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Hypertension in bone marrow transplanted patients
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Cyclosporine (CyA) can cause hypertension in bone marrow transplant patients. This study found that the hypertension is linked to kidney impairment, not the renin-angiotensin system.
Area of Science:
- Nephrology
- Cardiology
- Hematology
Background:
- Cyclosporine (CyA) is a crucial immunosuppressant used in bone marrow transplantation (BMT).
- Hypertension is a known complication of CyA therapy, but its underlying mechanisms require further elucidation.
Purpose of the Study:
- To investigate the etiological factors of cyclosporine-induced hypertension in bone marrow transplant patients.
- To differentiate between renal and renin-angiotensin system involvement in CyA-induced hypertension.
Main Methods:
- Prospective study of 10 BMT patients, monitoring blood pressure, plasma renin activity, and serum creatinine.
- Measurements taken one week before and three weeks after CyA administration.
- Comparison between hypertensive and normotensive patient groups.
Main Results:
- Four out of ten patients developed significant hypertension post-CyA administration.
- Hypertensive patients showed significantly lower plasma renin activity and a significant rise in serum creatinine compared to normotensive patients.
- Serum creatinine increase correlated with blood pressure elevation, while body weight and 6-keto PGF1 alpha levels remained unchanged.
Conclusions:
- Cyclosporine-induced hypertension in BMT patients is common.
- Hypertension is primarily associated with renal impairment rather than the renin-angiotensin axis.
- Monitoring renal function is crucial in BMT patients receiving cyclosporine.
Abstract:
Possible etiological factors of cyclosporine (CyA) induced hypertension were investigated in 10 bone marrow transplanted (BMT) patients followed during one week before and 3 weeks after transplantation. Diastolic blood pressure increased significantly after CyA in 4 patients (75 +/- 1 to 94 +/- 2 mmHg) but remained unchanged in 6 others (83 +/- 1 to 87 +/- 1 mmHg). Plasma renin activity on CyA was significantly lower in the hypertensive (0.6 +/- 0.1 ng/ml/hour) than in the normotensive group (1.1 +/- 0.2 ng/ml/hour). Serum creatinine rose significantly during CyA in hypertensive (0.70 +/- 0.04 to 0.99 +/- 0.07 mg/dl) but not in normotensive patients (0.74 +/- 0.06 to 0.81 +/- 0.03 mg/dl). The rise in serum creatinine was correlated with the increase of blood pressure. Neither body weight nor 6 keto PGF1 alpha plasma level changed during CyA. CyA dosage and plasma level were similar in hypertensive and normotensive patients. These data confirm the high incidence of CyA induced hypertension in BMT patients. In addition, they demonstrate that hypertension is not related to the renin-angiotensin axis but well to renal impairment.