HIV-associated nephropathy (HIVAN) is a condition characterized by rapid decrease of the renal function, generally associated with an advanced stage of the HIV infection. However, this is not the only type of kidney involvement seen in HIV-positive patients. As we are currently experiencing a global phenomenon of aging, so do HIV-infected patients, potentially registering an age-related chronic renal impairment.[1]

Case report

We present the case of a 44 year-old male patient, diagnosed with HIV infection at the age of 23 and started on antiretroviral therapy (ART) at the age of 35, who presented to our clinic for routine monitoring, completely asymptomatic, but the laboratory assessment revealed sudden-onset proteinuria (4 g of protein per 24-hour urine), accompanied by an increase in serum creatinine (1.4 mg/dL) and an estimated glomerular filtration rate (eGFR) decreased to 59 mL/min.

His clinical exam was not remarkable but his medical history included post-traumatic splenectomy and left nephrectomy at 23 years old and a subsequent diagnosis of HIV and HBV coinfection.Followed-up in our clinic for over 20 years,  the patient had an initially replicative HBV infection, but entered the immune-control state1 after 15 years, with positive HBs antigen positive HBe antibodies and undetectable HBV viral load. After another 6 years, he cleared the HBs antigen as well. At the time of evaluation, he was on ART for 9 years, highly adherent to therapy, currently at his second ART regimen due to side effects such as dyslipidemia and lipodystrophy. During the past 7 years the patient presented repeatedly negative HIV viral loads, with high CD4 counts (currently 1113 cells/cmm, and a nadir CD4 cell count of 513 cells/cmm 5 years previously). The HIV-associated kidney disease section of the European AIDS Clinical Society guidelines2 recommends starting therapy with angiotensinconverting-enzyme (ACE)-inhibitors or angiotensin-II receptor antagonists in case of proteinuria and/or hypertension, with close monitoring of potassium levels and eGFR. The target blood pressure should be below 130/80 mmHg and a healthy lifestyle should be prescribed, with targeted treatment of dyslipidemia, the avoidance of nephrotoxic drugs, and an adjustment of concomitant medication, when needed.2 We referred the patient to a nephrologist, and stage III chronic kidney disease was diagnosed, while raising the suspicion of HIVAN, by corroborating biochemical and imagistic ultrasound investigations. To establish the diagnosis, a kidney biopsy was recommended. However, given the relatively risk of post-biopsy bleeding, and considering the fact that the patient had a single kidney after his nephrectomy, a joint decision was made to postpone or defer the biopsy and a conservative management was implemented: treatment with ACE-inhibitor, with close monitoring of blood pressure and potassium levels. During the course of the following 5 years of monitoring, the renal function remained in a steady state, with persistent proteinuria at 3.3- 3.6 g/24 hours, creatinine values ranging from 1.4 to 1.6 mg/dL, and an eGFR between 52 and 59 mL/min. The patient remained asymptomatic, continued ART with persistent suppression of HIV replication and good immune status, and is currently considered for kidney transplant.

HIVAN is generally associated with advanced HIV disease,3 however, this was not the case in our patient. He did indeed present a long history (over 20 years) of HIV infection, but his CD4 cell count had always been high, and the HIV viral load had remained undetectable for over 7 years. HIVAN is characterized by nephrotic proteinuria in a bland urinalysis result, without peripheral edema, and with normal-to-large echogenic kidneys on ultrasound exam. 4,5 A correct HIVAN diagnosis is established through histopathology following kidney biopsy. However, in the case we have presented, the patient had suffered left nephrectomy at 23
years old and the risks of bleeding or other biopsy-associated complications were considered too high. Therefore, we were unable to confirm or deny the suspected diagnosis of HIVAN in this setting of suddenonset decrease in renal function. Conservative treatment prevented the deterioration of the renal function over the following 5 years

Given the asymptomatic course that kidney disease may have in HIV-positive patients, andconsidering the fact that some of the drugs included in ART regimens or prescribed for the treatment of HIV-associated comorbidities may influence renal function, routine evaluation of the kidney function should be consistently performed in HIV-positive patients, to ensure early diagnosis and prompt medical management to prevent further deterioration of the renal function.

1. Streinu-Cercel A. Hepatitis B in the spotlight. GERMS. 2011;1:5. [CrossRef]
2. European AIDS Clinical Society. EACS Guidelines. Version 7.1. November 2014. pg 12. Accessed on: 26 July 2015. Available at: http://www.eacsociety.org/ files/guidelines-7.1
3. Wyatt CM, Klotman PE. HIV-associated nephropathy (HIVAN), Post TW (Ed), UpToDate, Waltham, MA. Accessed on: 25 July 2015.
4. Yalavarthy R, Smith ML, Edelstein CL. HIV-associated nephropathy in Caucasians: case report and review of literature. Int J STD AIDS. 2008;19:789-90. [CrossRef]
5. Lu TC, Ross M. HIV-associated nephropathy: a brief review. Mt Sinai J Med. 2005;72:193-9.