Kidney Function

Hepatitis is a viral infection of the liver. In most cases, it causes a short-term illness that gradually clears up over a period of two or three weeks. However, in some cases, hepatitis leads to chronic infection that causes serious liver damage. Hepatitis C is a form of viral hepatitis that is transmitted primarily by the transfer of blood or blood products from one individual to another. It is being found more frequently in dialysis centers due to increased awareness of its existence and the availability of a test to detect it.

Another form of hepatitis, serum hepatitis, or Hepatitis B, may also occur in people on dialysis. The most common way that serum hepatitis spreads is through contact with blood. People receiving dialysis treatment are at a higher risk of acquiring Hepatitis C and (serum) Hepatitis B than others because of the nature of the treatment, possible contact with an infected needle (which should not occur) and because of blood transfusions. A test, known as the Hepatitis B Antigen test, determines who is infected with serum hepatitis. The spread of Hepatitis C and serum hepatitis may be prevented when the dialysis staff members practice universal precautions, as recommended by the Centers for Disease Control and Prevention (CDC), and when they isolate patients known to have a positive Hepatitis B Antigen test or abnormal liver enzymes. In addition, a Hepatitis B vaccine is available that is very effective in preventing infection with serum hepatitis.

Approximately 20% of post-transplant patients develop hyperglycemia, and 5-10% require therapy with oral hypoglycemic agents or insulin. Transient tubular glycosuria is also common.

Corticosteroid therapy is the most frequent cause of post-transplantation hyperglycemia. Steroids may increase production of glucose from gluconeogenesis, impair peripheral use of glucose, and cause elevation of glucogen levels by a direct anti-insulin effect at the cellular level. An undetermined threshold dose of corticosteroid may be required to provoke diabetes in susceptible individuals. Some studies have shown post-tranpslant diabetes to be related to steroid does, increased patient age, black race, a positive family history of diabetes, increased body weight, and human leukocyte antigen A28. These findings have not been consistent.

Typically, the onset of steroid diabetes is mild, without associated ketoacidosis; it may resolve on withdrawal or reduction of the steroid dose. Both cyclosporine and tacrolimus contribute to glucose intolerance by inhibiting insulin secretion by pancreatic beta cells and by inducing peripheral insulin resistance. Animal studies have revealed a decrease in islet cell insulin content as well as a severe degranulation and hydropic degeneration of islet cells after treatment with cyclosporine. Human studies have shown both improved glucose tolerance curves and insulin output after conversion from cyclosporine to azathioprine and prednisone. Cyclosporine dose reduction may improve glucose intolerance.