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The role of paraproteins in kidney damage in patients with lymphoproliferative diseases

https://doi.org/10.17650/1818-8346-2019-14-3-60-68

Abstract

Background. The course of lymphoproliferative diseases, in which the proliferation of a malignant clone is accompanied by the secretion of paraproteins, is often complicated by kidney damage. Perhaps kidney damage is associated with the physicochemical properties of monoclonal proteins.

The objective of the study was to determine the relationship between the type of monoclonal paraprotein, its level of secretion, and kidney damage in lymphoproliferative diseases

Materials and methods. A retrospective analysis of the data of 108 patients with lymphoproliferative diseases accompanied by paraproteinemia and kidney damage was performed. The age of the patients was 31–86 years (median 62.5 years). 78 out of 108 patients were diagnosed with chronic kidney disease (CKD). CKD was diagnosed in accordance with the clinical guidelines of KDIGO 2012.

Results. In patients with multiple myeloma, stage III CKD was diagnosed in 28 (35.9 %) cases, stage IV – in 14 (17.9 %), stage V – in 19 (24.4 %). High risk group for CKD included 10 (9.3 %) of 30 patients without CKD. 91 patients were diagnosed with concomitant diseases predisposing to the development of kidney damage. In the group of patients with paraproteinemic hemoblastosis in combination with CKD, the vast majority were patients with the presence of IgGκ and IgGλ blood paraproteins, free light chains (FLC), and Bence-Jones protein (BJ) in the urine. At the same time, patients with the secretion of IgDλ, IgAλ, IgAκ and IgMκ paraproteins were much less common. The highest level of pathological Ig of all classes and their structural components and fragments was observed in patients with stage III CKD, which is also characteristic of other laboratory markers in CKD. A negative correlation of glomerular filtration rate (GFR) with FLCκ in the blood (r = –0.21), GFR with BJκ (r = –0.35), GFR with FLCλ in the blood (r = –0.13), GFR c BJλ, which indicates a tendency to damage the kidneys of FLC and protein BJ.

Conclusion. In patients with lymphoproliferative diseases accompanied by monoclonal secretion of paraprotein and kidney damage with the development of CKD, in most cases IgGκ, IgGλ, FLCκ and FLCλ were determined in the blood, and protein BJ in urine. IgAκ, IgAλ, IgMκ, IgMλ, IgDλ paraproteins were determined much less frequently in serum. The highest level of pathological Ig and their structural components was observed in patients with stage III CKD. No association with quantitative level, type of paraprotein, and kidney damage was found. The role of FLC and BJ protein in the development of nephropathy is noted. The results of the study also show that with the development of the disease and kidney damage with subsequent progression of the stage of CKD in patients with lymphoproliferative diseases and proteinemia, there is a tendency to a temporary decrease in proteinuria and a compensatory increase in the number of paraproteins in the blood. This can be considered as one of the compensatory pathophysiological mechanisms of the protective function of the kidneys.

About the Authors

O. N. Pysarevskaya
N.N. Burdenko Main Military Clinical Hospital
Russian Federation

3 Gospital’naya Ploshchad’, Moscow 105094



A. N. Kotelnikova
N.N. Burdenko Main Military Clinical Hospital
Russian Federation

3 Gospital’naya Ploshchad’, Moscow 105094



S. P. Kazakov
N.N. Burdenko Main Military Clinical Hospital
Russian Federation

3 Gospital’naya Ploshchad’, Moscow 105094



N. P. Potekhin
N.N. Burdenko Main Military Clinical Hospital
Russian Federation

3 Gospital’naya Ploshchad’, Moscow 105094



O. A. Rukavitsyn
N.N. Burdenko Main Military Clinical Hospital
Russian Federation

3 Gospital’naya Ploshchad’, Moscow 105094



References

1. Kolina I.B., Bobkova I.N. Renal damage with malignant neoplasms. Klinitsist = Clinician 2014;(2):7–16. (In Russ.).

2. Rukavitsin O.A. Hematology: National guidelines. Moscow: GEOTAR-Media, 2015. 784 p. (In Russ.).

3. Rekhtina I.G., Mendeleeva L.P., Biryukova L.S. Draft clinical guidelines for the diagnosis and treatment of myeloma nephropathy. 2014. P. 5. (In Russ.).

4. Jagannath S., Richardson P.G., Munshi N.C. Multiple myeloma and other plasma cell dyscrasias. Physicians Practice 2016:1–21. Available at: http://www.physicianspractice.com.

5. Hoffbrand V., Pettit J. Color Atlas of Clinical Hematology. Moscow: Praktika, 2007. 274 p. (In Russ.).

6. Heher E.C., Rennke H.G., Laubach J.P., Richardson P.G. Kidney disease and multiple myeloma. Clin J Am Nephrol 2013;8(11):2007–17. DOI: 10.2215/CJN.12231212.

7. Leung N., Nasr S. Myeloma-related kidney disease. Adv Chronic Kidney Dis 2014; 21(1):36–47. DOI: 10.1053/j.ackd.2013.08.009.

8. Zakharova E.V., Stolyarevich E.S. Renal consequences of lymphoproliferative disorders and monoclonal gammopathy. Urol Nephrol Open Access J 2015;2(4):00047. DOI: 10.15406/unoaj.2015.02.00047.

9. Landgren О., Kyle R.A., Pfeiffer R.M. et al. Monoclonal gammopathy of undetermined significance (MGUS) consistently precedes multiple myeloma: a prospective study. Blood 2009;113(22):5412–7. DOI: 10.1182/blood-2008-12-194241.

10. Weiss B.M., Abadie J., Verna P. et al. A monoclonal gammopathy precedes multiple myeloma in most patients. Blood 2009;113(22):5418–22. DOI: 10.1182/blood-2008-12-195008.

11. Kyle R.A. Monoclonal gammopathy of undetermined significance. Natural history in 241 cases. Am J Med 1978;64:814–26.

12. Kozlovskaya L.V., Rameev V.V., Kogarko I.N. et al. Renal lesions associated with monoclonal gammopathy of undetermined significance: clinical forms, development mechanisms, treatment approaches Klinicheskaya meditsina = Clinical Medicine 2016;94(12):892–901. (In Russ.). DOI http://dx.doi.org/10.1882110023-2149-2016-94-12-892901.

13. Leung N., Bridoux F., Hutchison C.A. et al. Monoclonal gammopathy of renal significans: when MGUS is no longer undetermined or insignificant. Blood 2012;120(22):4292–5.

14. Pop V.P., Rukavitsin O.A. Multiple myeloma and related diseases. 3rd ed., Revised. Moscow: GEOTAR-Media, 2016. 224 p. (In Russ.).

15. Kowalewska J., Nicosia R.F., Smith K.D. et al. Patterns of glomerular injury in kidneys infiltrated by lymphoplasmacytic neoplasms. Hum Pathol 2011;42(6):898–903. DOI: 10.1016/j.humpath.2010.09.009.

16. Dzhumabaeva B.T., Biryukova L.S., Varshavsky V.A. et al. Clinical, laboratory, and morphological characteristics of kidney damage in lymphoproliferative disorders. Onkogematologiya = Oncohematology 2017;12(1):44–54. (In Russ.). DOI: 10.17650/18188346-2017-12-1-44-54.

17. Lien Y.H., Lai L.W. Pathogenesis, diagnosis and management of paraneoplastic glomerulonephritis. Nat Rev Nephrology 2011;7(2):85–95. DOI: 10.1038/nrneph.2010.171.

18. Official Journal of the International Society of Nephrology. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Vol 3, issue 1. 2013. Available at: http://www.kidneyinternational.org/.

19. Shilov E.M., Shvetsov M.Yu. Chronic kidney disease and nephroprotective therapy. Physician guideline. Moscow, 2012. P. 9. (In Russ.).

20. Kazakov S.P., Skvortsov S.V., Zukova E.E. et al. Prognostic value of homocysteine in patients with chronic kidney disease. Clin Chem Lab Med 2017;55(Special Suppl):1347.

21. Zhukova E.E., Skvortsov S.V., Kazakov S.P. et al. The relationship between serum and urine homocysteine levels in patients with chronic kidney disease. Laboratornaya sluzhba = Laboratory Service 2017;6(3):162–3. (In Russ.).


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For citations:


Pysarevskaya O.N., Kotelnikova A.N., Kazakov S.P., Potekhin N.P., Rukavitsyn O.A. The role of paraproteins in kidney damage in patients with lymphoproliferative diseases. Oncohematology. 2019;14(3):60-68. (In Russ.) https://doi.org/10.17650/1818-8346-2019-14-3-60-68

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ISSN 1818-8346 (Print)
ISSN 2413-4023 (Online)