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Living donor kidney transplantation in patients with hereditary nephropathies

Abstract

Patients with some hereditary nephropathies—including autosomal dominant polycystic kidney disease (ADPKD), Fabry disease and Alport syndrome—can progress to end-stage renal disease (ESRD) and are candidates for kidney transplantation. When considering whether a potential living donor is appropriate for a particular patient, clinicians should be aware of the increased risk of adverse outcomes for the donor and the recipient. Renal transplantation from a living related donor is not contraindicated in most nephropathies that have an autosomal recessive mode of inheritance (for example, autosomal recessive polycystic kidney disease and cystinosis). Renal transplant recipients with ADPKD, however, should only receive a kidney from a related donor if the disease has been excluded in the donor by imaging and/or genetic testing. Potential living related donors for patients with Alport syndrome should be evaluated carefully for the presence of microhematuria and microalbuminuria before a decision is made to perform transplantation, and mothers or heterozygous sisters of affected male recipients with X-linked Alport syndrome should be informed about the possible long-term increased risk of renal dysfunction associated with donation. Most patients with atypical hemolytic uremic syndrome should not receive a kidney transplant from a living donor because there is a high risk of disease recurrence and graft loss.

Key Points

  • Living donor kidney transplantation is often presented as the best option for patients awaiting renal transplantation, but patients whose renal failure is the result of an inherited disease might not be suitable candidates for living related transplantation

  • The possible occurrence of the same disease in the related living donor should be excluded before living donor transplantation is performed in a patient with a hereditary nephropathy

  • For living donor transplantation to be suitable for a particular patient, the risk of graft loss should not be higher than it would be if the patient received a graft from a deceased donor

  • Individuals with autosomal dominant polycystic kidney disease requiring renal transplantation should only receive a kidney from a relative if the disease has been excluded in that relative; if imaging data is equivocal, the potential living related donor should undergo molecular testing

  • Female heterozygotes for X-linked Alport syndrome who are considering donating a kidney should be informed about the long-term increased risk of renal dysfunction associated with kidney donation

  • Living donor kidney transplantation is contraindicated in patients with atypical hemolytic uremic syndrome because of the high risk of recurrence and the associated high risk of graft loss

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References

  1. Davis, C. L. & Delmonico, F. L. Living-donor kidney transplantation: a review of the current practices for the live donor. J. Am. Soc. Nephrol. 16, 2098–2110 (2005).

    Article  PubMed  Google Scholar 

  2. Mange, K. C., Joffe, M. M. & Feldman, H. I. Effect of the use or nonuse of long-term dialysis on the subsequent survival of renal transplants from living donors. N. Engl. J. Med. 344, 726–731 (2001).

    Article  CAS  PubMed  Google Scholar 

  3. Kasiske, B. L. et al. The evaluation of living renal transplant donors: clinical practice guidelines. Ad Hoc Clinical Practice Guidelines Subcommittee of the Patient Care and Education Committee of the American Society of Transplant Physicians. J. Am. Soc. Nephrol. 7, 2288–2313 (1996).

    CAS  PubMed  Google Scholar 

  4. Donne, R. L. et al. Recurrence of hemolytic uremic syndrome after live related renal transplantation associated with subsequent de novo disease in the donor. Am. J. Kidney Dis. 40, E22 (2002).

    Article  PubMed  Google Scholar 

  5. Grantham, J. J. Clinical practice. Autosomal dominant polycystic kidney disease. N. Engl. J. Med. 359, 1477–1485 (2008).

    Article  CAS  PubMed  Google Scholar 

  6. Torres, V. E., Harris, P. C. & Pirson, Y. Autosomal dominant polycystic kidney disease. Lancet 369, 1287–1301 (2007).

    Article  PubMed  Google Scholar 

  7. Gallagher, A. R., Germino, G. G. & Somlo, S. Molecular advances in autosomal dominant polycystic kidney disease. Adv. Chronic Kidney Dis. 17, 118–130 (2010).

    Article  PubMed  PubMed Central  Google Scholar 

  8. Hateboer, N. et al. Comparison of phenotypes of polycystic kidney disease types 1 and 2. European PKD1-PKD2 Study Group. Lancet 353, 103–107 (1999).

    Article  CAS  PubMed  Google Scholar 

  9. Bear, J. C. et al. Age at clinical onset and at ultrasonographic detection of adult polycystic kidney disease: data for genetic counselling. Am. J. Med. Genet. 18, 45–53 (1984).

    Article  CAS  PubMed  Google Scholar 

  10. Nicolau, C. et al. Autosomal dominant polycystic kidney disease types 1 and 2: assessment of US sensitivity for diagnosis. Radiology 213, 273–276 (1999).

    Article  CAS  PubMed  Google Scholar 

  11. Ravine, D. et al. Evaluation of ultrasonographic diagnostic criteria for autosomal dominant polycystic kidney disease 1. Lancet 343, 824–827 (1994).

    Article  CAS  PubMed  Google Scholar 

  12. Pei, Y. et al. Unified criteria for ultrasonographic diagnosis of ADPKD. J. Am. Soc. Nephrol. 20, 205–212 (2009).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  13. Zand, M. S. et al. Screening a living kidney donor for polycystic kidney disease using heavily T2-weighted MRI. Am. J. Kidney Dis. 37, 612–619 (2001).

    Article  CAS  PubMed  Google Scholar 

  14. Blumenfeld, J. D. Pretransplant genetic testing of live kidney donors at risk for autosomal dominant polycystic kidney disease. Transplantation 87, 6–7 (2009).

    Article  PubMed  PubMed Central  Google Scholar 

  15. Huang, E. et al. DNA testing for live kidney donors at risk for autosomal dominant polycystic kidney disease. Transplantation 87, 133–137 (2009).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Rossetti, S. et al. A complete mutation screen of the ADPKD genes by DHPLC. Kidney Int. 61, 1588–1599 (2002).

    Article  CAS  PubMed  Google Scholar 

  17. Veldhuisen, B. et al. A spectrum of mutations in the second gene for autosomal dominant polycystic kidney disease (PKD2). Am. J. Hum. Genet. 61, 547–555 (1997).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Hannig, V. L., Erickson, S. M. & Phillips, J. A. 3rd. Utilization and evaluation of living-related donors for patients with adult polycystic kidney disease. Am. J. Med. Genet. 44, 409–412 (1992).

    Article  CAS  PubMed  Google Scholar 

  19. Harris, P. C. & Rossetti, S. Molecular diagnostics for autosomal dominant polycystic kidney disease. Nat. Rev. Nephrol. 6, 197–206 (2010).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  20. Heidet, L. & Gubler, M. C. The renal lesions of Alport syndrome. J. Am. Soc. Nephrol. 20, 1210–1215 (2009).

    Article  CAS  PubMed  Google Scholar 

  21. Kashtan, C. E. Alport syndrome and thin glomerular basement membrane disease. J. Am. Soc. Nephrol. 9, 1736–1750 (1998).

    CAS  PubMed  Google Scholar 

  22. Tryggvason, K., Zhou, J., Hostikka, S. L. & Shows, T. B. Molecular genetics of Alport syndrome. Kidney Int. 43, 38–44 (1993).

    Article  CAS  PubMed  Google Scholar 

  23. Barker, D. F. et al. Identification of mutations in the COL4A5 collagen gene in Alport syndrome. Science 248, 1224–1227 (1990).

    Article  CAS  PubMed  Google Scholar 

  24. Jais, J. P. et al. X-linked Alport syndrome: natural history and genotype-phenotype correlations in girls and women belonging to 195 families: a “European Community Alport Syndrome Concerted Action” study. J. Am. Soc. Nephrol. 14, 2603–2610 (2003).

    Article  PubMed  Google Scholar 

  25. Martin, P. et al. High mutation detection rate in the COL4A5 collagen gene in suspected Alport syndrome using PCR and direct DNA sequencing. J. Am. Soc. Nephrol. 9, 2291–2301 (1998).

    CAS  PubMed  Google Scholar 

  26. Heiskari, N. et al. Identification of 17 mutations in ten exons in the COL4A5 collagen gene, but no mutations found in four exons in COL4A6: a study of 250 patients with hematuria and suspected of having Alport syndrome. J. Am. Soc. Nephrol. 7, 702–709 (1996).

    CAS  PubMed  Google Scholar 

  27. Feingold, J. et al. Genetic heterogeneity of Alport syndrome. Kidney Int. 27, 672–677 (1985).

    Article  CAS  PubMed  Google Scholar 

  28. Heidet, L. et al. Structure of the human type IV collagen gene COL4A3 and mutations in autosomal Alport syndrome. J. Am. Soc. Nephrol. 12, 97–106 (2001).

    CAS  PubMed  Google Scholar 

  29. Mochizuki, T. et al. Identification of mutations in the alpha 3(IV) and alpha 4(IV) collagen genes in autosomal recessive Alport syndrome. Nat. Genet. 8, 77–81 (1994).

    Article  CAS  PubMed  Google Scholar 

  30. Torra, R., Tazon-Vega, B., Ars, E. & Ballarin, J. Collagen type IV (α3- α4) nephropathy: from isolated haematuria to renal failure. Nephrol. Dial. Transplant. 19, 2429–2432 (2004).

    Article  PubMed  Google Scholar 

  31. Pescucci, C. et al. Autosomal-dominant Alport syndrome: natural history of a disease due to COL4A3 or COL4A4 gene. Kidney Int. 65, 1598–1603 (2004).

    Article  CAS  PubMed  Google Scholar 

  32. van der Loop, F. T. et al. Autosomal dominant Alport syndrome caused by a COL4A3 splice site mutation. Kidney Int. 58, 1870–1875 (2000).

    Article  CAS  PubMed  Google Scholar 

  33. Jais, J. P. et al. X-linked Alport syndrome: natural history in 195 families and genotype-phenotype correlations in males. J. Am. Soc. Nephrol. 11, 649–657 (2000).

    CAS  PubMed  Google Scholar 

  34. Flinter, F. Alport's syndrome. J. Med. Genet. 34, 326–330 (1997).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. Colville, D. et al. Ocular manifestations of autosomal recessive Alport syndrome. Ophthalmic Genet. 18, 119–128 (1997).

    Article  CAS  PubMed  Google Scholar 

  36. Kashtan, C. E. Women with Alport syndrome: risks and rewards of kidney donation. Nephrol. Dial. Transplant. 24, 1369–1370 (2009).

    Article  PubMed  Google Scholar 

  37. Gross, O., Weber, M., Fries, J. W. & Muller, G. A. Living donor kidney transplantation from relatives with mild urinary abnormalities in Alport syndrome: long-term risk, benefit and outcome. Nephrol. Dial. Transplant. 24, 1626–1630 (2009).

    Article  PubMed  Google Scholar 

  38. Badenas, C. et al. Mutations in the COL4A4 and COL4A3 genes cause familial benign hematuria. J. Am. Soc. Nephrol. 13, 1248–1254 (2002).

    CAS  PubMed  Google Scholar 

  39. Buzza, M., Wilson, D. & Savige, J. Segregation of hematuria in thin basement membrane disease with haplotypes at the loci for Alport syndrome. Kidney Int. 59, 1670–1676 (2001).

    Article  CAS  PubMed  Google Scholar 

  40. Voskarides, K. et al. COL4A3/COL4A4 mutations producing focal segmental glomerulosclerosis and renal failure in thin basement membrane nephropathy. J. Am. Soc. Nephrol. 18, 3004–3016 (2007).

    Article  CAS  PubMed  Google Scholar 

  41. Kashtan, C. E. Alport syndrome. An inherited disorder of renal, ocular, and cochlear basement membranes. Medicine (Baltimore) 78, 338–360 (1999).

    Article  CAS  Google Scholar 

  42. Kashtan, C. E. Renal transplantation in patients with Alport syndrome. Pediatr. Transplant. 10, 651–657 (2006).

    Article  PubMed  Google Scholar 

  43. Ding, J., Zhou, J., Tryggvason, K. & Kashtan, C. E. COL4A5 deletions in three patients with Alport syndrome and posttransplant antiglomerular basement membrane nephritis. J. Am. Soc. Nephrol. 5, 161–168 (1994).

    CAS  PubMed  Google Scholar 

  44. Kashtan, C. E., Butkowski, R. J., Kleppel, M. M., First, M. R. & Michael, A. F. Posttransplant anti-glomerular basement membrane nephritis in related males with Alport syndrome. J. Lab. Clin. Med. 116, 508–515 (1990).

    CAS  PubMed  Google Scholar 

  45. Branton, M. H. et al. Natural history of Fabry renal disease: influence of alpha-galactosidase A activity and genetic mutations on clinical course. Medicine (Baltimore) 81, 122–138 (2002).

    Article  CAS  Google Scholar 

  46. MacDermot, K. D., Holmes, A. & Miners, A. H. Anderson-Fabry disease: clinical manifestations and impact of disease in a cohort of 60 obligate carrier females. J. Med. Genet. 38, 769–775 (2001).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Galanos, J. et al. Clinical features of Fabry's disease in Australian patients. Intern. Med. J. 32, 575–584 (2002).

    Article  CAS  PubMed  Google Scholar 

  48. Nakao, S. et al. Fabry disease: detection of undiagnosed hemodialysis patients and identification of a “renal variant” phenotype. Kidney Int. 64, 801–807 (2003).

    Article  PubMed  Google Scholar 

  49. Popli, S. et al. Involvement of renal allograft by Fabry's disease. Am. J. Nephrol. 7, 316–318 (1987).

    Article  CAS  PubMed  Google Scholar 

  50. Loirat, C. & Niaudet, P. The risk of recurrence of hemolytic uremic syndrome after renal transplantation in children. Pediatr. Nephrol. 18, 1095–1101 (2003).

    Article  PubMed  Google Scholar 

  51. Bresin, E. et al. Outcome of renal transplantation in patients with non-Shiga toxin-associated hemolytic uremic syndrome: prognostic significance of genetic background. Clin. J. Am. Soc. Nephrol. 1, 88–99 (2006).

    Article  CAS  PubMed  Google Scholar 

  52. Noris, M. & Remuzzi, G. Atypical hemolytic-uremic syndrome. N. Engl. J. Med. 361, 1676–1687 (2009).

    Article  CAS  PubMed  Google Scholar 

  53. Caprioli, J. et al. Genetics of HUS: the impact of MCP, CFH, and IF mutations on clinical presentation, response to treatment, and outcome. Blood 108, 1267–1279 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  54. Neumann, H. P. et al. Haemolytic uraemic syndrome and mutations of the factor H gene: a registry-based study of German speaking countries. J. Med. Genet. 40, 676–681 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  55. Sellier-Leclerc, A. L. et al. Differential impact of complement mutations on clinical characteristics in atypical hemolytic uremic syndrome. J. Am. Soc. Nephrol. 18, 2392–2400 (2007).

    Article  CAS  PubMed  Google Scholar 

  56. Loirat, C. & Fremeaux-Bacchi, V. Hemolytic uremic syndrome recurrence after renal transplantation. Pediatr. Transplant. 12, 619–629 (2008).

    Article  CAS  PubMed  Google Scholar 

  57. Le Quintrec, M. et al. Complement mutation-associated de novo thrombotic microangiopathy following kidney transplantation. Am. J. Transplant. 8, 1694–1701 (2008).

    Article  CAS  PubMed  Google Scholar 

  58. Kavanagh, D. et al. Mutations in complement factor I predispose to development of atypical hemolytic uremic syndrome. J. Am. Soc. Nephrol. 16, 2150–2155 (2005).

    Article  CAS  PubMed  Google Scholar 

  59. Saland, J. M., Ruggenenti, P. & Remuzzi, G. Liver-kidney transplantation to cure atypical hemolytic uremic syndrome. J. Am. Soc. Nephrol. 20, 940–949 (2009).

    Article  CAS  PubMed  Google Scholar 

  60. Fremeaux-Bacchi, V. et al. Genetic and functional analyses of membrane cofactor protein (CD46) mutations in atypical hemolytic uremic syndrome. J. Am. Soc. Nephrol. 17, 2017–2025 (2006).

    Article  CAS  PubMed  Google Scholar 

  61. Richards, A. et al. Mutations in human complement regulator, membrane cofactor protein (CD46), predispose to development of familial hemolytic uremic syndrome. Proc. Natl Acad. Sci. USA 100, 12966–12971 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  62. Chan, M. R. et al. Recurrent atypical hemolytic uremic syndrome associated with factor I mutation in a living related renal transplant recipient. Am. J. Kidney Dis. 53, 321–326 (2009).

    Article  CAS  PubMed  Google Scholar 

  63. Levy, M. & Feingold, J. Estimating prevalence in single-gene kidney diseases progressing to renal failure. Kidney Int. 58, 925–943 (2000).

    Article  CAS  PubMed  Google Scholar 

  64. Latta, K. & Brodehl, J. Primary hyperoxaluria type I. Eur. J. Pediatr. 149, 518–522 (1990).

    Article  CAS  PubMed  Google Scholar 

  65. Amoroso, A. et al. AGXT gene mutations and their influence on clinical heterogeneity of type 1 primary hyperoxaluria. J. Am. Soc. Nephrol. 12, 2072–2079 (2001).

    CAS  PubMed  Google Scholar 

  66. Watts, R. W. Primary hyperoxaluria type I. QJM 87, 593–600 (1994).

    CAS  PubMed  Google Scholar 

  67. Brinkert, F. et al. Transplantation procedures in children with primary hyperoxaluria type 1: outcome and longitudinal growth. Transplantation 87, 1415–1421 (2009).

    Article  PubMed  Google Scholar 

  68. Millan, M. T. et al. One hundred percent patient and kidney allograft survival with simultaneous liver and kidney transplantation in infants with primary hyperoxaluria: a single-center experience. Transplantation 76, 1458–1463 (2003).

    Article  PubMed  Google Scholar 

  69. Saborio, P. & Scheinman, J. I. Transplantation for primary hyperoxaluria in the United States. Kidney Int. 56, 1094–1100 (1999).

    Article  CAS  PubMed  Google Scholar 

  70. Cochat, P. & Scharer, K. Should liver transplantation be performed before advanced renal insufficiency in primary hyperoxaluria type 1? Pediatr. Nephrol. 7, 212–218 (1993).

    Article  CAS  PubMed  Google Scholar 

  71. Gruessner, R. W. Preemptive liver transplantation from a living related donor for primary hyperoxaluria type I. N. Engl. J. Med. 338, 1924 (1998).

    Article  CAS  PubMed  Google Scholar 

  72. Monico, C. G., Rossetti, S., Olson, J. B. & Milliner, D. S. Pyridoxine effect in type I primary hyperoxaluria is associated with the most common mutant allele. Kidney Int. 67, 1704–1709 (2005).

    Article  CAS  PubMed  Google Scholar 

  73. van Woerden, C. S. et al. Clinical implications of mutation analysis in primary hyperoxaluria type 1. Kidney Int. 66, 746–752 (2004).

    Article  CAS  PubMed  Google Scholar 

  74. Scheinman, J. I., Najarian, J. S. & Mauer, S. M. Successful strategies for renal transplantation in primary oxalosis. Kidney Int. 25, 804–811 (1984).

    Article  CAS  PubMed  Google Scholar 

  75. Astarcioglu, I. et al. Primary hyperoxaluria: simultaneous combined liver and kidney transplantation from a living related donor. Liver Transpl. 9, 433–436 (2003).

    Article  PubMed  Google Scholar 

  76. Rosenblatt, G. S., Jenkins, R. D. & Barry, J. M. Treatment of primary hyperoxaluria type 1 with sequential liver and kidney transplants from the same living donor. Urology 68, 427.e7–427.e8 (2006).

    Article  Google Scholar 

  77. Jungraithmayr, T. C. et al. Primary focal segmental glomerulosclerosis—long-term outcome after pediatric renal transplantation. Pediatr. Transplant. 9, 226–231 (2005).

    Article  PubMed  Google Scholar 

  78. Cameron, J. S. Recurrent primary disease and de novo nephritis following renal transplantation. Pediatr. Nephrol. 5, 412–421 (1991).

    Article  CAS  PubMed  Google Scholar 

  79. Habib, R., Hebert, D., Gagnadoux, M. F. & Broyer, M. Transplantation in idiopathic nephrosis. Transplant. Proc. 14, 489–495 (1982).

    CAS  PubMed  Google Scholar 

  80. Ramos, E. L. & Tisher, C. C. Recurrent diseases in the kidney transplant. Am. J. Kidney Dis. 24, 142–154 (1994).

    Article  CAS  PubMed  Google Scholar 

  81. Striegel, J. E., Sibley, R. K., Fryd, D. S. & Mauer, S. M. Recurrence of focal segmental sclerosis in children following renal transplantation. Kidney Int. Suppl. 19, S44–S50 (1986).

    CAS  PubMed  Google Scholar 

  82. Niaudet, P. Genetic forms of nephrotic syndrome. Pediatr. Nephrol. 19, 1313–1318 (2004).

    Article  PubMed  Google Scholar 

  83. Weber, S. et al. NPHS2 mutation analysis shows genetic heterogeneity of steroid-resistant nephrotic syndrome and low post-transplant recurrence. Kidney Int. 66, 571–579 (2004).

    Article  CAS  PubMed  Google Scholar 

  84. Boute, N. et al. NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome. Nat. Genet. 24, 349–354 (2000).

    Article  CAS  PubMed  Google Scholar 

  85. Caridi, G. et al. Prevalence, genetics, and clinical features of patients carrying podocin mutations in steroid-resistant nonfamilial focal segmental glomerulosclerosis. J. Am. Soc. Nephrol. 12, 2742–2746 (2001).

    CAS  PubMed  Google Scholar 

  86. Becker-Cohen, R. et al. Recurrent nephrotic syndrome in homozygous truncating NPHS2 mutation is not due to anti-podocin antibodies. Am. J. Transplant. 7, 256–260 (2007).

    Article  CAS  PubMed  Google Scholar 

  87. Bertelli, R. et al. Recurrence of focal segmental glomerulosclerosis after renal transplantation in patients with mutations of podocin. Am. J. Kidney Dis. 41, 1314–1321 (2003).

    Article  CAS  PubMed  Google Scholar 

  88. Billing, H. et al. NPHS2 mutation associated with recurrence of proteinuria after transplantation. Pediatr. Nephrol. 19, 561–564 (2004).

    Article  PubMed  Google Scholar 

  89. Höcker, B. et al. Recurrence of proteinuria 10 years post-transplant in NPHS2-associated focal segmental glomerulosclerosis after conversion from cyclosporin A to sirolimus. Pediatr. Nephrol. 21, 1476–1479 (2006).

    Article  PubMed  Google Scholar 

  90. Ruf, R. G. et al. Patients with mutations in NPHS2 (podocin) do not respond to standard steroid treatment of nephrotic syndrome. J. Am. Soc. Nephrol. 15, 722–732 (2004).

    Article  PubMed  Google Scholar 

  91. Machuca, E. et al. Clinical and epidemiological assessment of steroid-resistant nephrotic syndrome associated with the NPHS2 R229Q variant. Kidney Int. 75, 727–735 (2009).

    Article  CAS  PubMed  Google Scholar 

  92. Tsukaguchi, H. et al. NPHS2 mutations in late-onset focal segmental glomerulosclerosis: R229Q is a common disease-associated allele. J. Clin. Invest. 110, 1659–1666 (2002).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Niaudet, P. Living donor kidney transplantation in patients with hereditary nephropathies. Nat Rev Nephrol 6, 736–743 (2010). https://doi.org/10.1038/nrneph.2010.122

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