Urologic manifestations in AIDS


According to who estimates, 40 million people worldwide were infected with HIV by December 2003; >80% occurred through sexual intercourse (1).
In people infected with the human immunodeficiency virus (HIV) both the CD4 T-cell count and the viral load are used to monitor disease progression to acquired immunodeficiency syndrome (AIDS). CD4 counts of <500/mm³ are associated with opportunistic infections and certain malignancies, so-called ‘AIDS-defining’ conditions (2).
People with AIDS are predisposed to urinary tract infection (UTI) by uncommon bacteria and pathogens, e.g. fungi, parasites and viruses, which many affect any urogenital organ; treatment should be culture-specific and long-term, because there is a tendency to recurrence, infection with multiple organisms and resistant isolates (2).


The Centers for Disease Control and Prevention definition of AIDS is an HIV-positive person with any AIDS-defining 3condition, or with a CD4 count of <200/mm (3). AIDS defining conditions are: • Candidiasis, esophageal, or lower respiratory tract; • Cervical cancer; • Coccidioidomycosis, disseminated or extrapulmonary; • Cryptococcosis, extrapulmonary; • Cryptosporidiosis, chronic intestinal; • Cytomegalovirus (CMV) infection (other than liver, spleen or nodes); • Encephalopathy, HIV-related; • Herpes simplex virus (HSV), chronic ulcer(s>1 month; or bronchitis, pneumonitis, esophagitis;

  • Histoplasmosis, disseminated or extrapulmonary;
  • Isosporiasis, chronic intestinal;
  • Kaposi’s sarcoma (KS);
  • Lymphoma, Burkitt’s, immunoblastic, or primary of the brain;
  • Mycobacterium tuberculosis, any site;
  • M. avium intracellular (MAI) or M. kansasiidisseminated or extrapulmonary;
  • Pneumocystis carinii pneumonia (PCP);
  • Progressive multifocal leukoencephalopathy;
  • Salmonella septicaemia, recurrent;
  • Toxoplasmosis of the brain;
  • Wasting caused by HIV.


When the CD4 count declines to <200/mm³the risk of opportunistic infection increases dramatically and prophylaxis with trimethoprim-sulphamethoxazole (TMP-SMX) can be used against PCP and Toxoplasmosis infection. When the CD4 count is <100/mm³, clarithromycin plus azithromycin will protect against M. avium complex infection (4-6). RENAL INFECTION AIDS patients are prone to kidney infections from unusual agents such as Salmonella, CMV, Mycobacteria, Candida, Cryptococcus, Histoplasma, Aspergillus, Coccidioidomyces, and PCP [8]. Renal candidal infection can result in collecting-system masses (‘fungus balls’) that may cause hydronephrosis. M. tuberculosis and Aspergillus infection of thekidney may be seen as several hypoechoic masses on renal US (5,7). HAEMATURIA Microscopic haematuria occurs in 20–35% of patients with HIV/AIDS, with greater haematuria as the CD4 count decreases. In young, asymptomatic, HIV-infected patients with microscopic haematuria, a urological evaluation can be safely omitted in the presence of normal renal function and a benign urological history, because the likelihood of finding significant pathology is low [4,9,10,11]. PROSTATITIS AND PROSTATIC ABSCESS The estimated incidence of acute bacterial prostatitis increases from 1–2% in the generapopulation to 3% in asymptomatic HIV-positive patients, and 14% in patients with AIDS. The incidence of prostatic abscesses in AIDS has decreased significantly with the advent of HAART, because they occur only in patients with very low CD4 counts [6]. Persistent subclinical prostatitis occurs in up to 29% of patients after successful treatment of cryptococcosis, and as this is an important reservoir for subsequent relapse of cryptoccocal meningitis, patients are given long-term antifungal prophylaxis (4). EPIDIDYMITIS HIV infection may first present with STDs which are severe, recurrent or resistant to conventional therapy, suppurative and/or antibiotic-resistant epididymitis, or Fournier’s gangrene (necrotizing fasciitis) of the genitalia (1). URETHRITIS HIV-infected patients with urethritis are presumptively treated for both Chlamydia and Gonorrhoea, because combined infection is found in 30–50% of cases (4). GENITAL ULCER DISEASE In the HIV-positive patient, genital ulcers are usually caused by STDs such as genital herpes, syphilis and chancroid, but they mayalso be part of a systemic illness such as herpes zoster or CMV, or may be related to drug therapy, e.g. with the antiviral agent foscarnet [4]. HIV patients with syphilis are more likely to encounter neurological complications and have a higher rate of treatment failure (4). CONDYLOMA ACUMINATUM Visible genital warts caused by human papillomavirus type 6 or 11 are found in 20%of HIV-infected patients, compared with 0.1% of the general population (4). MOLLUSCUM CONTAGIOSUM Molluscum contagiosum virus (MCV) infection, an STD in adults, occurs in 5–18% of HIV-positive patients. Lesions caused by MCV typically appear as flesh-coloured, umbilicated, raised papules (1–5 mm in diameter) or nodules (6–10 mm) which may be single or multiple. HIV-positive patients tend to develop giant (>1 cm) lesions or may have clustering of hundreds of small lesions, and are at greater riskfor secondary inflammation and bacterial infection (4).


Recurrent balanitis may be a presenting sign of HIV infection; ª75% of HIV-infected women have at least one episode of vulvovaginal candidiasis (4)


Bowen’s disease (carcinoma in situ) of the penile skin and labia is more common in the HIV-infected population. Squamous cell carcinoma and giant human papilloma virus-induced verrucous carcinoma of the penis also take on a more aggressive ourse in HIV-positive patients, and should (4,6).
Isolated cases of prostate cancer among HIV-infected men have been reported. Patients with localized prostate cancer may be offeredall the standard treatment options, dependingupon both standard considerations (tumour grade, stage, PSA level, comorbidities and patients’ desires) as well as HIV-considerations (CD4 count, viral load, opportunistic infections, HIV disease history and medications). Patients with AIDS and metastatic prostate cancer may respond poorly to androgen deprivation if they are hypogonadal before treatment [6].


Nephrocalcinosis can be found in up to 40%of kidneys of patients with AIDS examined atautopsy, but this does not appear to be clilinically signi?cant [2]. Indinavir (Crixivan) isa protease inhibitor of which ª20% is not metabolized and is excreted by the kidneys. Indinavir is most soluble at pH < 5, and therefore it tends to precipitate in alkaline urine [4,6]. The incidence of urolithiasis in patients receiving indinavir is 3–22% and isdose-related [4-6,12]. Indinavir calculi are radiolucent, but may act as a nidus for the formation of stones containing calcium oxalate and phosphate, which are radio-opaque [6]. In a study of patients on indinavironly 29% had indinavir-containing stones; the rest had calcium oxalate, ammonium acidurate or uric acid stones, attributable to underlying metabolic abnormalities [12]. PROGNOSIS OF HIV/AIDS Treatment with HAART has dramatically improved the survival and quality of life in HIV-positive patients [13]. With HAART and antibiotic prophylaxis, HIV-positive patients have a life-expectancy of >20 years. Patients with AIDS can anticipate a median survival of >48 months, and the interval from soropositivity to the development of AIDS is expected to increase significantly (4)

1. Wiersma R. HIV-positive African children with rectal fistulae. J Ped Surg 2003; 38: 62–4.

2. Heynes CF, Fisher M. BJU Int 2005;95: 709–16

3. Centers for Disease Control. 1993Revised Classification System for HIV Infection and Expanded Surveillance Case Definition for AIDS Among Adolescents and Adults, 2004

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6.Hyun G, Lowe FC. AIDS and the urologist. Urol Clin N Am 2003; 30: 101–9

7. O’Regan S, Russo P, Lapointe N, Rousseau E. AIDS and the urinary tract. J Acquir Immune De?c Syndr 1990; 3: 244–51

8. Zinn HL, Haller JO. Renal manifestations of AIDS in children. Pediatr Radiol 1999; 29: 558–61

9. Miles BJ, Melser M, Farah R, MarkowitzN, Fisher E. The urological manifestationsof the acquired immunode? ciency syndrome. J Urol 1989; 142: 771–3

10.Kaplan MS, Wechsler M, Benson MC. Urologic manifestations of AIDS. Urology 1987; 30: 441–3

11. Cespedes RD, Peretsman SJ, Blatt SP. The significance of hematuria in patients infected with the human immunodeficiency virus. J Urol 1995; 154: 1455–6

12. Nadler RB, Rubenstein JN, Eggener SE, Loor MM, Smith ND. The etiology of urolithiasis in HIV-infected patients. J Urol 2003; 169: 475–7

13. Gazzard B, Moyle G. Revision to the British HIV Association guidelines for antiretroviral treatment of HIV soropositive individuals. BHIVA Guidelines Writing Committee. Lancet 1998; 352: 314–6