Acute Renal Failure on Immune Reconstitution in an HIV‐Positive Patient with Miliary Tuberculosis

Abstract

Immune reconstitution syndrome following HAART in human immunodeficiency virus (HIV)-infected patients is characterized by inflammatory worsening of organ functions despite improvement in HIV surrogate markers of HIV infection. We describe a patient with miliary tuberculosis and urinary shedding of acid fast bacilli who developed acute renal failure 8 weeks after initiation of antituberculosis therapy and 6 weeks after initiation of HAART. The diagnostic workup and further course of disease implicated immune reconstitution syndrome as the cause of acute renal failure.

Histological Patterns of Polyomavirus Nephropathy: Correlation with Graft Outcome and Viral Load

“…secondary to tubular injury). Excessive tissue destruction may occur once the immune system recovers its capabilities (immune reconstitution response) (28,(33)(34)(35). Irrespective of the underlying etiopathogenesis, florid inflammatory responses in PVAN are often associated with parenchymal fibrosis (scarring) (9,29).…”

Immune reconstitution inflammatory syndrome (IRIS): review of common infectious manifestations and treatment options

“…The most frequently reported IRIS symptoms in response to previously treated or partially treated infections include reports of clinical worsening and recurrence of clinical manifestations of Mycobacterium tuberculosis (TB) and cryptococcal meningitis following initiation of ART [6,7,10,13,16,[25][26][27][28]. In noninfectious causes of IRIS, autoimmunity to innate antigens plays a likely role in the syndrome.…”

“…In most studies, TB-IRIS occurs within two months of ART initiation [6,7,10,11,25,35,45,48]. Among 43 cases of MTB-associated IRIS, the median onset of IRIS was 12-15 days (range 2-114 days), with only four of these cases occurring more than four weeks after the initiation of antiretroviral therapy [7,10,25,26,30].…”

“…In these patients, clinical deterioration occurs despite increased CD4 + Tlymphocyte counts and decreased plasma HIV-1 viral loads [4]. This clinical deterioration is a result of an inflammatory response or "dysregulation" of the immune system to both intact subclinical pathogens and residual antigens [5][6][7][8][9]. Resulting clinical manifestations of this syndrome are diverse and depend on the infectious or noninfectious agent involved.…”

“…Resulting clinical manifestations of this syndrome are diverse and depend on the infectious or noninfectious agent involved. These manifestations include mycobacterial-induced lymphadenitis [5], paradoxical tuberculosis reactions [6,7,10,11], worsening of progressive multifocal leukoencephalopathy (PML) [12], recurrence of cryptococcosis and Pneumocystis jirovecii pneumonia (PCP) [8,[13][14][15][16], Cytomegalovirus (CMV) retinitis [17], shingles [18], and viral hepatitis [19], as well as noninfectious phenomena [20].…”