Abstract Introduction HIV-associated nephropathy (HIVAN) and COVID-19-associated nephropathy (COVAN) are linked to APOL1 high-risk alleles (G1, G2) on chromosome 22q12, which greatly increase susceptibility to collapsing focal segmental glomerulosclerosis (cFSGS) and end-stage renal disease (ESRD), especially among African Americans (2,3,5,7). HIVAN involves direct HIV infection of renal cells, microcystic tubular changes, and advanced immunosuppression, resulting in an approximately 30-fold increased risk of progressing to ESRD if untreated (2,3,5,7,8,9,10). Antiretroviral therapy (ART) is essential and slows progression (3). In contrast, COVAN follows a “two-hit” model involving genetic predisposition and an inflammatory response to SARS-CoV-2 without direct kidney infection (7,10). Both cause acute kidney injury (AKI) and proteinuria but differ in mechanism and pathology (2,4,5,6,7). This report describes a 40-year-old male misdiagnosed with COVAN, later found to have HIVAN with AIDS and ESRD. Case In June 2025, a 40-year-old man with CKD stage G5/A3 was hospitalized for a hemorrhoidal bleed and developed acute renal failure (creatinine 5.95). Despite nephrology intervention, renal function worsened, prompting transplant evaluation. Genetic testing showed APOL1 G1/G1 high-risk alleles, and COVAN was suspected due to prior COVID-19 infection. During the workup, he tested positive for HIV, making him ineligible for transplant. In August, he presented with pneumonia, ESRD (creatinine 18.18), anemia, and electrolyte abnormalities requiring hemodialysis. PCR confirmed HIV-1 with a CD4 count of 1 cells/ul and PCP pneumonia. After starting ART and MAC prophylaxis, his pneumonia resolved, and he was discharged on scheduled dialysis. Discussion Distinguishing HIVAN from COVAN is challenging, particularly without biopsy. Anchoring bias—when clinicians fixate on an initial diagnosis despite new evidence—played a key role (13). The patient was labeled as having COVAN despite a COVID-19 infection three years earlier, positive HIV testing, AIDS-defining illness (PCP pneumonia), and APOL1 high-risk alleles, findings consistent with HIVAN. Literature supports that COVAN usually follows recent COVID-19 infection and can show renal recovery, unlike HIVAN (2,4,5,6,7). Given the patient’s HIV-1 infection, CD4 count of 1, APOL1 mutations, and renal failure requiring hemodialysis, this presentation aligns with HIVAN, demonstrating diagnostic anchoring. Conclusion This case describes a 40-year-old male initially misdiagnosed with COVAN but later found to have AIDS, PCP pneumonia, and ESRD requiring dialysis. After starting ART, MAC prophylaxis, and hemodialysis, he improved and was discharged. The case underscores anchoring bias and highlights the need for biopsy or miR193a urine testing in suspected HIVAN for early diagnosis and transplant referral. This abstract is funded by: None
Uhlen et al. (Fri,) studied this question.