudohypoaldosteronism
Follow-up: Pseudohypoaldosteronism
References
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References

  1. Melzi ML, Guez S, Sersale G, et al. Acute pyelonephritis as a cause of hyponatremia/hyperkalemia in young infants with urinary tract malformations. Pediatr Infect Dis J. Jan 1995;14(1):56-9. [Medline].

  2. Geller DS, Zhang J, Zennaro MC, et al. Autosomal dominant pseudohypoaldosteronism type 1: mechanisms, evidence for neonatal lethality, and phenotypic expression in adults. J Am Soc Nephrol. 2006;17:1429-1436. [Medline].

  3. Chitayat D, Spirer Z, Ayalon D, Golander A. Pseudohypoaldosteronism in a female infant and her family: diversity of clinical expression and mode of inheritance. Acta Paediatr Scand. Jul 1985;74(4):619-22. [Medline].

  4. Hogg R, Marks J, Marver D, Frolich J. Long-term observation in a patient with pseudohypoaldosteronism. Pediatr Nephrol. 1991;5:205-210. [Medline].

  5. Huang CL, Cha SK, Wang HR, Xie J, Cobb MH. WNKs: protein kinases with a unique kinase domain. Exp Mol Med. 2007;39:565-73. [Medline].

  6. Tobias JD, Brock JW III, Lynch A. Pseudohypoaldosteronism following operative correction of unilateral obstructive nephropathy. Clin Pediatr (Phila). Jun 1995;34(6):327-30. [Medline].

  7. Valimaki M, Pelkonen R, Tikkanem I, Fyhriquist F. Normal renin sensitivity to atrial natriuretic peptide in Gordon's syndrome. Pediatr Nephrol. 1992;6:44-45. [Medline].

  8. Chang SS, Grunder S, Hanukoglu A, et al. Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1. Nat Genet. Mar 1996;12(3):248-53. [Medline].

  9. Mansfield TA, Simon DB, Farfel Z, et al. Multilocus linkage of familial hyperkalaemia and hypertension, pseudohypoaldosteronism type II, to chromosomes 1q31-42 and 17p11-q21. Nat Genet. Jun 1997;16(2):202-5. [Medline].

  10. Abramson O, Zmora E, Mazor M, Shinwell ES. Pseudohypoaldosteronism in a preterm infant: intrauterine presentation as hydramnios. J Pediatr. Jan 1992;120(1):129-32. [Medline].

  11. Alon U, Kodroff MB, Broecker BH, et al. Renal tubular acidosis type 4 in neonatal unilateral kidney diseases. J Pediatr. Jun 1984;104(6):855-60. [Medline].

  12. Anand SK, Froberg L, Northway JD, et al. Pseudohypoaldosteronism due to sweat gland dysfunction. Pediatr Res. 1976;10:677-82. [Medline].

  13. Arai K, Tsigos C, Suzuki Y, et al. No apparent mineralocorticoid receptor defect in a series of sporadic cases of pseudohypoaldosteronism. J Clin Endocrinol Metab. Mar 1995;80(3):814-7. [Medline].

  14. Arai K, Tsigos C, Suzuki Y, et al. Physiological and molecular aspects of mineralocorticoid receptor action in pseudohypoaldosteronism: a responsiveness test and therapy. J Clin Endocrinol Metab. Oct 1994;79(4):1019-23. [Medline].

  15. Armanini D, Kuhnle U, Strasser T, et al. Aldosterone-receptor deficiency in pseudohypoaldosteronism. N Engl J Med. Nov 7 1985;313(19):1178-81. [Medline].

  16. Ballauff A, Wendel U, Kupke I, Kuhnle U. A partial form of hypoaldosteronism type I without sodium wasting. J Pediatr Endocrinol. 1994;7:57-60. [Medline].

  17. Bierich JR, Schmidt U. Tubular Na, K-ATPase deficiency, the cause of the congenital renal salt-losing syndrome. Eur J Pediatr. Jan 2 1976;121(2):81-7. [Medline].

  18. Bistritzer T, Evans S, Cotariu D, et al. Reduced Na+, K(+)-ATPase activity in patients with pseudohypoaldosteronism. Pediatr Res. Mar 1994;35(3):372-5. [Medline].

  19. Blachar Y, Kaplan BS, Griffel B, Levin S. Pseudohypoaldosteronism. Clin Nephrol. Jun 1979;11(6):281-8. [Medline].

  20. Brautbar N, Levi J, Rosler A, et al. Familial hyperkalemia, hypertension, and hyporeninemia with normal aldosterone levels. A tubular defect in potassium handling. Arch Intern Med. Apr 1978;138(4):607-10. [Medline].

  21. Chang S, Muller J, Rosler A. Molecular analysis of epithelial sodium channel subunits in pseudohypoaldosteronism type 1. J Am Soc Nephrol. 1996;7:1611.

  22. Cheek DB, Perry JA. A salt wasting syndrome in infancy. Arch Dis Child. 1958;33:252-256.

  23. Choate KA, Kahle KT, Wilson FH, et al. WNK1, a kinase mutated in inherited hypertension with hyperkalemia, localizes to diverse Cl- -transporting epithelia. Proc Natl Acad Sci USA. 2003;100:663-668. [Medline]. [Full Text].

  24. Claris Appiani A, Marra G, Tirelli SA, et al. Early childhood hyperkalemia: variety of pseudohypoaldosteronism. Acta Paediatr Scand. Nov 1986;75(6):970-4. [Medline].

  25. Cogan MC, Arieff AI. Sodium wasting, acidosis and hyperkalemia induced by methicillin interstitial nephritis. Evidence for selective distal tubular dysfunction. Am J Med. Mar 1978;64(3):500-7. [Medline].

  26. Cugini P, Natoli G, Gerlini G, et al. Erythrocyte transmembrane Na and K fluxes in pseudohypoaldosteronism. Biochem Med Metab Biol. Dec 1992;48(3):241-54. [Medline].

  27. Daughaday WH, Rendleman D. Severe symptomatic hyperkalemia in an adrenalectomized woman due to enhanced mineralocorticoid requirement. Ann Intern Med. Jun 1967;66(6):1197-203. [Medline].

  28. DuBose TD Jr. Hyperkalemic hyperchloremic metabolic acidosis: pathophysiologic insights. Kidney Int. Feb 1997;51(2):591-602. [Medline].

  29. Farfel Z, Iaina A, Levi J, Gafni J. Proximal renal tubular acidosis: association with familial normaldosteronemic hyperpotassemia and hypertension. Arch Intern Med. Dec 1978;138(12):1837-40. [Medline].

  30. Geller DS, Rodriguez-Soriano J, Vallo Boado A, et al. Mutations in the mineralocorticoid receptor gene cause autosomal dominant pseudohypoaldosteronism type I. Nat Genet. Jul 1998;19(3):279-81. [Medline].

  31. Gereda JE, Bonilla-Felix M, Kalil B, Dewitt SJ. Neonatal presentation of Gordon syndrome. J Pediatr. Oct 1996;129(4):615-7. [Medline].

  32. Gordon RD. Syndrome of hypertension and hyperkalemia with normal glomerular filtration rate. Hypertension. Feb 1986;8(2):93-102. [Medline].

  33. Gordon RD, Geddes RA, Pawsey CG, O'Halloran MW. Hypertension and severe hyperkalaemia associated with suppression of renin and aldosterone and completely reversed by dietary sodium restriction. Australas Ann Med. Nov 1970;19(4):287-94. [Medline].

  34. Greenberg D, Abramson O, Phillip M. Fetal pseudohypoaldosteronism: another cause of hydramnios. Acta Paediatr. May 1995;84(5):582-4. [Medline].

  35. Hanukoglu A. Type I pseudohypoaldosteronism includes two clinically and genetically distinct entities with either renal or multiple target organ defects. J Clin Endocrinol Metab. Nov 1991;73(5):936-44. [Medline].

  36. Hanukoglu A, Bistritzer T, Rakover Y, Mandelberg A. Pseudohypoaldosteronism with increased sweat and saliva electrolyte values and frequent lower respiratory tract infections mimicking cystic fibrosis. J Pediatr. Nov 1994;125(5 Pt 1):752-5. [Medline].

  37. Hanukoglu A, Fried D, Gotlieb A. Inheritance of pseudohypoaldosteronism. Lancet. Jun 24 1978;1(8078):1359. [Medline].

  38. Honour JW, Dillon MJ, Shackleton CH. Analysis of steroids in urine for differentiation of pseudohypoaldosteronism and aldosterone biosynthetic defect. J Clin Endocrinol Metab. Feb 1982;54(2):325-31. [Medline].

  39. Hummler E, Barker P, Gatzy J, et al. Early death due to defective neonatal lung liquid clearance in alpha-ENaC-deficient mice. Nat Genet. Mar 1996;12(3):325-8. [Medline].

  40. Kahle KT, Wilson FH, Leng Q, et al. WNK4 regulates the balance between renal NaCl reabsorption and K+ secretion. Nat Genet. Dec 2003;35(4):372-6. [Medline].

  41. Klemm SA, Gordon RD, Tunny TJ, Finn WL. Biochemical correction in the syndrome of hypertension and hyperkalaemia by severe dietary salt restriction suggests renin-aldosterone suppression critical in pathophysiology. Clin Exp Pharmacol Physiol. Mar 1990;17(3):191-5. [Medline].

  42. Komesaroff PA, Verity K, Fuller PJ. Pseudohypoaldosteronism: molecular characterization of the mineralocorticoid receptor. J Clin Endocrinol Metab. Jul 1994;79(1):27-31. [Medline].

  43. Kotchen TA, Welch WJ, Lorenz JN, Ott CE. Renal tubular chloride and renin release. J Lab Clin Med. Nov 1987;110(5):533-40. [Medline].

  44. Kuhnle U, Hinkel GK, Akkurt HI, Krozowski Z. Familial pseudohypoaldosteronism: a review on the heterogeneity of the syndrome. Steroids. Jan 1995;60(1):157-60. [Medline].

  45. Kuhnle U, Keller U, Armanini D. Immunofluorescence of mineralocorticoid receptors in peripheral lymphocytes: presence of receptor-like activity in patients with the autosomal dominant form of pseudohypoaldosteronism, and its absence in the recessive form. J Steroid Biochem Mol Biol. Dec 1994;51(5-6):267-73. [Medline].

  46. Kuhnle U, Nielsen MD, Tietze HU, et al. Pseudohypoaldosteronism in eight families: different forms of inheritance are evidence for various genetic defects. J Clin Endocrinol Metab. Mar 1990;70(3):638-41. [Medline].

  47. Landau D. Potassium handling in health and disease: lessons from inherited tubulopathies. Pediatr Endocrinol Rev. 2004;2:203-208. [Medline].

  48. Landau D. Potassium-related inherited tubulopathies. Cell Mol Life Sci. 2006;63:1962-8. [Medline].

  49. Levin TL, Abramson SJ, Burbige KA, et al. Salt losing nephropathy simulating congenital adrenal hyperplasia in infants with obstructive uropathy and/or vesicoureteral reflux--value of ultrasonography in diagnosis. Pediatr Radiol. 1991;21(6):413-5. [Medline].

  50. Limal JM, Rappaport R, Dechaux M, Morin C. Familial dominant pseudohypoaldosteronism. Lancet. Jan 7 1978;1(8054):51. [Medline].

  51. Luke RG, Allison ME, Davidson JF, Duguid WP. Hyperkalemia and renal tubular acidosis due to renal amyloidosis. Ann Intern Med. Jun 1969;70(6):1211-7. [Medline].

  52. Marra G, Goj V, Appiani AC, et al. Persistent tubular resistance to aldosterone in infants with congenital hydronephrosis corrected neonatally. J Pediatr. Jun 1987;110(6):868-72. [Medline].

  53. Mastrandrea LD, Martin DJ, Springate JE. Clinical and biochemical similarities between reflux/obstructive uropathy and salt-wasting congenital adrenal hyperplasia. Clin Pediatr (Phila). 2005;44:809-812. [Medline].

  54. Matthew PM, Manasra KB, Hamdan JA. Indomethacin and cation-exchange resin in the management of pseudohypoaldosteronism. Clin Pediatr (Phila). 1993;32:58-60. [Medline].

  55. Muhammad S, Mamish ZM, Tucci JR. Type II pseudohypoaldosteronism. Report of a case and review of the literature. J Endocrinol Invest. Jun 1994;17(6):453-7. [Medline].

  56. Oberfield SE, Levine LS, Carey RM, et al. Pseudohypoaldosteronism: multiple target organ unresponsiveness to mineralocorticoid hormones. J Clin Endocrinol Metab. Feb 1979;48(2):228-34. [Medline].

  57. Paver WKA, Pauline GJ. Hypertension and hyperpotassemia without renal disease in a young male. Med J Austr. 1964;2:305-306.

  58. Perimenis P, Wemeau JL, Vantyghem MC. Hypercalciuria [French]. Ann Endocrinol (Paris). 2005;66:532-539. [Medline].

  59. Peters TA, Levtchenko E, Cremers CW, et al. No evidence of hearing loss in pseudohypoaldosteronism type 1 patients. Acta Otolaryngol. 2006;126:237-239. [Medline].

  60. Proesmans W, Muaka B, Corbeel L, Eeckels R. Pseudohypoaldosteronism, a proximal tubular sodium wasting disease. J Pediatr. Apr 1978;92(4):678-9. [Medline].

  61. Rodriguez-Soriano J, Vallo A, Dominguez MJ. "Chloride-shunt" syndrome: an overlooked cause of renal hypercalciuria. Pediatr Nephrol. Apr 1989;3(2):113-21. [Medline].

  62. Rodriguez-Soriano J, Vallo A, Oliveros R, Castillo G. Transient pseudohypoaldosteronism secondary to obstructive uropathy in infancy. J Pediatr. 1983;103:375-380. [Medline].

  63. Roessler A. The natural history of salt-wasting disorders of adrenal and renal origin. J Clin Endocrinol Metab. 1984;59:689-700. [Medline].

  64. Sanderson IR, Carter EP, Dillon MJ, et al. Familial salivary gland insensitivity to aldosterone: a variant of pseudohypoaldosteronism. Horm Res. 1989;32(4):145-7. [Medline].

  65. Sanjad SA, Keenan BS, Hill LL. Renal hypoprostaglandism, hypertension, and type IV renal tubular acidosis reversed by furosemide. Ann Intern Med. Nov 1983;99(5):624-7. [Medline].

  66. Savage MO, Jefferson IG, Dillon MJ, et al. Pseudohypoaldosteronism: severe salt wasting in infancy caused by generalized mineralocorticoid unresponsiveness. J Pediatr. Aug 1982;101(2):239-42. [Medline].

  67. Schambelan M, Sebastian A, Rector FC Jr. Mineralocorticoid-resistant renal hyperkalemia without salt wasting (type II pseudohypoaldosteronism): role of increased renal chloride reabsorption. Kidney Int. May 1981;19(5):716-27. [Medline].

  68. Schindler AM, Bergman GE. Prospective diagnosis of pseudohypoaldosteronism. Pediatrics. Sep 1986;78(3):516-8. [Medline].

  69. Semmekrot B, Monnens L, Theelen BG, et al. The syndrome of hypertension and hyperkalaemia with normal glomerular function (Gordon's syndrome). A pathophysiological study. Pediatr Nephrol. Jul 1987;1(3):473-8. [Medline].

  70. Shalev H, Ohali M, Abramson O. Nephrocalcinosis in pseudohypoaldosteronism and the effect of indomethacin therapy. J Pediatr. Aug 1994;125(2):246-8. [Medline].

  71. Sheridan MB, Fong P, Groman JD, et al. Mutations in the beta-subunit of the epithelial Na+ channel in patients with a cystic fibrosis-like syndrome. Hum Mol Genet. 2005;14:3493-3498. [Medline].

  72. Shimkets RA, Warnock DG, Bositis CM, et al. Liddle's syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel. Cell. Nov 4 1994;79(3):407-14. [Medline].

  73. Shoker A, Morris G, Skomro R, Laxdal V. Pseudohypoaldosteronism with normal blood pressure. Clin Nephrol. Aug 1996;46(2):105-11. [Medline].

  74. Spitzer A, Edelmann CM Jr, Goldberg LD, Henneman PH. Short stature, hyperkalemia and acidosis: A defect in renal transport of potassium. Kidney Int. Apr 1973;3(4):251-7. [Medline].

  75. Stone RC, Vale P, Rosa FC. Effect of hydrochlorothiazide in pseudohypoaldosteronism with hypercalciuria and severe hyperkalemia. Pediatr Nephrol. Aug 1996;10(4):501-3. [Medline].

  76. Weinstein SF, Allan DM, Mendoza SA. Hyperkalemia, acidosis, and short stature associated with a defect in renal potassium excretion. J Pediatr. Sep 1974;85(3):355-8. [Medline].

  77. Wilson FH, Kahle KT, Sabath E, et al. Molecular pathogenesis of inherited hypertension with hyperkalemia: the Na-Cl cotransporter is inhibited by wild-type but not mutant WNK4. Proc Natl Acad Sci USA. 2003;100:680-684. [Medline]. [Full Text].

  78. Yang CL, Angell J, Mitchell R, Ellison DH. WNK kinases regulate thiazide-sensitive Na-Cl cotransport. J Clin Invest. 2003;111:1039-1045. [Medline]. [Full Text].

  79. Zennaro MC, Borensztein P, Jeunemaitre X, et al. No alteration in the primary structure of the mineralocorticoid receptor in a family with pseudohypoaldosteronism. J Clin Endocrinol Metab. Jul 1994;79(1):32-8. [Medline].

  80. Zennaro MC, Borensztein P, Soubrier F, et al. The enigma of pseudohypoaldosteronism. Steroids. Feb 1994;59(2):96-9. [Medline].

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Further Reading

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Keywords

pseudohypoaldosteronism, PHA, pseudohypoaldosteronism type I, PHA-I, Cheek and Perry syndrome, renal pseudohypoaldosteronism type I, AD renal PHA-I, multiple target organ pseudohypoaldosteronism, MTOD PHA-I, autosomal recessive PHA-I, AR PHA-I, early childhood hyperkalemia, renal tubular acidosis subtypes 4 and 5, RTA, pseudohypoaldosteronism type II, PHA-II, Gordon syndrome, adolescent hyperkalemic syndrome, Spitzer-Weinstein syndrome, mineralocorticoid-resistant hyperkalemia, renal tubular acidosis type IV subtype 3, metabolic acidosis, hypervolemia, renal salt wasting, hypotension, hypertension, chloride shunt syndrome, renal tube defects, short stature, urolithiasis, obstructive uropathy, urinary tract infection, tubulointerstitial nephritis, sickle cell nephropathy, systemic lupus erythematosus, amyloidosis, neonatal medullary necrosis, unilateral renal vein thrombosis, failure to thrive, adolescent hyperkalemic syndrome

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Contributor Information and Disclosures

Author

Robert J Ferry Jr, MD, Chief, Division of Pediatric Endocrinology and Diabetes, Le Bonheur Children's Medical Center, University of Tennessee Health Science Center at Memphis and St Jude Children's Research Hospital; Lieutenant Colonel (Medical Corps), 162nd Area Support Medical Company, Army National Guard
Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society
Disclosure: Nutropin Speakers Bureau Honoraria Speaking and teaching

Coauthor(s)

Jose F Pascual-y-Baralt, MD, Chief, Division of Pediatric Nephrology, San Antonio Military Pediatric Center; Clinical Professor, Department of Pediatrics, University of Texas Health Science Campus
Jose F Pascual-y-Baralt, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, American Society of Pediatric Nephrology, Association of Military Surgeons of the US, and International Society of Nephrology
Disclosure: Nothing to disclose.

Medical Editor

Arlan L Rosenbloom, MD, Adjunct Distinguished Service Professor Emeritus of Pediatrics, University of Florida; Fellow of the American Academy of Pediatrics; Fellow of the American College of Epidemiology
Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Florida Pediatric Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

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Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Lynne Lipton Levitsky, MD, Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor, Department of Pediatrics, Harvard University Medical School
Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and Arkansas Children's Hospital
Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research
Disclosure: Genentech, Inc. Honoraria Speaking and teaching; Pfiser, Inc. Honoraria Consulting

 
 
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