In May 2010 a 30-years-old African female patient with preexisting compensated renal failure was brought to the attention of the Infectious Disease Department for high fever, headache, abdominal pain, renal failure (serum blood urea nitrogen 35 mg/dl, creatinine 9.5 mg/dl), severe anemia (Hb 5 mg/dl), metabolic acidosis (arterial blood gas analysis: ph: 7.33; pCO2: 28 mmHg; HCO3-(c): 14,8 mmol/L), and high blood pressure 180/100. She was diagnosed with advanced HIV infection (CD4 count, 29/mul, HIV-1-RNA viral load >than 750 000 copies/ml) and disseminated tuberculosis (TB). (Quantiferon test was positive, and this result was confirmed by the study of the sputum which was positive for the presence of alcohol acid resistant bacilli.) Total body CT spotted the presence of an abdominal abscess, supposedly TBC related. The ophthalmological examination showed a normal fundus and a visual acuity of 20/20.
Antihypertensive therapy (Ramipril cp 5 mg 1 cp/day), three times a week, dialysis through groin venous access, and antituberculosis therapy (rifampicin cp 600 mg, 1 cp/day, isoniazid cp 200 mg, 1 cp + 1/2 cp/day, pyrazinamide cp 500 m, 3 cp/day, ethambutol cp 1000 mg, 1 cp 3/week, after dialysis and cotrimoxazole) were started. Calcium therapy was also administered occasionally after dialysis for a moderate hypocalcaemia (7.4 mg/dl, normal range 8.5-10.1 mg/dl).
In September she started antiretroviral therapy (ART): Lopinavir/Ritonavir cp 200/50 mg (2cp x 2/day) and raltegravir (Isentress) cp 400 mg (1 cp x 2/day). At this time her blood pressure was 130/80 mmHg.
After two weeks from the beginning of ART, she complained about severe asthenia, functional inability of her lower limbs, and severe loss of her sight. Her visual acuity at this time was limited to light perception in both eyes, pupils were equal, the pupillary reflex was torpid, and fundus examination showed a normal optic head and normal vascularization. Visual-evoked potential showed an increased latency and a decreased voltage. The other cranial nerves were observed to be intact. Lumbar puncture, executed at this time, showed no evidence of active central nervous system inflammation/infection. A new magnetic resonance imaging (MRI) (Figure 1(a)) of the brain revealed an abnormal T2 hyperintensity within both cerebellar and parietooccipital and frontal lobes. The classic features of neuroimages, combined with clinical presentation of decreased vision and headache, confirmed the diagnosis of PRES.
The patient underwent supportive therapy. She had a clinical improvement within a few days; new imaging (Figure 1(b)) showed bilateral white matter lesions with decreasing size, and her visual acuity returned to 20/20 in both eyes. The patient was discharged without neurological deficits 10 days later. After three months of followup, the patient is doing well, HI-viral load is suppressed, CD4 count has increased to 180/mul, and kidney function has improved substantially.