Surgical Correction of Posttransplant Renovascular Hypertension

Abstract

The incidence of renovascular hypertension in the transplanted kidney is reported to range between 5 and 15%. A review of 391 consecutive renal transplant patients revealed 16 patients (5.4%) with hypertension secondary to partial obstruction of renal arterial blood flow. The clinical course of this group of patients was marked by early normotension followed by progressive diastolic pressure elevation, with improving renal function and loss of accumulated excess volume. Five etiologic factors are responsible for impaired arterial flow in this group of patients. Indication for operation was based on hypertension and/or impaired renal function. Patch angioplasty using saphenous veins was the procedure of choice in most instances. The average blood pressure was 185 mmHg; systolic/125 mmHg; diastolic preoperatively, compared with 140 mmHg; systolic/90 mmHg: diastolic postoperatively. Twelve of 16 patients had good results, and improvement in renal function was observed in eight patients. Serum renin levels did not correlate well with the operative findings. The use of meticulous technique, combined with maximum use of autogenous tissue, is emphasized.

Estenose arterial nos transplantes renais

“…A etiologia da hipertensão arterial após transplante renal é múltipla e inclui muitas condições, tais como: rejeição do enxerto, toxicidade das drogas imunossupressoras, recorrência da doença renal original, doença dos rins nativos, hipertensão essencial e estenose da artéria renal 1,6,7,[10][11][12][13] . Destas condições, a estenose arterial é responsável por hipertensão em 10% dos transplantes e representa causa potencialmente curável 7,12,14 .…”

“…A presença de hipertensão em receptores de transplante renal é achado clínico em 50-60% dos casos, em longo prazo 7,10 . Dickerman et al 11 relatam que a incidência de hipertensão varia de 13 a 80% dos casos.…”

Hypertension in a Renal Transplant Recipient

“…A new bruit over the kidney or a marked change in the character of a preexisting bruit are also suggestive physical findings. Bruits were observed in 100, 88, 67, and 50% of patients reported by Ricotta et al [26], Dickerman et al [27], Goldman et al [28], and Pollini et al [3], respectively. Finally, a modest decrease in allograft function which is resistant or only transiently responsive to antirejection therapy is common in patients with RTAS [29].…”

“…The variability in incidence of this lesion, there fore, varies with selection of patients for arteriography as well as with the definition of 'hemodynamically signifi cant'. Thus, Grossman et al [36], Ricotta et al [26], and Dickerman et al [27] defined 'significant' stenosis as a 50, 70, or 80% reduction in intraluminal diameter, re spectively.…”

“…Occasionally the ste nosis is preanastomotic [26,27,33,36]. When the vascu lar reconstruction involves an end-to-side anastomosis between the renal artery and the external iliac artery, the overall incidence of RTAS apparently is the same, but the site is more commonly postanastomotic [36].…”