The Kidney in HIV and Aging (Updated 11/19/17)

  • Identify the cause and when possible treat all changes in renal function.
  • Renal function should be monitored at least twice annually using serum creatinine and other clinically available estimates of GFR.
  • Urinary albumin excretion should be measured at least annually.
  • Individuals with eGFR < 60ml/min (defined as CKD, NKF Stage 3a) should have a nephrologist involved in the patient care team.
  • Individuals with known CKD should be referred for planning for kidney replacement therapy when eGFR <15 ml/min.
  • In order to minimize the risk of acute kidney injury, careful monitoring and adjustment of drug dosing, should be performed.
  • Tenofovir alafenamide has shown reduced incidence of AKI and CKD compared to tenofovir disoproxil fumarate and should be the preferred formulation for older patients.

With the improvement in survival and disease progression due to antiretroviral therapy (ART) in people living with HIV (PLWH), chronic complications have significantly increased relative to HIV-related causes as the leading causes of morbidity and mortality.[1] Furthermore, several recent studies have shown an increase in renal disease among PLWH relative to HIV-uninfected controls.[2-4] The spectrum of kidney disease present in PLWH includes acute and chronic injury. Both the acute and chronic injuries may represent non-HIV conditions, HIV-associated nephropathy (HIVAN), and drug toxicity,[5] though the rates of HIVAN have been significantly reduced by antiretroviral treatment.[6]

The Aging Kidney and HIV Infection

Since glomerular filtration rate (GFR)-estimating equations began replacing serum creatinine for the evaluation of kidney function, the prevalence of diagnosed kidney disease in older adults has increased. As the normal kidney systematically loses function with age, it can be difficult to distinguish from disease processes.[7] The loss of renal reserve, however, makes the kidneys more susceptible to acute kidney injury, damage from other chronic illness, and toxic accumulation of renally cleared medications.

The structural changes of the aging kidney are classified as micro- or macro-anatomical. Micro-anatomical changes include nephrosclerosis, characterized by an increase in both focal and global glomerulosclerosis, tubular atrophy, interstitial fibrosis, and arteriosclerosis[8]; decrease in number of functional nephrons[9]; and nephron hypertrophy.[10] Macro-anatomical changes consist of declining cortical volume with an increase in parenchymal cysts and, less commonly, tumors.[11]

The effect of these changes leads to GFR decline which is thought to be physiologic due to its normal distribution.[12] There are no proven therapies to prevent age-related changes, which are thought to be irreversible once present. It is not yet clear if the decline in GFR is associated with increased mortality or progression to end stage renal disease (ESRD)[13].

While aging effects on kidneys may not increase risk of ESRD alone, it seems to contribute to increased disease progression for both acute and chronic kidney disease in PLWH[3]. As described in further detail elsewhere in this resource, PLWH are at increased risk of comorbidities which worsen their risk for acute and chronic kidney disease, including but not limited to Hepatitis B and C, tobacco use, hyperlipidemia, and diabetes mellitus (DM). Compared to patients with only HIV or DM, both of which increased risk of progression, comorbid DM and HIV significantly increased the risk of one or the other even after adjusting for traditional risk factors[14].

ART and Kidney Complications

PLWH are at increased risk of nephrotoxicity from several classes of ART, and from medications which may be used for opportunistic infections or other comorbid conditions. This risk is increased with underlying age-related changes. Caution should be taken using these agents in patient with a history of renal dysfunction or at high risk of kidney disease.  If unable to avoid, careful monitoring and adjustment of drug doses is recommended in all older PLWH.

The protease inhibitors (PIs) atazanavir and indinavir have both been associated with the development of crystalluria and AKI from both acute and chronic tubulointerstitial nephritis[15]. An analysis of renal impairment and ART exposure in the D.A.D. study cohort also showed that ritonavir-boosted lopinavir was an independent predictor of chronic renal impairment[16].

Tenofovir disproxil fumarate (TDF) causes both acute and chronic renal injury. The incidence estimates for acute kidney injury vary from 2 to 10%[17], though no specific characteristics are known to predict which individuals are at risk[18].  TDF is actively and primarily secreted in the proximal tubule and can cause tubular damage as a result of mitochondrial dysfunction. In the Johns Hopkins Clinical Cohort, patients receiving TDF experienced a greater decline in GFR over 3 years, though follow-up of the same cohort showed minimal difference[19], and an increase in renal dysfunction with concomitant PI use. Several studies have shown a statistically significant but mild to moderate progression with TDF use[20, 21], with at least 50% recovery to baseline function occurring in nearly all cases within 1 year after discontinuation[22].

Proximal tubulopathy (Fanconi syndrome), characterized by tubular proteinuria, glycosuria, hypophosphatemia, hypouricemia, hypokalemia, and renal tubular acidosis, is a recognized form of tenofovir toxicity[23]. No clear duration of use or other risk factors have been identified, but incidence was higher with co-administration of ritonavir[24]. Most cases resolve with discontinuation of TDF[23].

A newer prodrug of tenofovir, tenofovir alafenamide (TAF), approved in 2015, provides lower plasma concentrations of tenofovir. Patients receiving TAF had significantly smaller decreases in GFR than those receiving TDF, significantly less proteinuria, and significantly less loss of bone mineral density at the spine and hip without a significant change in virologic suppression [25, 26]. More recent studies have also shown changing from TDF-containing regiments to TAF-containing regimens was non-inferior for maintenance of viral suppression with improved renal function[27]. Though longer term follow-up is not yet available, the advantages of TAF over TDF for kidney and bone health make TAF a reasonable and preferred alternative for those at high risk of CKD.

Chronic Kidney Disease (CKD) in Persons with HIV

Reports of CKD in HIV-positive individuals vary significantly, from approximately 3% to 50% depending on the study population. Key factors include duration of HIV infection, access to ART, CD4 count, African heritage, age, coinfections (e.g., HCV), and other co-morbidities.

It is estimated that half of individuals with HIV infection and African heritage will develop HIVAN if left untreated, and is often associated with two alleles with APOL1 G1 and G2 mutations[28, 29]. In addition, a study published in 2017 showed racial disparities in the occurrence of DM, hypertension (HTN), and CKD persist[30]. HIVAN can progress to ESRD, and it generally presents in younger patients who have advanced HIV with nephrotic-range proteinuria and rapid progression without treatment.

Early use of ART has substantially reduced viral load in PLWH, and likewise kidney infection with HIV and the consequent development of HIVAN. Nevertheless, among HIV-positive individuals with CKD, up to 60% have evidence of focal segmental glomerulosclerosis (FSGS) with collapsing glomerulopathy typical of HIVAN on biopsy, representing a significant cause of CKD in this population [31, 32].

Another pattern of CKD in PLWH is HIV-immune complex kidney disease (HIVICK), the second most common diagnosis from kidney biopsy[33]. While this can present with a variety of histological changes, the clinical profile compared with HIVAN were patients who had more ART exposure, lower HIV viral loads, and higher CD4 and GFR estimates[34]. These cases are also predominantly seen in African-American patients, though may also be seen more commonly in those of European and Asian descent than HIVAN.

CKD in PLWH is mediated by factors related to the virus, the host, genetic predisposition, and environmental factors. The advent of ART has clearly decreased the progression of HIVAN to ESRD, and studies on its benefits for HIVICK show promise but remain conflicted[28].

Diagnosis and Management of CKD in Older PLWH

In order to identify individuals with kidney disease accurately and to make appropriate adjustments in drug dosing, ongoing efforts seek to identify the best clinically available means of accurately estimating GFR.

Initial studies using cystatin C measurements appeared promising, but recognition of limitations prompted evaluation of combinations of creatinine- and cystatin C-based equations [35-37]. Despite these efforts, considerable variability in results persists. These have been attributed to small numbers of subjects, the possibility that different methods perform differently in different subpopulations, and the lack of correlation with clinical outcomes [37]. Recent studies in PLWH indicate persistence of the limitations of these formulae [38].

Although the use of very accurate estimates of GFR within and across study populations is essential for establishing outcomes in clinical trials, using the same existing methods longitudinally in a clinical care setting are reliable in assessing stability or change of kidney function in individual persons. Furthermore, they provide general guidance in staging CKD.

Regarding GFR estimates for the adjustment of drug dosing, two studies in older individuals and PLWH concluded that the most commonly used creatinine-based methods (Cockcroft-Gault equation or Modified Diet in Renal Disease [MDRD] formulae) performed best [39, 40].

In older PLWH, multiple etiologies may contribute to loss of kidney function, e.g., aging, hypertension, diabetes, HIVAN, infections, obstructive uropathy, and acute kidney injury [41]. Thus, a change in kidney function and its likely cause must be identified to guide diagnosis-driven therapy that protects kidney function or reverses damage when possible.

In 2013, the Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group [42] report proposed clinical practice guidelines for the risk of CKD progression. These guidelines incorporate the cause of CKD, GFR category, and albuminuria category, where CKD is defined as abnormal kidney structure or function that is present for more than three months. For any given level of GFR, the greater the degree of albuminuria, the higher the risk for progression, including in PLWH [43]. Based on these criteria, in addition to eGFR, it is recommended to measure urinary albumin excretion (mg albumin/mg creatinine) to assess risk. Since the publication of these guidelines, commentary has suggested only minor modifications [43, 44].

A supplement to the 2013 KDIGO Guidelines was released in 2017 addressing CKD-Mineral and Bone Disorder (MBD)[45]. Though it did not specifically mention PLWH as a special population, MBD in older individuals with HIV is a well-described entity which is discussed further in Chapter 18.

The KDIGO Guidelines suggest involvement of a nephrologist in the care of all individuals with identified CKD (Stage3a), and certainly in all individuals with eGFR less than 30 ml/min. Prevention of progression of disease is an important goal prior to the time when referral for evaluation for dialysis and transplantation are required (eGFR less than 15 ml/min). In complex individuals with multiple comorbidities, such as older individuals with HIV infection, a nephrologist should be a part of the health care team when eGFR is less than 60ml/min [41].

Similar approaches that did not include measures of albumin excretion have been applied in individuals with HIV with reasonable predictive accuracy pf those who would develop CKD [46].

Given the importance of early detection of CKD as well as identification of modifiable risk factors, guidelines recommend that PLWH should have their GFR estimated at least twice yearly and have either a urinalysis or quantitative assessment of urinary protein excretion at least annually[47].

Kidney Transplantation in PLWH

In this era of improved survival with antiretroviral treatment of HIV-positive individuals with ESRD, kidney transplantation has become feasible. Similarly, increasing numbers of older individuals have also achieved satisfactory outcomes with organ transplantation. Yet, in both groups, recent studies have shown reduced graft function as compared to HIV-negative and younger individuals.

Canaud et al. [48] showed that, despite a lack of detectable HIV in the blood of individuals previously diagnosed with the virus, the kidney allograft becomes infected with HIV in 68% of biopsies, and a significant number develop clinical evidence of HIVAN in the transplanted kidney. Kidney infection correlated with, and could potentially be diagnosed by, detection of HIV DNA in the urine. This study suggests that nearly half of transplant recipients will have had episodes of acute rejection at the end of one year, double that of HIV-negative individuals [49].

Frassetto et al. [50] and Harbell et al. [51] have examined drug-drug interactions among allograft immunosuppressive agents and ART, finding a variety of complex interactions that require frequent monitoring of drug levels to avoid drug toxicities or inadequate immunosuppression.

Evidence that individuals with clinically diagnosed acute rejection also have kidney infection with HIV complicates selection of appropriate therapy in the face of a change in kidney function still further [48].

Despite these difficulties, adequate graft function at one and three years post-transplantation was present even in those who experienced an acute rejection episode, supporting the case for a continued role for transplantation in the management of older and HIV-positive individuals with ESRD [52].

Locke et al.[53] examined outcomes data from the Scientific Registry of Transplant Recipients from 2002-2011. Graft survival (GS) and patient survival (PS) was similar for HIV-positive recipients and HIV-negative matched control recipients (At 5 years: GS 85%, PS 89%). But HIV/HCV coinfected recipients had worse outcomes for both graft and patient (At 5 years: GS 76%, PS 67%).

Although transplantation of kidneys from HIV-positive donors into HIV-positive recipients was authorized in 2013, additional experience is needed before firm recommendations emerge [54, 55]. Nonetheless, this possibility increases the potential for donor availability.

Updated by Mehul Tejani, MD, MPH

October 2017

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