HIV-associated Immune Complex Kidney Disease with C3-dominant Deposition Induced by HIV Infection after Treatment of IgA Nephropathy

Abstract

A 57-year-old man was diagnosed with IgA nephropathy. Hematuria and proteinuria were improved by tonsillectomy plus methylprednisolone pulse therapy. Lymphadenopathy, hypocomplementemia and pancytopenia were observed six years later, and urinalysis abnormalities recurred. A biopsy revealed mesangial proliferative glomerulonephritis with C3-dominant deposition. Human immunodeficiency virus (HIV) antibody demonstrated positive conversion. He was diagnosed with HIV-associated immune complex kidney disease (HIVICK). The hematuria, proteinuria and hypocomplementemia were improved by reducing the HIV viral load through antiretroviral therapy. When C3-dominant deposition is observed on a renal biopsy, HIVICK must be differentiated.

Catechins: Therapeutic Perspectives in COVID-19-Associated Acute Kidney Injury

“…The viral invasion of renal tissue has been described as an important mechanism for the development of virus-associated kidney injury [ 126 , 127 ]. The detection of viral particles in urine and the absence of CD4+ and CD8+ T cells in kidney tissue for a long time after initial viral infection suggest that immune cells are not recruited to infected renal tissue as a viral strategy to establish persistent infection [ 128 , 129 , 130 ]. RAAS has also been shown to play a key role in renal dysfunctional and AKI [ 131 ].…”

Mechanistic Aspects and Therapeutic Potential of Quercetin against COVID-19-Associated Acute Kidney Injury

“…The pathological mechanisms behind virus-associated kidney injury manifestations are either immune complex deposition or immune reactions resulting in glomerular membrane proliferation, based on severe coagulopathy, endothelial damage, and increased vascular permeability [70,74,75]. Massive releases of myoglobin-, cytokine-, and humoral factor-mediated acute interstitial nephritis play an important role in many viral infections [67,76].…”

“…One relevant aspect in the incidence and outcome of AKI in viral infection is the presence of comorbidities and coinfection, particularly in those patients with a longer ICU stay and/or immunodeficiency [77,78]. In this context, HIV-infected patients may be predisposed to acquiring new viral coinfections added to HIV-associated nephropathy (HIVAN), immune complex kidney disease, thrombotic microangiopathy, and drug-related injury [75]. Thus, the kidney diseases found in HIV patients, such as immunotactoid glomerulopathy and fibrillary glomerulonephritis, are usually more severe and complex than other virus-associated kidney injuries [79].…”

“…An important feature of virus-associated kidney injury is the presence of virus in the urine for long periods after initial infection [80]. Considering that neither CD4+ nor CD8+ T cells are detected in the kidney, even after a long period of viral infection, increasing evidence that virus can infect renal tubules without the recruitment of immune cells as a viral strategy for persistent survival has been reported [54,75,79]. Ou et al [80] investigated the replication strategies and immune responses of kidney caused by the duck hepatitis A virus (DHAV) up to 280 days after virus infection.…”

Kidney damage in HIV infection: pathogenetic aspects, clinical and morphological variants and the role of antiretroviral therapy

“…По данным ряда исследователей, иммуноглобулин А-нефропатия при ВИЧ-инфекции протекает латентно с минимальными изменениями мочевого осадка [18]. Взаимосвязь иммуноглобулин А-нефропатии с ВИЧ была подтверждена наличием в крови и почечной ткани больных иммунных комплексов с антигенами ВИЧ [49,50]. Имеются сведения, что своевременная диагностика и адекватная АРТ значительно снижают риски прогрессирования ВИЧ-АБП [51].…”