METABOLIC
Impact of Serum Lipid Profiles and Hypertension on Chronic Renal Allograft Dysfunction A.R. Hamidian Jahromi, G.A. Raiss-Jalali, A. Malekhosseini, and P. Jan-Ghorban
T
RANSPLANTATION is the preferred treatment modality for many patients with end-stage renal disease (ESRD), because it offers an improved quality of life over both hemodialysis and peritoneal dialysis.1,2 Transplantation is an expensive procedure for both the patient and the government, and there are some limitations for retransplantation of patients with a failed kidney transplant. Despite the efforts of tissue-typing laboratories and transplant nephrologists to avoid immunologic responses to foreign antigens in the transplanted kidney, allograft dysfunction remains the most important cause of graft loss.3 Death from cardiovascular disease is a major cause of morbidity and mortality among both dialysis and renal transplant patients.4,5 In addition to being important risk factors for
cardiovascular disease, hypertension (HTN) and hyperlipidemia both of which are extremely common in posttransplant patients, may accelerate the deterioration of renal function in transplanted kidney.6,7 Both HTN and hyperlipidemia exert a cumulative effect on the risk of cardiovascular disease.8 MATERIALS AND METHODS This prospective study included 93 patients transplanted in Nemazee Hospital of Shiraz University between April 1999 and From Organ Transplant Unit, Nemazee Hospital, Shiraz, Iran. Address reprint requests to A.R. Hamidian Jahromi, Organ Transplantation Unit, Nemazee Hospital, P.O. Box 71937, Shiraz, Iran.
Fig 1. The comparison of average serum lipid profile levels in renal transplant patients prior to and after transplantation until 1 year, in 3-month intervals.
© 2003 by Elsevier Science Inc. 360 Park Avenue South, New York, NY 10010-1710 Transplantation Proceedings, 35, 259 –262 (2003)
0041-1345/03/$–see front matter doi:10.1016/S0041-1345(02)03837-X 259
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Fig 2. Distribution of relative frequency in renal transplant patients with hypercholestrolemia and hypertriglyceridemia prior to and after transplantation until 1 year in 3-month intervals. July 2000. The patients’ time on dialysis prior to transplantation, the drug history, the BUN, creatinine, and blood pressures were checked in patients at 1 month intervals, and triglyceride (TG), cholesterol, LDL, and HDL, at 3-month intervals. For the purpose of this study, graft dysfunction was defined as a serum creatinine ⬎1.8 mg/dL, hypertriglyceridemia as serum TG ⬎250 mg/dL, hypercholestrolemia as serum cholesterol ⬎200 mg/dL and hypertension as BP ⬎ 140/90 on at least two occasions or treatment with antihypertensive medications. Patients in the hypertensive group were divided into controlled and uncontrolled patients (CH, UH) (BP ⬎ 140/90 on at least two monthly visits). Blood chemistry values was all measured in the same laboratory with kinetic (UV) methods. Results were analyzed using SPSS-10 software with results interpreted by t-test, chi-square, phi and cramer tests.
RESULTS
The patients had been on dialysis for an average of 4.7 years prior to transplantation (PTT). Development of renal allo-
Fig 3. The relative frequency of development renal allograft dysfunction in the first year posttrasplant period in three groups of patients.
graft dysfunction did not show any relationship with the duration that the patient had been on dialysis before transplantation. In our group of patients 71.7% were hypertensive and 23.9% had uncontrolled hypertension. Serum TG, cholesterol, and LDL levels showed a significant increase in the first 3-month interval after transplantation (P ⬍ .05) but HDL changes during that period were not significant. (P ⬎ .05) (Fig 1). Hypertriglyceridemia was seen in 21.4% of patients prior to transplantation and changed to 30%, 27.1%, 23.9%, and 23.8% at 3-month intervals thereafter. Hypercholesterolemia was seen in 27.3% of patients and increased to 64.9%, 62.5%, 62.9%, and 56.7% of patients at 3 months, 6 months, 9 months, and 12 months posttransplant, respectively (Fig 2). Uncontrolled hypertensive patients had an increased risk of developing chronic renal allograft dysfunction compared with controlled hypertension and normotensive patients. (P
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Fig 4. The mean serum lipid profile levels in uncontrolled hypertensive renal transplant patients in two groups of patients with and without renal allograft dysfunction prior to and after transplantation until 1 year in 3-month intervals.
⬍ .0005) (Fig 3). Mean posttransplant serum TG, cholesterol and LDL levels were higher among patients developing renal allograft dysfunction than patients without renal allograft dysfunction, during the first year posttransplant, but the difference was not significant (P ⬎ .05). Uncontrolled hypertensive patients showed an increased risk of developing renal allograft dysfunction, hypercholesterolemia, hypertriglyceridemia, and high LDL levels (for all P ⬍ .05) during the first year posttransplant (Fig 4).
DISCUSSION
In previous studies on serum lipid profiles and blood pressure in postrenal transplant patients, hypertriglyceridemia (with the same range as our study) was seen in 9% to 66% hypercholesterolemia in 16% to 78%, and hypertension in 25% to 95% of patients.3 Our results on serum lipid profiles and blood pressure in postrenal transplant patients were also in these ranges. In some studies the mean duration that the patient had been on dialysis prior to transplantation
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ranged between 1 and 8 years; our data were in that range (4.7 years).9 Two theories were presented on the relationship between dialysis duration and development of renal allograft dysfunction. In some studies better graft survival was seen in patients with longer periods of dialysis; the results were consider to be due to better patient compliance. In other studies, shorter graft survival times and more episodes of allograft dysfunction as well as greater organ damage and metabolic derangements10 were observed in these patients. In our study, no relationships were seen. In this survey, hypertension was the main predictor of renal allograft dysfunction and hyperlipidemia seemed to function as an additive factor in the presence of hypertension. The cumulative effect of hypertension and hyperlipidemia on the development of chronic nephropathy seems to support the theories of the role of atherosclerosis.
dysfunction. Therefore, control of lipid profiles in uncontrolled hypertensive patients must be aggressively pursued.
CONCLUSION
Control of blood pressure and lipid profiles in renal transplant patients seems to increase graft survival time. Hyperlipidemia appears to have a cumulative effect with hypertension on the development of chronic renal allograft
REFERENCES 1. Jofre R, Lopez-Gamez J, Moreno F, et al: Am J Kidney Dis 32:93, 1998 2. Hathaway DK, Winsett RP, Johnson C, et al: Clin Transplant 12:168, 1998 3. First MR: Am J Kidney Dis 22:477, 1993 4. Lindholm A, Albrechtsen D, Frodin L, et al: Transplantation 60:451, 1995 5. Kasiske BL: Am J Med 1988:985, 1988 6. Bumgardner GL, Wilson GA, Tso PL, et al: Transplantation 60:1418, 1995 7. Curtis J: Kidney Int 52:S75, 1997 8. Castalli WP, Garrison RJ, Wilson WF, et al: JAMA 256:2835, 1986 9. Carpenter CB, Milford EL, Sayegh MH: In: Braunwald E (ed): Harrison’s Pinciples of Internal Medicine. New York: McGraw-Hill; 2001, p 1567 10. Skorecki K, Green J, Brener BM: In: Braunwald E (ed): Harrison’s Pinciples of Internal Medicine. New York: McGrawHill; 2001, p 1551