Renal dysfunction and destruction of renal structures are very common complications of HIV infection, and approximately 5-10% of HIV patients suffer from a pathologically distinct kidney disease known as HIV nephropathy. This nephropathy usually progresses rapidly to end-stage renal disease requiring life support by hemodialysis. Many HIV-related renal abnormalities, including HIV nephropathy, can occur at any stage of HIV disease from early asymptomatic infection to advanced AIDS, with renal failure and electrolyte disturbances more common in people with AIDS. HIV nephropathy can be an early or exclusive manifestation of HIV, in some cases even before the production of anti-HIT7 antibodies, and HIV nephropathy can be the first and only manifestation of HIV disease in children born with HIV. HIV nephropathy can be an important clinical manifestation in infants born to serologically positive mothers. Tea consumption may reduce the efficacy of AIDS 1. HIV-associated nephropathy (HIV AN) The basis of the histophilic nature of HIV is the complex, not simply because CD4 receptors are attached to the surface of susceptible cells, and the intracellular replication of HIV is generally cytotoxic. In the kidney, tubular cells and glomerular epidermal cells are severely damaged, resulting in “leakage” of filtered proteins and nephrotic syndrome. Severe proteinuria is the precursor to HIV nephropathy. Ureaemia, proteinuria, or both occur in 90% of HIV-infected patients, and most patients (89%) have urine protein amounts exceeding 1 gram per day or more. Focal segmental glomerulosclerosis (FSGS) is the typical renal lesion exhibited by patients with HIV AN. The disease progresses rapidly after the appearance of HIV renal damage and most die within 16 weeks after the discovery of renal damage, and the pathology shows enlarged kidneys with smooth cortical surfaces. Early renal damage showed diffuse glomerular membrane enlargement with very mild glomerulosclerosis under microscopy. Segmental sclerosis occurs in a variable number of glomeruli and is characterized by proliferation of epithelial cells containing coarse cytoplasmic vesicles and atrophy of the capillary wall or due to protein deposition (hyaline degeneration) to the disappearance of capillaries with foam cells (lipid-filled mononuclear cells) in the lumen. The glomerular capsule lumen is usually enlarged and tubular damage is very extensive. The clinical manifestations of HIV nephropathy are synthesized as follows: severe proteinuria, azotemia, water-electrolyte disorders, sarcohematuria, normal blood pressure, normal or enlarged kidneys, and acute progressive renal insufficiency. Normal blood pressure becomes a distinctive feature of HIV nephropathy, the cause of which is difficult to explain. Urine sedimentation tests often show severe proteinuria, ovoid fatty vesicles, and steaturia. A large number of giant wax-like tubular shapes are the characteristic manifestation of HIV nephropathy. The enlarged kidneys may be due to: (1) rapid disease progression without sufficient time for all glomeruli to sclerose and fibrosis; (2) unlike other chronic renal failures, HIV nephropathy shows significant glomerular dilatation and numerous microscopic-like vesicles; (3) interstitial edema, with dramatic serum albumin reduction disproportionate to moderate proteinuria (<10 mg/day), possibly associated with malnutrition Once HIV nephropathy occurs, it will rapidly progress and deteriorate to end-stage nephropathy, with inconsistent reporting of time in different studies, but mostly 6 to 12 months, with a mean of 9 months. 2. Water, electrolyte and acid-base balance disorders are common in patients with advanced AIDS. Hyponatremia is the most common dielectric disorder in HIV-infected patients, and up to 36%-56% of hospitalized patients are hyponatremic. In these patients, hypovolemia caused by gastrointestinal fluid loss is the most common cause of hyponatremia. Adrenal hypofunction is another cause of hyponatremia. Although pathologic changes of the adrenal glands are often reported at autopsy, less than 5% of patients clinically present with significant adrenal hypofunction. Hyponatremia, hyperkalemia, metabolic acidosis without an anion gap, hypovolemia, renal salt loss, and mild renal insufficiency are often present in mixed presentations. Drugs are also an important cause of water and electrolyte disturbances during the treatment of HIV-infected patients and can cause abnormal manifestations similar to those of adrenal insufficiency. Hyperkalemia and non-anion gap metabolic acidosis have been found to occur in patients receiving parenteral administration of pentamidine. Disulfiramycin B is associated with hypernatremia, hypokalemia, hypomagnesemia, renal tubular acidosis, and renal insufficiency. Treatment of AIDS-related malignancies with chemotherapeutic agents can cause water and electrolyte disorders directly through nephrotoxicity or sustained vomiting and diarrhea resulting in gastrointestinal fluid loss. 3. Acute renal failure Acute renal failure occurs in 20% to 40% of AIDS patients, and is one of the complications of HIV infection. It can be secondary to prerenal azotemia caused by insufficient fluid intake or excessive loss of gastrointestinal fluid. Renal ischemia caused by hypertension, sepsis, or application of nephrotoxic drugs can lead to tubular necrosis. Acute interstitial nephritis is another complication caused by drug therapy for HIV-related disease. Opportunistic infections, renal parenchymal invasion by lymphoma or Kapozi's sarcoma, and amyloidosis caused by subcutaneous narcotic abuse can lead to interstitial nephritis. Other renal lesions, such as hepatitis B-induced membranous glomerulonephritis, acute glomerulonephritis secondary to bacterial infection, renal parenchymal infections directly caused by CMV, fungi, and mycobacteria, and hemolytic-uremic syndrome, are associated with renal insufficiency in HIV-infected patients.