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Published in: BMC Infectious Diseases 1/2021

Open Access 01-12-2021 | Kidney Injury | Case report

Continuous hypergammaglobulinemia and proteinuria after the recovery of the visceral Leishmaniasis: a case report

Authors: Linfeng Zou, Gang Chen, Yangzhong Zhou, Wei Ye, Yubin Wen, Limeng Chen, Xuemei Li

Published in: BMC Infectious Diseases | Issue 1/2021

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Abstract

Background

Kidney involvement of visceral Leishmaniasis is previously reported, but knowledge is limited. Hypergammaglobulinemia is common in visceral leishmaniasis patients. Whether hypergammaglobulinemia after leishmaniasis depletion can cause kidney injury is not well reported yet.

Case presentation

We reported a patient who recovered from visceral Leishmaniasis but showed persistent hypergammaglobulinemia and elevated urinary protein. Kidney biopsy showed glomerular hypertrophy with mild segmental mesangial proliferation without tubulointerstitial involvement in light microscopy. No immune complex deposit was found in the mesangial area by neither immunofluorescent staining nor electronic microscope. Increased lysosomes were observed in proximal tubules by electronic microscope. Valsartan was administered to decrease urinary protein, and no immune-suppressive therapy was added. The urinary protein and serum IgG level gradually dropped, and serum creatinine level remained stable during three- month follow up.

Conclusions

Hypergammaglobulinemia is unlikely to cause renal structural or functional damage in the short term. Angiotensin blockade significantly reduced urine protein, with a minor effect on IgG elimination.
Literature
1.
go back to reference WHO Expert Committee on the Control of the Leishmaniases & World Health Organization: Control of the leishmaniases: report of a meeting of the WHO Expert Committee on the Control of Leishmaniases. Geneva: World Health Organization; 2010. WHO Expert Committee on the Control of the Leishmaniases & World Health Organization: Control of the leishmaniases: report of a meeting of the WHO Expert Committee on the Control of Leishmaniases. Geneva: World Health Organization; 2010.
2.
go back to reference Shamsian S, et al. Clinical and Laboratory Findings of Visceral Leishmaniasis in Children Hospitalized in Mashhad, Northeastern Iran: A Twenty-Year Retrospective Study. Iran J Parasitol. 2020;15(4):495–9. Shamsian S, et al. Clinical and Laboratory Findings of Visceral Leishmaniasis in Children Hospitalized in Mashhad, Northeastern Iran: A Twenty-Year Retrospective Study. Iran J Parasitol. 2020;15(4):495–9.
3.
go back to reference Meneses GC, et al. Visceral leishmaniasis-associated nephropathy in hospitalised Brazilian patients: new insights based on kidney injury biomarkers. Tropical Med Int Health. 2018;23(10):1046–57.CrossRef Meneses GC, et al. Visceral leishmaniasis-associated nephropathy in hospitalised Brazilian patients: new insights based on kidney injury biomarkers. Tropical Med Int Health. 2018;23(10):1046–57.CrossRef
4.
go back to reference Verde FAAL, et al. Renal tubular dysfunction in human visceral Leishmaniasis (Kala-azar). Clin Nephrol. 2009;71(5):492–500.CrossRef Verde FAAL, et al. Renal tubular dysfunction in human visceral Leishmaniasis (Kala-azar). Clin Nephrol. 2009;71(5):492–500.CrossRef
5.
go back to reference Ortiz M, et al. Glomerulonephritis and cryoglobulinemia: first manifestation of visceral Leishmaniasis. Clin Nephrol. 2015;83(6):370–7.CrossRef Ortiz M, et al. Glomerulonephritis and cryoglobulinemia: first manifestation of visceral Leishmaniasis. Clin Nephrol. 2015;83(6):370–7.CrossRef
6.
go back to reference Duarte MI, et al. Interstitial nephritis in human kala-azar. Trans R Soc Trop Med Hyg. 1983;77(4):531–7.CrossRef Duarte MI, et al. Interstitial nephritis in human kala-azar. Trans R Soc Trop Med Hyg. 1983;77(4):531–7.CrossRef
7.
go back to reference Dutra M, et al. Renal involvement in visceral Leishmaniasis. Am J Kidney Dis. 1985;6(1):22–7.CrossRef Dutra M, et al. Renal involvement in visceral Leishmaniasis. Am J Kidney Dis. 1985;6(1):22–7.CrossRef
8.
go back to reference Chaigne V, et al. A patient with visceral Leishmaniasis and acute renal failure in necrotizing glomerulonephritis. Nephrologie. 2004;25(5):179–83.PubMed Chaigne V, et al. A patient with visceral Leishmaniasis and acute renal failure in necrotizing glomerulonephritis. Nephrologie. 2004;25(5):179–83.PubMed
9.
go back to reference Enríquez R, et al. Membranoproliferative glomerulonephritis due to visceral leishmaniasis in an HIV patient. Am J Case Rep. 2015;16:8–11.CrossRef Enríquez R, et al. Membranoproliferative glomerulonephritis due to visceral leishmaniasis in an HIV patient. Am J Case Rep. 2015;16:8–11.CrossRef
10.
go back to reference Alex S, et al. Nephrotic syndrome complicating chronic visceral Leishmaniasis: re-emergence in patients with AIDS. Clin Nephrol. 2008;70(1):65–8.PubMed Alex S, et al. Nephrotic syndrome complicating chronic visceral Leishmaniasis: re-emergence in patients with AIDS. Clin Nephrol. 2008;70(1):65–8.PubMed
11.
go back to reference Olliaro PL, et al. Treatment options for visceral Leishmaniasis: a systematic review of clinical studies done in India, 1980-2004. Lancet Infect Dis. 2005;5(12):763–74.CrossRef Olliaro PL, et al. Treatment options for visceral Leishmaniasis: a systematic review of clinical studies done in India, 1980-2004. Lancet Infect Dis. 2005;5(12):763–74.CrossRef
12.
go back to reference Makaritsis KP, et al. Polyclonal hypergammaglobulinemia and high smooth-muscle autoantibody titers with specificity against filamentous actin: consider visceral Leishmaniasis, not just autoimmune hepatitis. Int J Infect Dis. 2009;13(4):e157–60.CrossRef Makaritsis KP, et al. Polyclonal hypergammaglobulinemia and high smooth-muscle autoantibody titers with specificity against filamentous actin: consider visceral Leishmaniasis, not just autoimmune hepatitis. Int J Infect Dis. 2009;13(4):e157–60.CrossRef
13.
go back to reference Silva-Barrios S, et al. Innate immune B cell activation by Leishmania donovani exacerbates disease and mediates Hypergammaglobulinemia. Cell Rep. 2016;15(11):2427–37.CrossRef Silva-Barrios S, et al. Innate immune B cell activation by Leishmania donovani exacerbates disease and mediates Hypergammaglobulinemia. Cell Rep. 2016;15(11):2427–37.CrossRef
14.
go back to reference Sartori A, et al. Immune complex glomerulonephritis in experimental kala-azar. II: detection and characterization of parasite antigens and antibodies eluted from kidneys of Leishmania donovani-infected hamsters. Clin Exp Immunol. 1992;87(3):386–92.CrossRef Sartori A, et al. Immune complex glomerulonephritis in experimental kala-azar. II: detection and characterization of parasite antigens and antibodies eluted from kidneys of Leishmania donovani-infected hamsters. Clin Exp Immunol. 1992;87(3):386–92.CrossRef
15.
go back to reference Galle J. Reduction of proteinuria with angiotensin receptor blockers. Nat Clin Pract Cardiovasc Med. 2008;5(Suppl 1):S36–43.CrossRef Galle J. Reduction of proteinuria with angiotensin receptor blockers. Nat Clin Pract Cardiovasc Med. 2008;5(Suppl 1):S36–43.CrossRef
16.
go back to reference Ryman JT, Meibohm B. Pharmacokinetics of monoclonal antibodies. CPT Pharmacometrics Syst Pharmacol. 2017;6(9):576–88.CrossRef Ryman JT, Meibohm B. Pharmacokinetics of monoclonal antibodies. CPT Pharmacometrics Syst Pharmacol. 2017;6(9):576–88.CrossRef
17.
go back to reference Tabrizi MA, Tseng CM, Roskos LK. Elimination mechanisms of therapeutic monoclonal antibodies. Drug Discov Today. 2006;11(1–2):81–8.CrossRef Tabrizi MA, Tseng CM, Roskos LK. Elimination mechanisms of therapeutic monoclonal antibodies. Drug Discov Today. 2006;11(1–2):81–8.CrossRef
18.
go back to reference Waldmann TA, Strober W, Mogielnicki RP. The renal handling of low molecular weight proteins. II. Disorders of serum protein catabolism in patients with tubular proteinuria, the nephrotic syndrome, or uremia. J Clin Invest. 1972;51(8):2162–74.CrossRef Waldmann TA, Strober W, Mogielnicki RP. The renal handling of low molecular weight proteins. II. Disorders of serum protein catabolism in patients with tubular proteinuria, the nephrotic syndrome, or uremia. J Clin Invest. 1972;51(8):2162–74.CrossRef
19.
go back to reference Zoja C, et al. Protein overload stimulates RANTES production by proximal tubular cells depending on NF-kappa B activation. Kidney Int. 1998;53(6):1608–15.CrossRef Zoja C, et al. Protein overload stimulates RANTES production by proximal tubular cells depending on NF-kappa B activation. Kidney Int. 1998;53(6):1608–15.CrossRef
20.
go back to reference Daher EF, et al. Renal function improvement with pentavalent antimonial agents in patients with visceral Leishmaniasis. Am J Nephrol. 2011;33(4):332–6.CrossRef Daher EF, et al. Renal function improvement with pentavalent antimonial agents in patients with visceral Leishmaniasis. Am J Nephrol. 2011;33(4):332–6.CrossRef
Metadata
Title
Continuous hypergammaglobulinemia and proteinuria after the recovery of the visceral Leishmaniasis: a case report
Authors
Linfeng Zou
Gang Chen
Yangzhong Zhou
Wei Ye
Yubin Wen
Limeng Chen
Xuemei Li
Publication date
01-12-2021
Publisher
BioMed Central
Published in
BMC Infectious Diseases / Issue 1/2021
Electronic ISSN: 1471-2334
DOI
https://doi.org/10.1186/s12879-021-05819-z

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