A RARE COINFECTION OF LEPTOSPIRA AND HEPATITIS A PRESENTING AS IMMUNE COMPLEX-MEDIATED GLOMERULONEPHRITIS

Infection-related glomerulonephritis (IRGN) is a form of immune complex-mediated kidney injury that typically follows bacterial infections, most notably by streptococci or staphylococci. Leptospira and Hepatitis A virus (HAV) are endemic pathogens known to cause systemic illness with hepatic and renal involvement, though their role in triggering IRGN is rare. We report a rare case of IRGN associated with coinfection by Leptospira and Hepatitis A virus in an immunocompetent adult, highlighting the importance of thorough infectious workup before initiating immunosuppressive therapy.

A 45-year-old male with no prior comorbidities presented with Jaundice, cola colored urine, decreased urine output, and new-onset hypertension for 20 days. He had a history of fever for five days initially. The patient was referred to our center for evaluation of worsening renal function and oliguria, having undergone five sessions of hemodialysis before referral. On arrival, he was afebrile with a blood pressure of 160/90 mmHg, icterus, and pedal edema. Initial investigations showed Hb 10g/dL, serum creatinine 3.23 mg/dL, AST 44 U/L, ALT 114 U/L, and Total/direct bilirubin 2.42/1.17mg/dL. Urine routine microscopy showed 2+ proteinuria with 20 to 50 RBCs. Urine Protein creatinine ratio (uPCR)was 2.8.  Serum C3 was low. His anti-nuclear antibody and anti-neutrophil cytoplasmic antibody were negative. Further workup showed negative serologies for Hepatitis B, C, and HIV with CRP of 80mg/dL and Procalcitonin of 0.7 ng/mL. Blood and urine cultures were negative. Tests for malaria parasites, dengue, scrub typhus, and hepatitis E were negative. Leptospira IgM and Hepatitis A IgM were positive with a titer of 13.9 units and a 5.43 S/CO ratio (Reactive), respectively. (Table 1)

Light microscopy of the kidney biopsy revealed enlarged glomeruli, characterized by diffuse mesangial and endocapillary hypercellularity, as well as neutrophil infiltration. Cellular crescent formation was noted over 3 glomeruli (12.5%). (Figure 01) Immunofluorescence study showed 2+/3+ intensity granular staining of mesangial and capillary walls by IgG, C3, kappa, and lambda light chains. (Figures 02 A/B) It was suggestive of an immune complex-mediated diffuse proliferative glomerulonephritis.

He was empirically treated with ceftriaxone and doxycycline with supportive treatment. There was a gradual improvement in renal and liver function and urine output without further dialysis. After 15 days, he had serum creatinine of 1.4 mg/dL, uPCR of 0.37, with normal urine output. Repeat serology of Leptospira IgM and Hepatitis A IgM were negative with a titer of 8.12 units and 0.17 S/CO ratio. The qualitative assay for Leptospira and Hepatitis A IgG was negative. At 6-month follow-up, he was normotensive with serum creatinine of 0.9 mg/dL and uPCR of 0.16.

This case emphasizes the need to consider IRGN in patients presenting with acute kidney injury and nephritic features in the setting of recent febrile illness. To our knowledge, coinfection with Leptospira and HAV causing IRGN in an adult has not been previously reported, making this a rare but important clinical observation. Whether these infections acted synergistically or sequentially to trigger glomerular injury is unclear. Our case expands the clinical spectrum of IRGN and highlights the importance of a thorough infectious workup before starting immunosuppression.