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Kidney injury is a significant complication of HIV infection. HIV-associated nephropathy (HIVAN) is the most commonly described form and one of the leading causes of end-stage renal disease in this population. Another form of renal involvement in HIV infection is related to glomerular deposition of immune complexes (HIVICK), which typically occurs after years of disease and can have varied renal manifestations depending on the extent and location of glomerular deposits.
The present study describes a young patient with immune complex renal disease as the initial manifestation of acute HIV infection.
CASE REPORT:
The patient, a 32-year-old male, sought medical attention due to uncontrolled blood pressure, dyspnea, progressive edema and a weight gain of 6 kg in the last 7 days. Previously overweight (BMI = 27.8), insulin-dependent type 1 diabetes diagnosed at 7 years old with adequate glycemic control and mild proteinuria, with no macrovascular complications. Also diagnosed with hypertension for the past 2 years with adequate control. Recent tests showed normal renal function, urine analysis with 1+ proteinuria and an albumin/creatinine ratio of 189 mg/g.
Admitted with hypertensive emergency and acute kidney injury. Admission laboratory results: Creatinine 2.6 mg/dL (CKD-EPI 32.6 mL/min/1.73m²), Urea 105 mg/dL, mild metabolic acidosis, no electrolyte imbalances, urine analysis with 3+ protein, no glucosuria, hematuria, or leukocyturia; non-nephrotic proteinuria (2.6g/24h); hemoglobin level indicating anemia – Hb 9.9 g/dL. Kidney ultrasound showed both normal size and good corticomedullary ratio.
HIV serology was reactive in the investigation despite a recent negative test. Viral load was 420 thousand copies with a CD4 cell count of 913/mm³. He presented with symptoms suggestive of acute HIV infection including persistent fever, low C-reactive protein and negative cultures during hospitalization. Rheumatological tests were negative, except for the consumption of complement C3 fraction. He rapidly progressed to worsening renal function, oliguria and severe acidosis, requiring the initiation of renal replacement therapy. A videolaparoscopic renal biopsy revealed findings suggestive of Diffuse Proliferative Glomerulonephritis (DPGN), awaiting immunofluorescence to characterize immune complex-mediated injury.
HLA-B57 testing was performed due to contraindication to Tenofovir use- considering severe renal dysfuction and suspected diagnosis of HIVICK. The decision was to initiate Abacavir, Lamivudine and Dolutegravir. Patient was discharged still anuric, undergoing regular hemodialysis with no signs of renal recovery.
Renal manifestations in HIV are multifactorial including factors such as injuries directly related to the viral infection, treatment-related nephrotoxicity, pre- and post-renal causes, comorbidities, pre-existing renal disease and coinfections. Immune complex-mediated lesions typically occur after years of illness, usually in patients with good disease control. There are no reported cases in the literature of HIVICK as the initial renal manifestation of acute HIV infection.