Renal Alterations Secondary to Visceral Leishmaniasis: A Scoping Review.

Abstract

Background: Visceral leishmaniasis (VL) is an endemic and neglected disease in several countries. In addition to affecting the visceral tissues, kidney alterations are recurrent and result from the pathophysiological implications of infection or drug action during treatment. This review mapped and described renal changes, renal biomarkers, and treatment-related nephrotoxicity in humans with confirmed VL.

Methods: This scoping review was conducted in accordance with the Joanna Briggs Institute Manual for Evidence Synthesis and the PRISMA-ScR guidelines. PubMed, SciELO, ScienceDirect, Scopus, and Web of Science. were searched with no temporal or geographical restrictions. We included studies involving humans with confirmed VL that reported renal alterations, kidney injury biomarkers, or treatment-related nephrotoxicity. Two reviewers independently screened the records and extracted data. Study selection was documented using the PRISMA-ScR flowchart.

Results: In total, 1,444 studies were identified, of which 15 met the eligibility criteria. The included studies reported a wide spectrum of renal alterations in VL, including urinary abnormalities, kidney injury biomarkers, and acute kidney injury. Glomerular and tubulointerstitial changes, such as mesangial alterations, membranoproliferative patterns, cryoglobulinemia, interstitial nephritis, and impaired urinary concentrating ability, have also been described. Reports have also addressed the potential treatment-related nephrotoxicity.

Conclusion: This scoping review identified diverse renal alterations in patients with VL, ranging from functional changes and urinary abnormalities to glomerular and tubulointerstitial involvement. Evidence has also described biomarkers of kidney injury and potential treatment-related nephrotoxicity. The heterogeneity and limited data highlight the need for robust research to clarify the underlying mechanisms, diagnostic markers, and optimal management.