Purpose of review HIV-associated nephropathy (HIVAN) is characterized histologically by a collapsing form of FSGS, microcystic tubular dilation, interstitial inflammation and fibrosis. In this review, we provide a summary of the current state of knowledge about the mechanisms involved in the pathogenesis of HIVAN. Recent Findings Two variants in the ApoL1 gene have been identified as the susceptibility alleles that account for a majority of the increased risk of FSGS and non-diabetic ESRD in Blacks. HIVAN1 and HIVAN 2 are the other host susceptibility genes that have been identified in animal models for HIVAN. HIV infects renal tubular epithelial cells likely through direct cell-cell transmission. Both in vivo and in vitro evidence suggests that nef and vpr are the key viral genes mediating HIVAN. Nef induces podocyte dysfunction whereas Vpr induces RTEC apoptosis. Summary HIVAN results from direct infection by HIV-1 and expression of viral genes, especially nef and vpr, in renal epithelial cells in a genetically susceptible host. The infected renal epithelium acts as a separate viral compartment from the blood and facilitates evolution of strains distant from blood. Dysregulation of several host cellular pathways, including those involved in cell cycle and apoptosis, ultimately results in the unique histopathological syndrome of HIVAN.

Introduction Approximately 15% of HIV-infected individuals have comorbid diabetes. Studies suggest that HIV and diabetes have an additive effect on chronic kidney (CKD) progression; however, this observation may be confounded by differences in traditional CKD risk factors. Methods We studied a national cohort of HIV-infected and matched HIV-uninfected individuals who received care through the Veterans Healthcare Administration. Subjects were divided into four groups based on baseline HIV and diabetes status, and the rate of progression to an estimated glomerular filtration rate (eGFR) < 45ml/min/1.73m2 was compared using Cox-proportional hazards modeling to adjust for CKD risk factors. Results 31,072 veterans with baseline eGFR ≥ 45ml/min/1.73m2 (10,626 with HIV only, 5,088 with diabetes only, and 1,796 with both) were followed for a median of 5 years. Mean baseline eGFR was 94ml/min/1.73m2, and 7% progressed to an eGFR < 45ml/min/1.73m2. Compared to those without HIV or diabetes, the relative rate of progression was increased in individuals with diabetes only [adjusted hazard ratio (HR) 2.48; 95% confidence interval (CI) 2.19–2.80], HIV only [HR 2.80, 95% CI 2.50–3.15], and both HIV and diabetes [HR 4.47, 95% CI 3.87–5.17]. Discussion Compared to patients with only HIV or diabetes, patients with both diagnoses are at significantly increased risk of progressive CKD even after adjusting for traditional CKD risk factors. Future studies should evaluate the relative contribution of complex comorbidities and accompanying polypharmacy to the risk of CKD in HIV-infected individuals, and prospectively investigate the use of cART, glycemic control, and adjunctive therapy to delay CKD progression.

The Organ Procurement Transplant Network/United Network for Organ Sharing (OPTN/UNOS) has increased the amount of data collected before and after donation and increased the duration of donor followup to 2 years, yet there is evidence that reporting is incomplete. We examined the frequency of missing data in the OPTN/UNOS donor follow-up registry and found that reporting rates were low, particularly for donors who may have limited access to health care. We argue that a national donor follow-up registry is essential to ensure transparency in ascertaining long-term health outcomes among all living donors and in providing assessments of quality assurance within transplant programs. We have suggested approaches to strengthen the donor follow-up registry system. These include setting clear and high standards for follow-up reporting, a system of incentives and penalties that would motivate transplant centers to comply with these standards and would encourage donors to follow-up and lifelong follow-up reporting by primary care providers. We argue that the US government must provide funding to support a donor follow-up registry that can allow for meaningful and valid conclusions, in recognition of donors' public service and to maintain trust in the system of living organ donation.

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The majority of patients with prevalent BE participating in an endoscopic surveillance program overestimated their chances of developing adenocarcinoma of the esophagus. Efforts to improve education of such patients with BE are warranted.

Because creatinine is heavily weighed in the MELD (model for end-stage liver disease) score, we sought to determine the impact of MELD-based organ allocation on outcomes after transplantation in the preand post-MELD eras, focusing on recipients over age 65 on dialysis prior to transplant. A total of 20 196 patients from the UNOS database were analyzed. Comparing the pre-MELD to MELD era, there was a 41% increase in patients on dialysis (p < 0.0001), and a 117% increase in combined liver/kidney transplants (p < 0.0001). In the pre-MELD era, 1-year patient survival in recipients greater and less than age 65 on dialysis who received liver transplant alone was 56.8% and 76.4%, respectively (p = 0.13). In the MELD era these rates were 50.7% and 77.8% (p = 0.04). In the pre-MELD era, 1-year patient survival in recipients greater and less than age 65 on dialysis who underwent combined liver/kidney transplantation was 25.0% and 83.2%, respectively (p = 0.0002). In the MELD era, these rates were 67.0% and 82.5% (p = 0.18). In conclusion, a greater proportion of patients in the MELD era are on dialysis prior to transplant, and more receive combined liver/kidney transplants compared with the pre-MELD era. Candidates over age 65 who are on dialysis at the time of transplant have decreased survival after isolated liver transplantation.

Importance of the field Human immunodeficiency virus (HIV) infection is associated with the development of a wide spectrum of kidney diseases. HIV-associated nephropathy (HIVAN) is the most common cause of chronic kidney disease (CKD) in HIV-infected individuals and predominantly affects patients of African ancestry. HIVAN is a leading cause of end-stage renal disease (ESRD) among African-Americans. Areas covered in this review an overview of the spectrum of kidney disease in patients with HIV; current pharmacologic interventions to treat kidney disease in HIV. What the reader will gain Knowledge regarding the most common causes of kidney disease in HIV-infected patients and principals related to pharmacotherapy in HIV-infected patients with kidney disease. Take home message Kidney disease is an important cause of morbidity and mortality in HIV-infected patients and the most common cause of chronic kidney disease in this population is HIV-associated nephropathy, which is caused by viral infection of the renal epithelium. Several medications that are commonly used in HIV-infected patients can have adverse effects on the kidneys and the doses of many antiretroviral medications need to be adjusted in patients with impaired renal function.