● Avascular necrosis is ischemic bone necrosis affect the femoral condyles, tibial plateau, talus, and humeral head.
● The prevalence is typically 6% to 15% but may be as high as 52% in patients treated with high-dose of corticosteroids.
● In renal transplant patients, the ischemia occurs very early, often within 12 weeks of transplantation.
● Patient experience pain, limitation of ROM and limping during activity of the hip. By activity insidious onset of pain will appear and with disease progression, pain occur at rest and affect ROM and function.
Plain Language Summary 
After transplantation, inactivity and postoperative malnutrition lead to BMI and muscle atrophy, pre-exciting metabolic bone disease or mass accompanied by treatment by immunosuppressive therapy such as high doses of corticosteroids, lead to cellular hypertrophy and toxicity. Fat embolism is formed due to elevated lipid levels lead to micro emboli and endothelial cell changes causing venous stasis, an increased intra-osseous pressure and bone necrosis. Once osteonecrosis begins, 80% of the femoral heads will collapse, if not treated. Conservative treatment options including bed rest, reduced weight bearing, analgesics, deep heat modalities, braces, and ROM exercises but unfortunately, pain des not relieved 100%. AVN characterized by inflammatory changes and ischemia which occur in the first stage and lead to pain and edema. Using of NMES during early stage increase cell membrane adenosine receptors which have an anti-inflammatory effect accompanied by decrease the production of free radicles and this lead to decrease the pain. The anti-inflammatory effect reduced by NMES, decrease the breakdown of the cartilage and increase angiogenesis and improve bone formation through increase osteoblasts and decrease the osteoclasts.