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The performance of HIV infection - Urinary system

Renal dysfunction, renal structural damage are very common complication of HIV infection, about 5 ~ 10% of HIV patients suffering from a pathological unique kidney disease, known as HIV nephropathy. Such rapid progress is usually in need of kidney dialysis to sustain life by the end of the period of renal disease. Many HIV-related kidney abnormalities, including HIV nephropathy, can occur in any stage of HIV disease, one from the early asymptomatic infection to advanced AIDS, including kidney failure and electrolyte disorders more common in people with AIDS in the. HIV nephropathy HIV can also be an early or only performance in some cases even before the birth of anti-HIT7 antibodies, HIV nephropathy can also be born in serology-positive mothers of infants, one of the important clinical manifestations.


1.HIV-associated nephropathy (HIV AN) HIV's addicted organization is based on the complex, not just because the surface of susceptible cells with CD4 receptors, HIV replication in cells in general have a toxicity. In the kidney, the renal tubular cells, glomerular epithelial cells were seriously damaged, resulting in filtering protein "leakage" producing nephrotic syndrome. Heavy proteinuria is a prelude to HIV nephropathy. Urea, hyperlipidemia, proteinuria, or both occurred in 90% of simultaneous HIV-infected patients, the majority of patients (89%), urinary protein of more than 1 g per day or more.

Focal segmental glomerulosclerosis (FSGS) is the HIV AN patients show a typical kidney disease, HIV disease after renal damage occurs the rapid progress of the discovery of more than 16 weeks after renal injury deaths increased renal pathology can be seen , the cortical surface is smooth. Early kidney damage under a microscope showed diffuse glomerular membrane increased, with minimal glomerular sclerosis. The number of occurrence ranging from segmental glomerular sclerosis, which is characterized by a thick cytoplasm containing vacuoles of epithelial cell proliferation, capillary wall collapse, or because of protein deposition (hyaline degeneration) and to the capillaries disappear, cavity foam cells (lipid filled with mononuclear cells). Glomerular cysts are usually expanded, tubular damage is extensive.