Increased plasma renin and aldosterone in patients treated with cisplatin-based chemotherapy for metastatic germ-cell tumors.

Abstract

Twenty-four normotensive males in complete remission (CR) for 9+ to 54+ months after cisplatin-based chemotherapy for metastatic germ-cell tumors were evaluated for evidence of alterations in the renin-aldosterone axis and renal function. Abnormally high ambulatory plasma renin activity was seen in 14 of 19 patients with 24-hour urine sodium excretion greater than 50 mEq. This was correlated with elevated ambulatory plasma aldosterone (P = .009) and 24-hour urinary aldosterone excretion (P = .01). The mean serum magnesium value (1.34 +/- .05 mEq/L) was subnormal. Therapy resulted in an increase in serum creatinine during treatment (P less than .0001), an increase in BUN (P less than .01), and decrease in serum phosphorus (P less than .001). The relationship between the alterations in the renin-aldosterone axis and abnormal renal tubular function remains to be determined. In view of reports of cardiovascular toxicity after treatment for germ-cell tumors, and evidence individually linking both magnesium deficiency and increased plasma renin activity (PRA) to cardiovascular consequences, these abnormalities in renin and magnesium metabolism suggest that patients treated with cisplatin-based chemotherapy should be carefully observed for the development of delayed cardiovascular toxicities.

Bone morphogenetic protein signalling activity distinguishes histological subsets of paediatric germ cell tumours

“…Furthermore, significant therapy‐related toxicity occurs in many patients treated with cisplatin, etoposide and bleomycin, including pulmonary fibrosis (Osanto et al. , 1992), renal insufficiency (Bosl et al. , 1986; Hansen et al.…”

“…While cisplatin-based combination chemotherapy has been very successful in the treatment of GCTs (Einhorn & Donohue, 1977;Williams et al, 1987), survival is still suboptimal for patients in high-risk groups and those whose tumours are not susceptible to cisplatin (Frazier & Amatruda, 2009). Furthermore, significant therapy-related toxicity occurs in many patients treated with cisplatin, etoposide and bleomycin, including pulmonary fibrosis (Osanto et al, 1992), renal insufficiency (Bosl et al, 1986;Hansen et al, 1988;Bokemeyer et al, 1996) and ototoxicity (Bokemeyer et al, 1996;Strumberg et al, 2002). Children are particularly vulnerable to late effects of therapy, especially ototoxicity and pulmonary abnormalities (Hale et al, 1999).…”

Worm-like thrombus in left main coronary artery after cytostatic treatment

“…Elevated plasma von Willebrand factor level [5], additional thrombophilia such as acquired protein C deficiency [6], increased platelet aggregation [7], hyperreninemia and hyperaldosteronemia [8] and hypomagnesaemia-induced vasospasm [9] are thought to be responsible for the underlying pathogenesis.…”

Review of Late Complications of Treatment and Late Relapse in Testicular Cancer

“…This evidence should be considered along with reports of hyperreninemia, hypomagnesemia, and hyperaldosteronemia in normotensive men after cisplatin-based chemotherapy for TC. 8,21 Clustering of cardiovascular risk factors resembling the metabolic syndrome was seen in TC patients who had undergone chemotherapy and had an increased PAI-1, 16 raising the question of the indirect effect of chemotherapy-induced metabolic and hormonal changes on the development of premature atherosclerosis. Indirect Cisplatin Effects: Gietema et al 22 first reported on the association between the metabolic syndrome and low testosterone levels in TC survivors who underwent chemotherapy.…”