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Renovascular hypertension in kidney transplant recipients (KTR): main risk factors
254A
POSTERS: Secondary Hypertension
AJH–May 2003–VOL. 16, NO. 5, PART 2
P-594 TREATMENT AND LONG-TERM FOLLOW-UP OF RENOVASCULAR HYPERTENSION (RVHT) DUE TO GRAFT RENAL ARTERY STENOSIS (GRAS) IN RENAL TRANSPLANT PATIENTS Anna Oliveras, Ma Josep Soler, Susana Va´ zquez, Marisa Mir, Josep M. Puig, Josep Lloveras. Hospital Universitari del Mar, Barcelona, Spain. The development of GRAS is a recognized cause of hypertension (HT) after renal transplantation. Revascularization seems to improve blood pressure (BP) control and renal function or to prevent them from worsening at least. 31 patients with GRAS diagnosed by arteriography were followed throughout 24 months. Six of them received medical treatment, 19 patients underwent primary surgical revascularization (SR) and percutaneous transluminal angioplasty (PTA) was performed in the 6 remaining patients (⫹ stent in 1/6). Renal function was assessed by serum creatinine (SCr) and 24h-creatinine clearance (CrCl), and systolic, diastolic and mean BP (SBP, DBP, MBP) were also evaluated at diagnosis and at 1,6,12 and 24 months, as well as the number of antihypertensive drugs required at each period. Statistical analyses: analysis of variance by repeated measurements. No significant differences were found between groups of treatment whereby results are showed considering all patients together: We conclude that 1) SBP, DBP and MBP significantly deMonth 0 (m0)
Month 1 (m1)
Month 24 (m24)
SBP (mmHg) 173,2 (⫾29,4) 147,1 (⫾20,7) 143,7 (⫾21,0) DBP (mmHg) 97,3 (⫾15,9) 84,7 (⫾11,2) 86,0 (⫾13,1) MBP (mmHg) 122,6 (⫾19,3) 105,4 (⫾13,5) 105,2 (⫾15,0) SCr (mg/dl) 2,17 (⫾0,93) 2,23 (⫾0,99) 2,43 (⫾1,46) ClCr (ml/min) 54,37 (⫾26,07) 52,3 (⫾24,4) 55,42 (⫾27,08) Drugs (N) 2,03 (⫾1,13) 1,73 (⫾1,23) 2,03 (⫾1,16)
P1
P2
0,004 0,001 0,001 0,727 0,316 –
0,085 0,689 0,516 0,563 0,794 0,532
P1: (m13m0); P2: (m243m1); N ⫽ number of antihypertensive drugs
creased at 1 month after SR or PTA and this reduction was maintained from then on. 2) At 24 months the decrease of BP was similar in the three groups of treatment. 3) There was not significative change in the number of antihypertensive drugs taken after treatment, although it could be observed a trend towards a decrease in the PTA group and towards an increase in the medical treatment group. 4) Renal function did not change initially neither throughout time in any group of treatment. Key Words: Renovascular hypertension, Renal Transplantation, Treatment
P-595 RENOVASCULAR HYPERTENSION IN RENAL TRANSPLANTED PATIENTS: CLINICAL FEATURES AND MODE OF PRESENTATION Anna Oliveras, Ma Josep Soler, Josep Parrilla, Marisa Mir, Josep M. Puig, Josep Lloveras. Hospital Universitari del Mar, Barcelona, Spain. Renovascular hypertension due to graft renal artery stenosis (GRAS) may cause hypertension (HT) after renal transplantation (RT). The early detection and treatment of this disease can improve blood pressure control and prevent patients from graft dysfunction. We describe the main characteristics of a cohort of 34 out of 503 renal transplant recipients in whom GRAS was diagnosed by arteriography. Features of GRAS population: age: 45,5yr (⫾12,6); males: 74,3%; cardiovascular diseases and risk factors prior to RT: current or previous smokers: 40%; HT: 82,9%, diabetes mellitus (DM): 22,9%, dislipemia (DL): 78,8%, occlusive vascular disease: 28,6% (stroke: 5,9%, ischaemic cardiopathy: 11,4%, peripheral vascular disease 11,4%). Features of RT: acute tubular necrosis (ATN): 48,6% (average time in dialysis after RT: 11,8 days); cold ischaemia time: 20hr⫾10,8; acute rejection episodes: ⱕ 1 in 91,1%; number of arteries ⫽ 1 in 78,8%;
anastomosis type: end-to-side to common iliac artery (54,5%), external iliac artery (33,3%), end-to-end to hypogastric artery (12,1%). Features of donor: age: 42,6yr (⫾17,6); males: 37,5%; cadaveric donor: 91,4%; HT: 28,6%. Features of GRAS disease: incidence: 6,7%, localization: ostium/proximal: 62,9%; middle renal artery: 8,6%; outside renal artery: 14,3%. Abdominal bruit: 42,9%. Diagnostic suspicion: HT⫹abdominal bruit: 38,2%; acute renal failure after ACEI or AT-II receptors antagonists: 17,6%; new-onset HT or impaired control of previous HT: 14,7%; renal function worsening⫹HT: 11,8%; abdominal bruit alone: 2,9%; intermittent claudication: 2,9%. We conclude from our data that: 1) GRAS is prevalent in patients with classical cardiovascular risk factorsHT, DM and DL- and in those with organ target damage such as ischaemic cardiac and peripheral vascular diseases. 2) Poor controlled or refractory HT with or without bruit rises clinical suspicion in ⬎50% of GRAS but an abdominal bruit is heard in ⬍50%. 3) Acute renal failure after treatment with ACEI or AT-II receptor antagonists lead to diagnosis in 17,6% of GRAS. 4) Acute rejection episodes or ATN do not account for a major incidence of GRAS. Key Words: Renovascular Secondary Hypertension
Hypertension,
Renal
Transplantation,
P-596 RENOVASCULAR HYPERTENSION IN KIDNEY TRANSPLANT RECIPIENTS (KTR): MAIN RISK FACTORS Ma Josep Soler, Anna Oliveras, Susana Va´ zquez, Marisa Mir, Josep M. Puig, Josep Lloveras. Hospital Universitari del Mar, Barcelona, Spain. Renal artery stenosis in renal transplanted patients (RAS-RT) is a rather common cause of reversible hypertension and graft dysfunction. Our aim is to ascertain the possible risk factors for RAS-RT. 34 RAS-RT were diagnosed by arteriography in a cohort of 503 KTR who underwent renal transplantation (RT) between 1979 and 2002 (incidence: 6,7%). Univariate analyses were performed for several donor and recipient variables (2 test). Significant variables were then analyzed by a multivariate Cox proportional hazards model. Results (A ⫽ RAS-RT vs. B ⫽ non RASRT): Univariate Analyses Diseases Prior to RT Hypertension (HT) Diabetes mellitus (DM) Isch. cardiopathy (IC) Dislipemia (DL)
A
B
P
82,9% 22,9% 11,4% 78,8%
65,2% 3,7% 3,1% 6,1%
0,033 ⬍0,001 0,037 ⬍0,001
Multivariate Analyses OR
95% CI
P
– – – 4,5 1,2–17,1 0,028 – – – 50,4 19,8–128,7 ⬍0,001
The following analyzed variables were not significative risk factors for RAS-RT: age, gender, cigarette smoking, HT post RT, stroke, peripheral vascular disease, acute rejection episodes, cytomegalovirus infection, laboratory parameters -renal function, lipid profile, 24h- proteinuria, fibrinogenemia, serum potassium, hematocrit-, donor age and donor HT, donor type (cadaveric or living-related), acute tubular necrosis, cold ischaemia time, anastomotic type and number of arteries. We conclude from our study that: 1) diabetes mellitus and dislipemia prior to RT are independent risk factors for renal artery stenosis in renal transplanted patients. 2) Hypertension and ischaemic cardiac disease appeared also to be risk factors in the univariate analyses, but not in the multivariate model. Key Words: Renovascular Hypertension, Renal Transplantation, Risk Factors
POSTERS: Secondary Hypertension
AJH–May 2003–VOL. 16, NO. 5, PART 2
P-594 TREATMENT AND LONG-TERM FOLLOW-UP OF RENOVASCULAR HYPERTENSION (RVHT) DUE TO GRAFT RENAL ARTERY STENOSIS (GRAS) IN RENAL TRANSPLANT PATIENTS Anna Oliveras, Ma Josep Soler, Susana Va´ zquez, Marisa Mir, Josep M. Puig, Josep Lloveras. Hospital Universitari del Mar, Barcelona, Spain. The development of GRAS is a recognized cause of hypertension (HT) after renal transplantation. Revascularization seems to improve blood pressure (BP) control and renal function or to prevent them from worsening at least. 31 patients with GRAS diagnosed by arteriography were followed throughout 24 months. Six of them received medical treatment, 19 patients underwent primary surgical revascularization (SR) and percutaneous transluminal angioplasty (PTA) was performed in the 6 remaining patients (⫹ stent in 1/6). Renal function was assessed by serum creatinine (SCr) and 24h-creatinine clearance (CrCl), and systolic, diastolic and mean BP (SBP, DBP, MBP) were also evaluated at diagnosis and at 1,6,12 and 24 months, as well as the number of antihypertensive drugs required at each period. Statistical analyses: analysis of variance by repeated measurements. No significant differences were found between groups of treatment whereby results are showed considering all patients together: We conclude that 1) SBP, DBP and MBP significantly deMonth 0 (m0)
Month 1 (m1)
Month 24 (m24)
SBP (mmHg) 173,2 (⫾29,4) 147,1 (⫾20,7) 143,7 (⫾21,0) DBP (mmHg) 97,3 (⫾15,9) 84,7 (⫾11,2) 86,0 (⫾13,1) MBP (mmHg) 122,6 (⫾19,3) 105,4 (⫾13,5) 105,2 (⫾15,0) SCr (mg/dl) 2,17 (⫾0,93) 2,23 (⫾0,99) 2,43 (⫾1,46) ClCr (ml/min) 54,37 (⫾26,07) 52,3 (⫾24,4) 55,42 (⫾27,08) Drugs (N) 2,03 (⫾1,13) 1,73 (⫾1,23) 2,03 (⫾1,16)
P1
P2
0,004 0,001 0,001 0,727 0,316 –
0,085 0,689 0,516 0,563 0,794 0,532
P1: (m13m0); P2: (m243m1); N ⫽ number of antihypertensive drugs
creased at 1 month after SR or PTA and this reduction was maintained from then on. 2) At 24 months the decrease of BP was similar in the three groups of treatment. 3) There was not significative change in the number of antihypertensive drugs taken after treatment, although it could be observed a trend towards a decrease in the PTA group and towards an increase in the medical treatment group. 4) Renal function did not change initially neither throughout time in any group of treatment. Key Words: Renovascular hypertension, Renal Transplantation, Treatment
P-595 RENOVASCULAR HYPERTENSION IN RENAL TRANSPLANTED PATIENTS: CLINICAL FEATURES AND MODE OF PRESENTATION Anna Oliveras, Ma Josep Soler, Josep Parrilla, Marisa Mir, Josep M. Puig, Josep Lloveras. Hospital Universitari del Mar, Barcelona, Spain. Renovascular hypertension due to graft renal artery stenosis (GRAS) may cause hypertension (HT) after renal transplantation (RT). The early detection and treatment of this disease can improve blood pressure control and prevent patients from graft dysfunction. We describe the main characteristics of a cohort of 34 out of 503 renal transplant recipients in whom GRAS was diagnosed by arteriography. Features of GRAS population: age: 45,5yr (⫾12,6); males: 74,3%; cardiovascular diseases and risk factors prior to RT: current or previous smokers: 40%; HT: 82,9%, diabetes mellitus (DM): 22,9%, dislipemia (DL): 78,8%, occlusive vascular disease: 28,6% (stroke: 5,9%, ischaemic cardiopathy: 11,4%, peripheral vascular disease 11,4%). Features of RT: acute tubular necrosis (ATN): 48,6% (average time in dialysis after RT: 11,8 days); cold ischaemia time: 20hr⫾10,8; acute rejection episodes: ⱕ 1 in 91,1%; number of arteries ⫽ 1 in 78,8%;
anastomosis type: end-to-side to common iliac artery (54,5%), external iliac artery (33,3%), end-to-end to hypogastric artery (12,1%). Features of donor: age: 42,6yr (⫾17,6); males: 37,5%; cadaveric donor: 91,4%; HT: 28,6%. Features of GRAS disease: incidence: 6,7%, localization: ostium/proximal: 62,9%; middle renal artery: 8,6%; outside renal artery: 14,3%. Abdominal bruit: 42,9%. Diagnostic suspicion: HT⫹abdominal bruit: 38,2%; acute renal failure after ACEI or AT-II receptors antagonists: 17,6%; new-onset HT or impaired control of previous HT: 14,7%; renal function worsening⫹HT: 11,8%; abdominal bruit alone: 2,9%; intermittent claudication: 2,9%. We conclude from our data that: 1) GRAS is prevalent in patients with classical cardiovascular risk factorsHT, DM and DL- and in those with organ target damage such as ischaemic cardiac and peripheral vascular diseases. 2) Poor controlled or refractory HT with or without bruit rises clinical suspicion in ⬎50% of GRAS but an abdominal bruit is heard in ⬍50%. 3) Acute renal failure after treatment with ACEI or AT-II receptor antagonists lead to diagnosis in 17,6% of GRAS. 4) Acute rejection episodes or ATN do not account for a major incidence of GRAS. Key Words: Renovascular Secondary Hypertension
Hypertension,
Renal
Transplantation,
P-596 RENOVASCULAR HYPERTENSION IN KIDNEY TRANSPLANT RECIPIENTS (KTR): MAIN RISK FACTORS Ma Josep Soler, Anna Oliveras, Susana Va´ zquez, Marisa Mir, Josep M. Puig, Josep Lloveras. Hospital Universitari del Mar, Barcelona, Spain. Renal artery stenosis in renal transplanted patients (RAS-RT) is a rather common cause of reversible hypertension and graft dysfunction. Our aim is to ascertain the possible risk factors for RAS-RT. 34 RAS-RT were diagnosed by arteriography in a cohort of 503 KTR who underwent renal transplantation (RT) between 1979 and 2002 (incidence: 6,7%). Univariate analyses were performed for several donor and recipient variables (2 test). Significant variables were then analyzed by a multivariate Cox proportional hazards model. Results (A ⫽ RAS-RT vs. B ⫽ non RASRT): Univariate Analyses Diseases Prior to RT Hypertension (HT) Diabetes mellitus (DM) Isch. cardiopathy (IC) Dislipemia (DL)
A
B
P
82,9% 22,9% 11,4% 78,8%
65,2% 3,7% 3,1% 6,1%
0,033 ⬍0,001 0,037 ⬍0,001
Multivariate Analyses OR
95% CI
P
– – – 4,5 1,2–17,1 0,028 – – – 50,4 19,8–128,7 ⬍0,001
The following analyzed variables were not significative risk factors for RAS-RT: age, gender, cigarette smoking, HT post RT, stroke, peripheral vascular disease, acute rejection episodes, cytomegalovirus infection, laboratory parameters -renal function, lipid profile, 24h- proteinuria, fibrinogenemia, serum potassium, hematocrit-, donor age and donor HT, donor type (cadaveric or living-related), acute tubular necrosis, cold ischaemia time, anastomotic type and number of arteries. We conclude from our study that: 1) diabetes mellitus and dislipemia prior to RT are independent risk factors for renal artery stenosis in renal transplanted patients. 2) Hypertension and ischaemic cardiac disease appeared also to be risk factors in the univariate analyses, but not in the multivariate model. Key Words: Renovascular Hypertension, Renal Transplantation, Risk Factors