COVID-19 in an HIV-positive kidney transplant recipient.

We report a case of a 50-year-old male with a history of HIV and kidney transplant who presented with SARS-CoV-2. We also present a review of COVID-19 cases in kidney transplant recipients.

In sickness and in health: Living HIV positive kidney donation from a wife to her husband, with 7 years' post-transplant follow-up.

Human immunodeficiency virus (HIV) infection was traditionally considered an absolute contraindication for kidney transplantation. After the introduction of ART, several studies have demonstrated comparable patient and graft outcomes between HIV-negative and HIV-positive kidney recipients. The US Congress passed the HIV Organ Policy Equity (HOPE) Act in 2013, which permits research in the area of HIV-positive to HIV-positive transplantation. HIV-infected living donation is also permitted under the HOPE Act. However, there is a concern regarding the safety of kidney donation in an HIV-infected person, given the risk of renal disease associated with HIV infection. We report here the case of successful kidney transplantation from HIV-positive living donor to HIV-positive recipient performed in our center on July 2012. To the best of our knowledge, this is the earliest case done in this medical context to be reported in the literature, therefore, potentially carrying several important messages to the transplantation community. In the present case, the living-donor kidney transplant was performed between a married couple infected with same strain of HIV-1, both on effective ART with efficiently suppressed viral replication and satisfactory pre-transplantation immune status.

APOL1 Renal Risk Variants: Fertile Soil for HIV-Associated Nephropathy.

Apolipoprotein L1 (APOL1) genetic variants are potent risk factors for glomerular disease, but one or more additional factors are required for expression of glomerular disease. Uncontrolled or poorly controlled human immunodeficiency virus (HIV) infection is the most potent susceptibility factor for APOL1 nephropathy that has been identified to date. APOL1 variants are associated with HIV-associated nephropathy (HIVAN), a podocyte disease, but not with HIV-immune complex disease, primarily a disease of the mesangium. The mechanism by which HIV brings out the latent glomerular disease risk remains to be defined. There are at least two classes of candidate mechanisms to explain the potent interaction between HIV-1 and APOL1. First, APOL1 variant proteins and HIV accessory proteins implicated in HIVAN may target the same or related intracellular pathways in podocytes. Recent data suggest roles for interleukin 1b and transcription factor EB. Second, features of uncontrolled HIV infection, including increased circulating factors such as interferon, may drive APOL1 gene transcription or act upon podocytes in other ways. Deeper probing of APOL1-HIV interactions may yield insights that will aid in understanding HIVAN, APOL1 nephropathy, and podocyte biology.

Immunomodulatory Role of Complement Proteins in the Neuropathology Associated with Opiate Abuse and HIV-1 Co-Morbidity.

The complement system which is a critical mediator of innate immunity plays diverse roles in the neuropathogenesis of HIV-1 infection such as clearing HIV-1 and promoting productive HIV-1 replication. In the development of HIV-1 associated neurological disorders (HAND), there may be an imbalance between complement activation and regulation, which may contribute to the neuronal damage as a consequence of HIV-1 infection. It is well recognized that opiate abuse exacerbates HIV-1 neuropathology, however, little is known about the role of complement proteins in opiate induced neuromodulation, specifically in the presence of co-morbidity such as HIV-1 infection. Complement levels are significantly increased in the HIV-1-infected brain, thus HIV-induced complement synthesis may represent an important mechanism for the pathogenesis of AIDS in the brain, but remains underexplored. Anti-HIV-1 antibodies are able to initiate complement activation in HIV-1 infected CNS cells such as microglia and astrocytes during the course of disease progression; however, this complement activation fails to clear and eradicate HIV-1 from infected cells. In addition, the antiretroviral agents used for HIV therapy cause dysregulation of lipid metabolism, endothelial, and adipocyte cell function, and activation of pro-inflammatory cytokines. We speculate that both HIV-1 and opiates trigger a cytokine-mediated pro-inflammatory stimulus that modulates the complement cascade to exacerbate the virus-induced neurological damage. We examined the expression levels of C1q, SC5b-9, C5L2, C5aR, C3aR, and C9 key members of the complement cascade both in vivo in post mortem brain frontal cortex tissue from patients with HAND who used/did not use heroin, and in vitro using human microglial cultures treated with HIV tat and/or heroin. We observed significant expression of C1q and SC5b-9 by immunofluorescence staining in both the brain cortical and hippocampal region in HAND patients who abused heroin. Additionally, we observed increased gene expression of C5aR, C3aR, and C9 in the brain tissue of both HIV-1 infected patients with HAND who abused and did not abuse heroin, as compared to HIV negative controls. Our results show a significant increase in the expression of complement proteins C9, C5L2, C5aR, and C3aR in HIV transfected microglia and an additional increase in the levels of these complement proteins in heroin-treated HIV transfected microglia. This study highlights the a) potential roles of complement proteins in the pathogenesis of HIV-1-related neurodegenerative disorders; b) the combined effect of an opiate, like heroin, and HIV viral protein like HIV tat on complement proteins in normal human microglial cells and HIV transfected microglial cells. In the context of HAND, targeting selective steps in the complement cascade could help ameliorating the HIV burden in the CNS, thus investigations of complement-related therapeutic approaches for the treatment of HAND are warranted.

Renal transplantation in HIV-positive patients - No more a scare!

Human immunodeficiency virus (HIV) infection has posed as a major global health epidemic for almost three decades. With the advent of highly active antiretroviral therapy in 1996 and the application of prophylaxis and management of opportunistic infections, acquired immunodeficiency syndrome mortality has decreased markedly. The most aggressive HIV-related renal disease is end-stage renal disease due to HIV-associated nephropathy. Presence of HIV infection used to be viewed as a contraindication to renal transplantation for multiple reasons; concerns for exacerbation of an already immunocompromised state by administration of additional immunosuppressants; the use of a limited supply of donor organs with unknown long-term outcomes. Multiple studies have reported promising outcomes at three to five years after kidney transplantations in patients treated with highly active antiretroviral therapy, and HIV is no longer a contraindication for renal transplant. Hence, we present eight HIV-positive patients who received live-related renal transplantation at our center and their follow-up.

Viral-Associated GN: Hepatitis C and HIV.

Viruses are capable of inducing a wide spectrum of glomerular disorders that can be categorized on the basis of the duration of active viremia: acute, subacute, or chronic. The variable responses of the adaptive immune system to each time period of viral infection results mechanistically in different histologic forms of glomerular injury. The unique presence of a chronic viremic carrier state with either hepatitis C (HCV) or HIV has led to the opportunity to study in detail various pathogenic mechanisms of viral-induced glomerular injury, including direct viral infection of renal tissue and the development of circulating immune complexes composed of viral antigens that deposit along the glomerular basement membrane. Epidemiologic data show that approximately 25%-30% of all HIV patients are coinfected with HCV and 5%-10% of all HCV patients are coinfected with HIV. This situation can often lead to a challenging differential diagnosis when glomerular disease occurs in this dual-infected population and requires the clinician to be familiar with the clinical presentation, laboratory workup, and pathophysiology behind the development of renal disease for both HCV and HIV. Both of these viruses can be categorized under the new classification of infection-associated GN as opposed to being listed as causes of postinfectious GN as has previously been applied to them. Neither of these viruses lead to renal injury after a latent period of controlled and inactive viremia. The geneses of HCV- and HIV-associated glomerular diseases share a total dependence on the presence of active viral replication to sustain renal injury so the renal disease cannot be listed under "postinfectious" GN. With the new availability of direct-acting antivirals for HCV and more effective combined antiretroviral therapy for HIV, successful remission and even regression of glomerular lesions can be achieved if initiated at an early stage.

Impact of APOL1 polymorphism and IL-1ß priming in the entry and persistence of HIV-1 in human podocytes.

BACKGROUND: Patients of African ancestry with untreated HIV-1 infection and carrying the G1 or G2 kidney disease risk variants (Vs) at the APOL1 gene have a tenfold higher risk of developing HIV-associated nephropathy (HIVAN) compared to those with the non-risk wild type (WT) G0 variant. However, the mechanistic contribution of the APOL1 allelic state to kidney injury in HIV-1 infection remains to be elucidated. RESULTS: Non-risk WT APOL1 is associated with lower intracellular levels of HIV-1 in conditionally immortalized human podocytes, while the over expression of G1 or G2 risk Vs significantly increases viral accumulation. The priming of podocytes with exogenous IL-1ß facilitates HIV-1 entry, via the up-regulation of DC-SIGN. The over expression of APOL1 G1 and G2 risk Vs in combination with an increase in IL-1ß levels causes a greater increase in viral concentration than either condition alone. In turn, HIV-1 and exogenous IL-1ß together induce a de novo secretion of endogenous IL-1ß and an increase of APOL1 gene expression. CONCLUSIONS: Our findings indicate that the presence of risk Vs of APOL1 is permissive of HIV-1 persistence in human podocytes in synergy with IL-1ß, a cytokine that characterizes the inflammatory milieu of acute and chronic phases of HIV-1 infection. The elucidation of these molecular mechanisms explains, at least in part, the higher frequency of HIVAN in populations carrying the risk polymorphic genetic variant of APOL1 gene.

[The role of immune factors in the progression of chronic kidney diseases in HIV infection].

AIM: To determine the significance of immune factors in the pathogenesis of kidney injuries in HIV infection, by investigating the cellular and cytokine components of an immune response. MATERIALS AND METHODS: Thirty HIV-infected patients (mean age 31.7±6.2 years) with chronic kidney disease (CKD) were examined. A comparison group consisted of 10 HIV-infected patients without signs of kidney injury. A control group included 24 healthy individuals to analyze immune status and 15 people to estimate the normal values of the cytokine composition. The cellular composition of lymphocytes on a typical immunogram was determined on a flow cytofluorometer; the serum concentrations of cytokines were measured on a multichannel photometer. RESULTS: The HIV-infected patients with kidney injury displayed significant reductions in the absolute (0.2·109/l and 0.4·109/l, respectively; р=0.015) and relative (14.75 and 22%, respectively; р=0.005) counts of CD3+/CD4+ cells and in the immunoregulatory index (0.2 and 0.4, respectively; р=0.014) as compared to those in HIV-infected patients without kidney disease (р≤0.05) with a rise in the number of cytotoxic T cells (CD3+/CD8+). The HIV-infected patients showed a preponderance of immunosuppressive cytokine compositions, as indicated by the high levels of transforming growth factor-ß (a more than 50-fold increase) and by a statistically significant rise in the level of tumor necrosis factor-α (TNF-α) (with CD4+ lymphocyte counts more or less than 200 cells/µl - 19.0 and 24.2 pg/ml, respectively; p=0.017; with HIV RNA levels more and less than 100,000 copies/ml - 24.4 and 19.7 pg/ml, respectively; p=0.012). CONCLUSION: The HIV-infected patients with CKD developed kidney injury in the presence of a more pronounced decrease in blood T helper lymphocyte subpopulation levels with a predominance of proinflammatory and immunosuppressive responses. TNF-α in combination with immunosuppression and high viral loads was established to play a leading role in the development of kidney injury in HIV infection.

Clinical characteristics and outcomes of HIV-associated immune complex kidney disease.

BACKGROUND: The pathogenesis and natural history of HIV-associated immune complex kidney disease (HIVICK) is not well understood. Key questions remain unanswered, including the role of HIV infection and replication in disease development and the efficacy of antiretroviral therapy (ART) in the prevention and treatment of disease. METHODS: In this multicentre study, we describe the renal pathology of HIVICK and compare the clinical characteristics of patients with HIVICK with those with IgA nephropathy and HIV-associated nephropathy (HIVAN). Poisson regression models were used to identify risk factors for each of these pathologies. RESULTS: Between 1998 and 2012, 65 patients were diagnosed with HIVICK, 27 with IgA nephropathy and 70 with HIVAN. Black ethnicity and HIV RNA were associated with HIVICK, receipt of ART with IgA nephropathy and black ethnicity and CD4 cell count with HIVAN. HIVICK was associated with lower rates of progression to end-stage kidney disease compared with HIVAN and IgA nephropathy (P < 0.0001). Patients with HIVICK who initiated ART and achieved suppression of HIV RNA experienced improvements in estimated glomerular filtration rate and proteinuria. CONCLUSIONS: These findings suggest a pathogenic role for HIV replication in the development of HIVICK and that ART may improve kidney function in patients who have detectable HIV RNA at the time of HIVICK diagnosis. Our data also suggest that IgA nephropathy should be viewed as a separate entity and not included in the HIVICK spectrum.

Late onset of HIVAN in a young female - a case report.

INTRODUCTION: Human Immunodeficiency Virus associated Nephropathy (HIVAN) is a relatively frequent pathology among HIV patients, especially in black patients. Among about 800 HIV-infected patients from the Western Romania cohort, mainly of subtype F, none were diagnosed documented with renal biopsy with HIV-associated nephropathy. Renal alterations etiology seems to be complex. Several renal abnormalities have been described among HIV-infected patients. Patient, Methods and Results: We discuss the case of a 24-year-old white Caucasian female HIV-infected in 1990 by horizontal transmission, in her first year of life. She was diagnosed as late-presenter stage C3 at the age of 10, when she was admitted in coma secondary to toxoplasmic encephalitis. The clinical evolution was favorable under antiretroviral treatment until 2003 when dyslipidemia and arterial hypertension appeared. The first clinical manifestations of nephropathy were detected in 2006, with altered values of creatinine clearance. A 7-year follow-up of renal impairment shows a descending trend of creatinine clearance values. We analyzed the repeated ultrasound findings and renal biopsy was performed in 2013 revealing aspects of HIVAN. It has become obvious that HIVAN is caused by direct effects of HIV-1 virus over kidney structure and also that within the renal cells, viral replication is still permitted. In our case, the viral load peaked in 2011 at the same time the renal function significantly deteriorated. Her lifestyle changes must be taken under consideration - in the last year she has been under a low protein regimen. Compliance to antiretroviral treatment improves survival rate with a delayed deterioration of renal function to end-stage renal disease. CONCLUSIONS: Renal biopsy remains the most important feature in order to diagnose HIVAN. Suspicion of HIVAN diagnosis should be taken under consideration in the presence of constant proteinuria as well as decreased creatinine clearance levels.

Expression of substance P, neurokinin-1 receptor and immune markers in the brains of individuals with HIV-associated neuropathology.

The tachykinin neuropeptide substance P (SP) has an important signaling role in both the nervous and the immune systems. Two naturally occurring variants of the neurokinin-1 receptor (NK1R) mediate the effects of SP, full-length receptor (NK1R-F) and a truncated form (NK1R-T) that lacks 96 amino acid residues at the C-terminus. We previously reported decreased expression of the NK1R-F in the CNS of HIV-positive individuals in comparison to HIV-negative control subjects. There were no differences in the expression of the NK1R-T in the same groups. In the current study, we quantified the expressions of SP precursor mRNA preprotachykinin (TAC1), NK1R (full and truncated forms), viral load (HIV-gag) and several proinflammatory and immune markers (CD4, CCR5, CXCR4, fractalkine, IL-6, IL-10, CCL2, CCL20 and CD163) in the frontal cortex of autopsied brains from HIV-1-positive individuals with or without HIV-associated neuropathology. The expressions of SP and, to lesser extent, NK1R-F were decreased while the expressions of CXCR4, CCR5 and CCL2 were increased in CNS of individuals with HIV-associated neuropathology. There was no change in HIV loads associated with neuropathology; however, we found a positive correlation between viral loads and the expression of haptoglobin-hemoglobin scavenger receptor CD163. An analysis of CSF from corresponding samples demonstrated an increase in proinflammatory markers (CCL2 MIP-1α and MIP-1ß) associated with neuropathology. Although our data confirm the overall inflammatory nature of HIV-associated neuropathology, we observed a decrease in the expression of SP and NK1R-F, which is also associated with other forms of neuroinflammation.

The changing pattern of glomerular disease in HIV and hepatitis C co-infected patients in the era of HAART.

Previous reports have suggested a poor renal prognosis in patients with HIV and HCV co-infection with a preponderance of immune complex mediated glomerular disease on biopsy. Although the benefits of HAART on HIVAN are known, its impact on co-infected patients is unclear. We describe the renal biopsy findings and renal outcome in 29 co-infected patients in the HAART era and compare them to findings in 14 historical controls reported from our institution in the pre-HAART era. Our present cohort was predominantly male and Black with the majority reporting a history of intravenous (i.v.) drug use. Renal biopsy findings included 16 patients with immune complex mediated glomerular disease and 14 patients with FSGS, of which only 3 had collapsing features and/or tubular microcysts typical of HIVAN. Five patients had other biopsy diagnoses not directly related to viral infection. Median renal survival in our cohort was 15.6 months - significantly better than the 1.7 months seen our pre-HAART cohort. The modern cohort's improved renal outcome occurred despite older patients, longer HIV infection and similar levels of renal insufficiency. Our data indicate a changing epidemiology and natural history of renal disease in the HAART era with less immune complex mediated glomerular disease and more non-collapsing FSGS of the usual type. The marked improvement is likely to be multifactorial, including use of antiretroviral and anti-HCV therapies, RAAS antagonists, earlier nephrology referral and generally improved medical care.

[Glomerular diseases in HIV-infected patients: clinical and morphological evaluation].

AIM: To evaluate the clinical and morphological variants of kidney abnormalities in HIV-infected patients. SUBJECTS AND METHODS: Thirty HIV-infected patients (60% men and 40% women) aged 26 to 54 years (mean age 31.6 +/- 4.7 years) who had undergone diagnostic needle renal biopsy were examined. The indication for the biopsy was nephrotic syndrome (NS) (isolated or concurrent acute nephritic syndrome) and/or decreased renal function. The morphological study of biopsy specimens included light microscopy and immunofluorescence assay. RESULTS: In the examined HIV-infected patients, the histological variants of kidney abnormalities presented with immune complex glomerulonephritis (ICGN) in 26 cases and with focal segmental glomerulosclerosis (FSGS) in 4 cases. The clinical manifestations of ICGN were as follows: NS (61.5%), acute nephritic syndrome (in more than one third of the patients) concurrent with hematuria, as well as mainly grades 2-3 arterial hypertension (AH) (12/14) and renal dysfunction. Immune complex glomerulopathies were marked by polymorphism in the renal morphological pattern with fluorescence during immunofluorescence microscopy in most cases of virtually all classes of immunoglobulins (IgA, IgM, IgG) and complement system fragments (C3, C1q). FSGS was clinically characterized by NS concurrent with AH, hematuria. The morphological subtypes of FSGS were exhibited by apical, perihilar, and nonspecific variants in 1, 1, and 2 cases, respectively. By the time the signs of renal dysfunction appeared, the HIV-infected patients with glomerulopathy were found to have a high viral load (HIV RNA >100 000 copies/ml) and low CD4 lymphocyte levels (< or = 200 in 1 microl). CONCLUSION: In our study, the morphological pattern of chronic glomerulonephritis showed a preponderance of immune complex nephropathies with the clinical manifestations of acute nephritic syndrome and/or NS concurrent with hematuria. High viremia and depressed immune system may be risk factors for nephropathy.

Hepatitis C virus viremia increases the incidence of chronic kidney disease in HIV-infected patients.

BACKGROUND: Several studies have reported on an association between hepatitis C virus (HCV) antibody status and the development of chronic kidney disease (CKD), but the role of HCV viremia and genotype are not well defined. METHODS: Patients with at least three serum creatinine measurements after 1 January 2004 and known HCV antibody status were included. Baseline was defined as the first eligible estimated glomerular filtration rate (eGFR) (Cockcroft-Gault equation), and CKD was either a confirmed (>3 months apart) eGFR of 60 ml/min per 1.73 m or less for patients with a baseline eGFR more than 60 ml/min per 1.73 m or a confirmed 25% decline in eGFR for patients with a baseline eGFR of 60 ml/min per 1.73 m or less. Incidence rates of CKD were compared between HCV groups (anti-HCV-negative, anti-HCV-positive with or without viremia) using Poisson regression. RESULTS: Of 8235 patients with known anti-HCV status, 2052 (24.9%) were anti-HCV-positive of whom 983 (47.9%) were HCV-RNA-positive, 193 (9.4%) HCV-RNA-negative and 876 (42.7%) had unknown HCV-RNA. At baseline, the median eGFR was 97.6 (interquartile range 83.8-113.0) ml/min per 1.73 m. During 36123 person-years of follow-up (PYFU), 495 patients progressed to CKD (6.0%) with an incidence rate of 14.5 per 1000 PYFU (95% confidence interval 12.5-14.9). In a multivariate Poisson model, patients who were anti-HCV-positive with HCV viremia had a higher incidence rate of CKD, whereas patients with cleared HCV infection had a similar incidence rate of CKD compared with anti-HCV-negative patients. There was no association between CKD and HCV genotype. CONCLUSION: Compared with HIV-monoinfected patients, HIV-positive patients with chronic rather than cleared HCV infection were at increased risk of developing CKD, suggesting a contribution from active HCV infection toward the pathogenesis of CKD.

Chronic kidney disease associated with perinatal HIV infection in children and adolescents.

BACKGROUND: This study describes the incidence, clinical and demographic characteristics, and spectrum of chronic kidney disease (CKD) in youths with perinatal HIV-1 infection. METHODS: Retrospective analysis between May 1993 and December 2006 of subjects with renal disease followed in the Pediatric AIDS Clinical Trials Group 219/219C multicenter study examining the long-term consequences of perinatal HIV infection. Diagnosis confirmation was made utilizing a questionnaire mailed to research sites. Participants with CKD of other etiology than HIV were excluded. Outcome measures were biopsy-diagnosed CKD and, in the absence of biopsy, HIV-associated nephropathy (HIVAN) using established clinical criteria. RESULTS: Questionnaires on 191 out of 2,102 participants identified 27 cases of CKD: 14 biopsy-diagnosed and 6 clinical cases of HIVAN, and 7 biopsy-diagnosed cases of immune complex-mediated kidney disease (lupus-like nephritis, 3; IgA nephropathy, 2; membranous nephropathy, 2). Incidence rates for CKD associated with HIV in pre-highly active antiretroviral therapy (HAART) (1993-1997) and HAART (1998-2002, 2003-2006) eras were 0.43, 2.84, and 2.79 events per 1,000 person years respectively. In multivariate analysis, black race and viral load ≥100,000 copies/mL (rate ratios 3.28 and 5.05, p ≤ 0.02) were associated with CKD. CONCLUSIONS: A variety of immune complex-mediated glomerulonephritides and HIVAN occurs in this population. Black race and uncontrolled viral replication are risk factors for CKD associated with HIV.

Alloantigen-specific response is preserved and autoimmunity is maintained in an HIV-positive patient with immunoglobulin A nephropathy undergoing renal transplantation: a warning about long-term reduction in immunosuppression--a case report.

We report the case of a 43-year-old patient with HIV infection treated with antiretroviral therapy, which was complicated by immunoglobulin A (IgA) nephropathy and renal failure, who subsequently was transplanted using a deceased donor kidney transplant. During the late posttransplant period we detected specific anti-donor HLA antibodies showing a preserved alloantigen response. A renal biopsy showed no acute cellular or humoral rejection, an absence of pericapillary C4d deposits or SV40 infected cells, but demonstrated IgA mesangial deposits and mild interstitial fibrosis probably related to calcineurin inhibitor toxicity. This case shows that allo- and autoimmune responses are preserved despite immunosuppressive treatment and original HIV disease. It warns of the importance of maintaining optimal monitoring and immunosuppressive strategies among HIV-positive recipients who become solid organ transplant recipients.

HIV-associated immune complex glomerulonephritis with "lupus-like" features.

Renal structural abnormalities in HIV/AIDS infected patients have been infrequently and incompletely reported in patients from sub-Saharan Africa. We report an immune complex glomerulonephritis with "lupus-like" features in a ten-year-old HIV+ boy who was evaluated at the University Hospital of Kinshasa. The light microscopic examination of the renal biopsy displayed a predominantly membranoproliferative glomerulonephritis with prominent focal segmental necrotizing injury, numerous wire-loops, and a spiky membranous nephropathy. In addition, there were prominent tubular injury, microcysts filled with periodic acid-Schiff (PAS) positive casts, edema and an inflammatory infiltrate of the interstitium, features of a classic HIV-associated nephropathy (HIVAN). Electron microscopy revealed large subendothelial, intra-membranous, subepithelial and mesangial deposits. The combination of these findings, while being consistent with lupus nephritis WHO grade IV/V, the tubulointerstitial HIVAN-like changes and the absence of clinical evidence of lupus disease favored an HIV-associated immune complex glomerulonephritis with "lupus-like features".

Treatment of HIV-associated nephropathies.

In patients with HIV, the use of highly active antiretroviral therapy has improved life expectancy. At the same time, this increase in life expectancy has been associated with a higher frequency of chronic kidney disease due to factors other than HIV infection. Besides HIV-associated nephropathy, a number of different types of immune complex and non-immune complex-mediated processes have been identified on kidney biopsies, including vascular disease (nephrosclerosis), diabetes, and drug-related renal injury. In this setting, renal biopsy needs to be considered in order to obtain the correct diagnosis in individual patients with HIV and kidney impairment. Many issues regarding the optimal treatment of the different pathological processes affecting the kidneys of these patients have remained unresolved. Further research is needed in order to optimize treatment and renal outcomes in patients with HIV and kidney disease.

ABO incompatible renal transplantation in an HIV-seropositive patient.

To date, there have been no reports of successful ABO blood group incompatible renal transplantation in HIV patients. We describe a case of a 47-year-old African American man with end-stage renal disease secondary to HIV-induced nephropathy who underwent a live unrelated (spouse) donor ABO blood group incompatible transplant using an intravenous immunoglobulin/plasmapheresis preconditioning regimen with interleukin-2 receptor antagonist induction along with tacrolimus and mycophenolate mofetil maintenance. The postoperative course was complicated by two acute cellular rejection (Banff Ia) episodes that were successfully managed with corticosteroid boluses and the addition of corticosteroids to maintenance immunosuppression. Antibody-mediated rejection was not observed on biopsy. The patient reached a serum creatinine nadir of 2.0 mg/dL on postoperative day 20, which has now been maintained for 170 days. His current CD4 count was 410 cells/microL.