Objectives: This study proposes to evaluate risk factors for kidney disease in HIV patients treated chronically and correlate with microalbuminuria measurements. Methods: Review charts and analyses of microalbuminuria in subgroup of HIV patients treated at Ceara/Brazil. Results: 149 patients, 69.1% male, mean 38.5 years old, infection mean 86.8 months. Mean Creatinine Clearance 110.2%, Creatinine 0.97, Urea 27.76 mg/dl, CD4+ 600.37 cels/mm 3 and detectable viral load 530.59 copies with 61.7% undetectable. Mean Dosages of microalbuminuria/24h 147, 46 ± 820, 45 (N = 48) and microalbuminuria (mg/dl) 32.05 ± 85.25 (N = 43). Kidney Diseases Classification analyses evidenced 6.4% patients in stages ≥3 and 6.2% presented altered Microalbuminuria/24h. Patients using Tenofovir (TDF) 27.27% had Stage 2 and protease inhibitors (PI) had 4.1% in Stage 3. Proteinuria was observed in 5% stage ≥3. Association PI/TDF had 4.1% in Stage 3. No statistical difference between CD4 > or < 350 cels/mm 3 and microalbuminuria/24h > 300 mg (p = 0.69); detectable/undetectable viral load and microalbuminuria/24h (p = 0.63) or stage ≥3 (p = 0.17); relation to Diabetes or arterial hypertension and microalbuminuria 24 h (p = 0.5 and p = 0.21); relation stage ≥3 and microalbuminuria/24h (p = 0.33); relation HIV diagnoses >/< 60 months and stage ≥3 (p = 0.51); or microalbuminuria/24h and TDF (p = 0.4), PI (p = 1), TDF/PI (p = 0.69), Atazanavir (p = 0.4) or Lopinavir/r (p = 1) regimens. There was statistical significance comparing age > or < 50 years and stage ≥3 (p = 0.001) without difference with age > or < 50 years and microalbuminuria/24h (p = 0.55) or microalbuminuria mg/d (p = 0.32). Relating comorbidities risk (Diabetes Mellitus plus Systemic Arterial Hypertension) to Kidney Diseases, it was found that 55.5% patients in Stage 3 or above with comorbidities compared with 15% with comorbidities in lower stages (P = 0.005). Nevertheless, comorbidities presence was not associated with microalbuminuria (p = 0.08). Conclusion: Kidney disease is a real risk for HIV patients and stages ≥3 have to be early detected. Microalbuminuria dosage did not demonstrate more sensibility than proteinuria to early diagnoses, even related to antiretroviral drugs. Major risk factor for kidney damage evidenced to be older than 50 years and there was no protective effect from CD4 or undetectable viral load.
Objectives: Report a case of Tay-Sachs disease. Methods: A complete ophthalmologic examination, retinography and blood dosage of hexosaminidase A (EHA) activity were performed. Results: A one year and seven months old male with a history of generalized tonic-clonic seizures, with delayed neuropsychomotor development from the eighth month of life. At the ophthalmologic examination the patient did not fix or follow objects, with bilateral horizontal nystagmus. The fundoscopy revealed an image of “cherry-red spot” in the macula in both eyes. Dosage of EHA activity confirmed diagnosis of Tay-Sachs disease. Conclusion: Tay-Sachs Disease is a genetic disease with an autosomal recessive inheritance pattern characterized by deficiency of EHA activity, leading to the accumulation of sphingolipids in neuronal cells that results in progressive neurological dysfunction. In the retina, there is deposition in the ganglion cells, resulting in the appearance of cherry-red spot macula. There is no curative treatment, aiming at the therapy, only the clinical support in the patient.
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