Abstract
In a scholarly essay entitled Nature, Nurture, and Human Affairs, Scriver (1981) discussed the biologic origins of rickets in terms that can be modified for the better understanding of many other conditions, symptoms, or abnormalities in which a common phenotype (for example hematuria) may be the result of environmental factors, genetic factors, or an interaction between the two [1]. Before the introduction of vitamin D into milk in the Province of Quebec, the vast majority of cases of rickets treated at The Montreal Childrens’ Hospital were the result of vitamin D deficiency; only a few cases of inherited rickets were seen. Following the addition of vitamin D to milk, only one case of vitamin-D-deficiency rickets was seen; thus the inherited forms of rickets came to represent the majority of rickets cases admitted, although the prevalence of these cases remained the same. In Scriver’s words, “The rickets volume was greatly decreased but the heritability of rickets had increased greatly because the origin of rickets had shifted from an extrinsic cause (vitamin D deficiency) to intrinsic causes (Mendelian causes of phosphate homeostasis).” A similarly dramatic, but less well-documented change has occurred in the biologic origins of hematuria in North America and possibly in Europe. Poststreptococcal glomerulonephritis was, in the past, the most frequent cause of hematuria in North America.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Scriver CR: Nature, nurture, and human affairs. Trans Roy Soc Can 19:211–232, 1981.
Norman MI: An office approach to hematuria and proteinuria. Pediatr Clin N Am 34:545–560, 1987.
Trachtman H, Weiss RA, Bennett B, Greifer I: Isolated hematuria in children: indications for a renal biopsy. Kidney Int 25:94–99, 1984.
Rodriguez-Iturbe B, Rubio L, Garcia R: Attack rate of poststreptococcal nephritis in families. A prospective study. Lancet i:401–403, 1981.
Welch TR, Beischel L, Balakrishnan K, et al.: Major histocompatibility complex extended haplotype in membranoproliferative glomerulonephritis. N Engl J Med 314:1476–1481, 1986.
Jackson EC, McAdams J, Strife CF, Forristal J, Welch TR, West CD: Differences between membranoproliferative glomerulonephritis Types I and III in clinical presentation, glomerular morphology, and complement perturbation. Am J Kidney Dis 9:115–1120, 1987.
Reveille JD, Bias WB, Winkelstein JA, Provost TT, Dorsch CA, Arnett FC: Familial systemic lupus erythematosus: immunogenetic studies in eight families. Medicine 62:21–35, 1983.
Clarkson AR, Woodroffe AJ, Bannister KM, et al.: The syndrome of Ig A nephropathy. Clin Nephrol 21:7–14, 1984.
Gregory MC, Hammond ME, Brewer ED: Renal deposition of cytomegalovirus antigen in immunoglobulin-A nephropathy. Lancet ii:11–14, 1988.
Wyatt RJ, Rivas ML, Julian BA, et al.: Regionalization in hereditary IgA nephropathy. Am J Hum Genet 41:36–50, 1987.
Hasstedt SJ, Atkin CL: X-linked inheritance of Alport syndrome: family P revisited. Am J Hum Genet 35:1241–1251, 1983.
Hasstedt SJ, Atkin CL, San Juan AC Jr: Genetic heterogeneity among kindreds with Alport syndrome. Am J Hum Genet 38:940–953, 1986.
Yoshikawa N, Matsuyama S, Ito H, et al.: Nonfamilial hematuria associated with glomerular basement membrane alterations characteristic of hereditary nephritis: comparison with hereditary nephritis. J Pediatr 111:519–524, 1987.
Atkin CL, Gregory MC, Border WA: Alport syndrome. In: Schrier RW, Gottschalk CW (eds): Diseases of the Kidney. Boston: Little, Brown and Co., 1988, pp. 617–641.
Atkin CL, Hasstedt SJ, Menlove L, et al.: Mapping of Alport syndrome to the long arm of the X chromosome. Am J Hum Genet 42:249–255, 1988.
Perkoff GT, Stephens FE, Dolowitz DA, Tyler FH: A clinical study of hereditary interstitial pyelonephritis. Arch Intern Med 88:191–200, 1951.
Tishler PV: Healthy female carriers of a gene for the Alport syndrome: importance for genetic counseling. Clin Genet 16:291–294, 1979.
Preus M, Fraser FC: Genetics of hereditary nephropathy with deafness (Alport’s disease). Clin Genet 2:331–337, 1971.
MacNeill E, Shaw RF: Segregation ratios in Alport’s syndrome. J Med Genet 10:23, 1973.
Piel CF, Biava CG, Goodman JR: Glomerular basement membrane attenuation in familial nephritis and “benign” hematuria. J Pediatr 101:358–365, 1982.
McConville JM, West CD, McAdams AJ: Familial and nonfamilial benign hematuria. J Pediatr 69:207–214, 1966.
Marks M, Drummond KN: Benign familial hematuria. Pediatrics 44:590–593, 1969.
Favus MJ: Familial forms of hypercalciuria. Prevention and treatment of kidney stones. NIH Consensus Development Conference. March 28–30, 1988, pp. 23–27.
Coe EL, Parks JA, Moore ES: Familial idiopathic hypercalciuria. N Engl J Med 300:337–340, 1979.
Beathard GA, Granholm NA: Development of the characteristic ultrastructural lesion of hereditary nephritis during the course of the disease. Am J Med 62:751–756, 1977.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1990 Kluwer Academic Publishers
About this chapter
Cite this chapter
Kaplan, P., Turner, M.E., Kaplan, B.S. (1990). Genetics of Familial Hematuria. In: Spitzer, A., Avner, E.D. (eds) Inheritance of Kidney and Urinary Tract Diseases. Topics in Renal Medicine, vol 9. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1603-9_6
Download citation
DOI: https://doi.org/10.1007/978-1-4613-1603-9_6
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4612-8887-9
Online ISBN: 978-1-4613-1603-9
eBook Packages: Springer Book Archive