Renal tubular dysfunction in human visceral leishmaniasis (Kala-azar)

Verde, Francisco Agenor Araújo Lima; Verde, Frederico Araújo Lima; Daher, Elizabeth De Francesco; Santos, Gustavo Martins dos; Neto, Augusto Saboia; Verde, Eduardo

doi:10.5414/cnp71492

Cited by 24 publications

(10 citation statements)

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“…The peak of his serum IgG level was above 100 g/L, mainly consisting of IgG1. Similar findings were observed in patients with visceral leishmaniasis [4,12]. A mice experiment suggested that the extremely high IgG might be caused by endosomal Toll-like receptor activation [13].…”

Section: Discussionsupporting

confidence: 76%

“…However, understandings of kidney involvement are still limited. Clinical observation revealed acute kidney injury [3] and renal tubular dysfunction [4]. Pathologically, both glomerulonephritis [5] and interstitial nephritis [6] have been reported.…”

Section: Discussionmentioning

confidence: 99%

“…This might suggest that proximal tubular injury happens without clinical significance. A case series of visceral Leishmaniasis reported clinical presentations of proximal tubular damage with alteration in low-molecule protein, glucose, and uric acid reabsorption [4]. Another leishmaniasis case series reported elevated kidney injury molecule-1, a proximal tubule injury biomarker [3].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2021

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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.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

et al. 2021

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“…In humans with VL, several clinical signs of renal involvement have been described. In addition to acute kidney injury (AKI), urinary abnormalities, such as oliguria, proteinuria, hematuria, pyuria 6 , 48 – 50 , tubulointerstitial nephritis, and GN were described in patients with VL 49 – 56 . A prospective study demonstrated that approximately 60% of hospitalized patients with VL presented evidence of mild renal impairment.…”

Section: Introductionmentioning

confidence: 99%

“…Cystatin C has been considered a better marker of renal function due to its heightened levels in the early stages of AKI than other relevant markers 61 – 63 . Other studies reported a decrease in glomerular filtration rate (GFR) in patients with chronic VL, a phenomenon attributed to factors such as fluid loss, hypotension, and immunological glomerular disease 64 . Furthermore, proteinuria described in patients with VL predominantly consisted of low molecular weight protein fractions that migrated alongside gamma globulins 56 .…”

Section: Introductionmentioning

confidence: 99%

A link between circulating immune complexes and acute kidney injury in human visceral leishmaniasis

Corrêa-Castro,

Silva-Freitas,

de Paula

et al. 2024

Sci Rep

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Visceral leishmaniasis (VL) is an infectious disease caused by Leishmania infantum. Clinically, VL evolves with systemic impairment, immunosuppression and hyperactivation with hypergammaglobulinemia. Although renal involvement has been recognized, a dearth of understanding about the underlying mechanisms driving acute kidney injury (AKI) in VL remains. We aimed to evaluate the involvement of immunoglobulins (Igs) and immune complexes (CIC) in the occurrence of AKI in VL patients. Fourteen VL patients were evaluated between early treatment and 12 months post-treatment (mpt). Anti-Leishmania Igs, CIC, cystatin C, C3a and C5a were assessed and correlated with AKI markers. Interestingly, high levels of CIC were observed in VL patients up to 6 mpt. Concomitantly, twelve patients met the criteria for AKI, while high levels of cystatin C were observed up to 6 mpt. Plasmatic cystatin C was positively correlated with CIC and Igs. Moreover, C5a was correlated with cystatin C, CIC and Igs. We did not identify any correlation between amphotericin B use and kidney function markers in VL patients, although this association needs to be further explored in subsequent studies. Our data reinforce the presence of an important renal function impairment during VL, suggesting the involvement of Igs, CIC, and C5a in this clinical condition.

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