Renal transplant rejection is categorised in to 3 namely hyeracute, acute and chronic rejection.

Hyperacute rejection occurs immediately, leading to thrombosis. Immediate kidney removal should be performed. Acute rejection can occur most frequently in first 3 months with mild or severe presentations. It is usually mediated by cellular effector mechanism but humoral mechanism may play a role. Chronic rejection occurs gradually with decline of renal function, which can be detected as early as 6 months posttransplantation. It is commonly associated with proteinuria and hypertension. The transplanted kidney will undergo hypertrophy initially and the glomerular filtration rate (GFR) will be increased. It will eliminate waste products, toxins and foreign substance. It helps in regulation of water and electrolyte balances. Long term arterial pressure is regulated by secreting renin. In addition, acid base balance will be maintained. Erythropoietin would be secreted which is essential in production of erythrocytes. Calcitriol, an active form of vitamin D, required for normal bone deposition and calcium reabsorption in the gastrointestinal tract will be synthesised by the kidney. It is also involved in gluconeogenesis during prolonged fasting periods. (Hall, 2011)

Most kidney transplant recipient experiences decrease in renal function after 1 year of transplant. Recurrent disease, chronic rejection, nephrotoxicity by cyclosporine, hypertension and secondary focal glomerulosclerosis contribute to chronic renal transplant dysfunction. Patients are subjected to complications of long term immunosuppression medications. Adverse effects of Aathioprine are jaundice, anemia and alopecia. Mycophenolate sodium causes slight gastrointestinal toxicity and minimal bone suppression. Glucocorticoids cause impaired wound healing, increased risk of infection, and hypoalbuminemia, leading to generalized and symmetric edema. Cyclosporine contributes to nephrotoxicity , hirsutism, diabetes, hepatotoxicity, tremor and gingival hyperplasia. (Chandraker, Milford, & Sayegh, Harrison's Principles of Internal Medicine, 2012) Sclerodematous skin changes also occur (Fish & Massad, 2011) The remaining kidney will undergo physiological atrophy. This is the result of renal blood flow and GFR when it is ligated during renal transplantation. Advantages of renal transplant are improved quality of life without the need of hemodialysis, less restriction on diet and fluid intake and increased survival rates. It has been reported that the survival rate of during the first posttransplantation in all kidney recipients is higher than 95%. Patients receiving renal transplant particularly diabetic patient, has a survival benefit as compared to dialysis. The overall survival is 26% and 80 % at 5 year without and with renal transplant respectively. (Humar & Dunn, 2010) Complications of renal transplantation are chronic dysfunction and failure, de novo diabetes development. Posttransplantation patients are also associated with vascular complications like renal artery stenosis and thrombosis, infarction, arteriovenous fistulas, pesudoanuerysms and renal vein thrombosis. They are more susceptible during to infections and graft rejection. Neurologic complications like tremors, parasthesia, stroke disabling pain syndrome and leukoencehalopathy.

Advantage of hemodialysis is that close monitoring of patients can be carried out during in center hemodialysis. Technique failure rate is usually low. Disadvantages include multiple visits each week to dialysis centre and several complication of hemodialysis. One of the most common complications is hypotension, particularly in diabetic patients. Gastrointestinal disturbances like nausea and vomiting frequently occur during the first hour of dialysis (Rocco & Moossaci, 2009). Muscle cramps commonly occur during dialysis. The patients receiving their first dialysis experience anaphylactoid reactions to dialyzer. Cardiovascular mortality rates are higher in patients receiving hemodialysis than in posttransplantation patients. (Liu & Chertow, 2012).

Bibliography Hall, J. E. (2011). CHAPTER 26 Urine Formantion by The Kidneys. In J. E. Hall, & A. C. Guyton, Guyton and Hall Textbook of Medical Physiology. Philadelpia: Saunders Elsevier. Chandraker, A., Milford, E., & Sayegh, M. (2012). Harrison's Principles of Internal Medicine. New York: McGraw Hill. Fish, R., & Massad, M. (2011). Tintinalli's Emergency Medicine : A Comprehensive Study Guide 7th ed. New York: McGraw Hill. Humar, A., & Dunn, D. (2010). Chapter 11 Transplantation . In F. Brunicardi, D. Andersen, T. Billar, D. Dunn, J. Hunter, J. Matthew, et al., Schwartz's Principles of Surgery. New York: McGraw Hill. Rocco, M., & Moossaci, S. (2009). Chapter 50 Hemodialysis. In E. Lerma, J. Berns, & A. Nissenson, CURRENT Diagnosis & Treatment : Nephrology & Hypertension. New York: McGraw Hill. Liu, K., & Chertow, G. (2012). Chapter 281 Dialysis in the Treatment of Renal Failure. In D. Longo, A. Fauci, S. Kasper, J. Jameson, & J. Loscalzo, Harrison's Princinples of Internal Medicine. New York: McGraw Hill.

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