Abstract. The present study surveyed 69 patients with aldosteronoma to study the clinical implications of renal cysts demonstrated in computed tomography. Patients who had cysts (n=16, 23.2%) were older and had a longer duration of hypertension and more severe hypokalemia than those without cysts (n=53). Patients with cysts therefore had longer-term, more severe hypokalemia than those without cysts. Endogeneous creatinine clearance (Ccr), measured in 61 patients, was significantly lower in patients with cysts (58.4 ± 7.1 ml/min, n=16) than in those without cysts (77.3 ± 7.1 ml/min, n=45, P=0.0039). This significant difference was observed even after adjusting for covariables (age, duration of hypertension, and serum potassium) between the two groups by analysis of covariance (ANCOVA). No significant difference was observed in gender, blood pressure, serum creatinine, plasma aldosterone, or PRA. Age, serum potassium levels, and systolic and diastolic blood pressure were the significant determinants in predicting Ccr in a backward stepwise multiple regression analysis (r=0.505, n=61, P=0.0025). Cysts were graded into four classes on the basis of number and size. Cyst grading correlated negatively with Ccr at a Spearman rank correlation (p= -0.33, n=61, P=0.0103). The incidence of chronic renal failure was significantly higher in patients with cysts (18.8%) than in patients without (0%) in a Fischer's exact probability test (P=0.0107). Thus, both renal cysts and dysfunction arose and/or developed from common roots, i.e., the duration and severity of hypokalemia, in primary aldosteronism.In addition, we surveyed 27 patients with pheochromocytoma. Patients with renal cysts (n=8) had a significantly longer duration of hypertension than those without cysts. No significant difference was observed in Ccr between patients with and those without cysts. Thus, a significant link between renal cysts and Ccr was a specific feature of primary aldosteronism, but not of pheochromocytoma.In summary, the renal cysts in primary aldosteronism should be recognized as a significant complication representing the extent of renal injury and dysfunction.Key words: Hypertension, Hypokalemia, Creatinine clearance , CT, Nephrocalcinosis (Endocrine Journal 43: 261-268,1996) PRIMARY aldosteronism causes hypertension, hypokalemia, and metabolic alkalosis. Each of these independent factors can potentially cause renal tissue injury. Hypertension causes nephrosclerosis (renal vascular and glomerular injuries) [1,2]. Hypokalemia causes vacuolation, degeneration and
Abstract. Systemic and nonspecific stress response effects on the cellular defense mechanism were studied in the male rat kidney. Two days after laparotomy-induced surgical stress, rats showed increased serum corticosterone and renal cortical reduced glutathione (GSH). Rats were then injected s.c. with mercuric chloride (HgC12) to oxidatively injure renal tubuli. Increased serum creatinine levels indicated that laparotomy pretreatment lessened renal damage. To study the effects of the activated pituitary-adrenal axis on renal cortical GSH content and vulnerability to subsequent oxidative injury, rats were injected s.c. with ACTH on two consecutive days. ACTH administration increased both corticosterone and aldosterone. These rats showed increased, dose-dependent renal cortical GSH content, i.e., controls (n=7): 1.25 ± 0.23 ,umol/g tissue, daily dose of 10 µg/100 gBW (n=7):1.53 ± 0.24 µmol/g tissue, and daily dose of 40 µg/100 gBW (n=7): 2.31 ± 0.23 µm01/g tissue. Rats receiving daily doses of 40 µg of ACTH/100 gBW acquired resistance to oxidative injury, indicated by serum creatinine levels: controls (n=6), 22 ± 4 µmol/L; HgCl2 (n=6),145 ± 88 ,umol/L; ACTH and HgCl2 (n=6), 37 ± 11 ,umol/L. Morphological evidence indicated that ACTH pretreatment in HgCl2-injected rats prevented renal tissue from inflammatory cell infiltration but not from tubular degeneration. Cellular GSH content of LLC-PK1 cells, porcine renal-tubule-derived culture cells, increased significantly in incubation with dexamethasone or aldosterone, suggesting that adrenal steroids directly stimulate renal cell GSH. We demonstrated that stress or ACTH administration activates the defense mechanism in the kidney via increased GSH. This stress-activatable defense system may therefore indicate a connection between endocrine stress response and the cellular defense mechanism.
Abstract. A small subgroup of primary aldosteronism due to aldosteronoma, named aldosteroneproducing renin-responsive adenoma (AP-RA), has been reported to masquerade as idiopathic hyperaldosteronism (IHA) because of the responsiveness of the plasma aldosterone concentration (PAC) to upright posture (UP). We found two patients with AP-RA in 19 patients with aldosteronoma who were examined by UP stimulation and were treated surgically. In 17 patients with typical aldosteroneproducing adenoma (APA), PAC decreased or increased only slightly (less than 200% of the basal level); in contrast, it increased to over 300% of the basal level in two patients with AP-RA. The two groups were comparatively studied as to their hormonal levels, adrenal computed tomography (CT) scan and histological findings in order to clarify the characteristics of AP-RA. Basal PAC was within the normal range (11.1 and 13.0 ng/dl) in AP-RA but in APA it ranged from 14.8 to 58.1 ng/dl with a mean of 32.3 ± 2.7 ng/dl. The diameters of the adenoma in AP-RA were apparently smaller (6 and 9 mm) than those in APA ranged from 10 to 25 mm with a mean of 15.5 ± 1.1 mm. After a contrast medium was injected at CT scan, the density of the normal adrenal gland adjacent to the adenoma increased but that of the adenoma did not in APA, making a clear distinction between the adenoma and the gland. On the other hand, the density of the adenoma and gland increased to almost the same degree in AP-RA. Thus, in AP-RA it was difficult to detect adrenal tumor by CT scan because of its size and because of the response to the contrast medium. Adenomas in both groups were mainly composed of clear cells, and no histological difference was found between the two groups. In summary, AP-RA was rarely present in primary aldosteronism and should be carefully diagnosed as primary aldosteronism because of normal PAC. Its PAC increased over to 300% of the basal level. It was showed that AP-RA are difficult to distinguish from IHA not only because of the similar responsiveness of PAC to UP but also because of difficulties in detecting adrenal tumor by adrenal CT scanning.
The significance of stress-induced hypogonadism remains unclear. Since plasma testosterone and LH have renotropic activity that is other than reproductive, we hypothesize that stress-induced hypogonadism is an adaptive response to protect the kidney. To examine this hypothesis, we prepared hypogonadal male rats with different levels of LH and testosterone through orchiectomy (castration), through chronic treatment with a slowly secreted form of gonadotropin-releasing hormone agonist (GnRHA; GnRHA pretreatment), or through both treatments concomitantly (castration with GnRHA pretreatment). Castrated rats had undetectable plasma testosterone and high plasma LH. GnRHA-pretreated rats had low plasma testosterone and normal plasma LH. Castrated rats with GnRHA pretreatment had undetectable plasma testosterone and normal plasma LH. We compared their sensitivity to HgCl2 nephrotoxicity and found that, when a low dose of HgCl2 (1.5 mg/kg body weight (BW)) was injected s.c. to induce acute renal failure, endogenous creatinine clearance (Ccr) decreased from 390 +/- 30 to 94 +/- 17 ml/h per kg BW in intact (unpretreated) rats. Such a decrease in Ccr was completely prevented in castrated rats (388 +/- 30 ml/h per kg BW) and partially prevented in GnRHA-pretreated rats (216 +/- 40 ml/h per kg BW). When a high dose of HgCl2 (2.25 mg/kg BW) was injected, half of the eight intact rats died but castrated rats and GnRHA-pretreated rats survived (P < 0.05). The elevated resistance in castrated rats was reduced when plasma LH was reduced with GnRHA pretreatment, but was restored by additional pretreatment with ovine LH (40 micrograms/day), as evidenced by changes in Ccr. Elevated resistance in castrated rats was also reduced by the administration of testosterone propionate. In conclusion, hypogonadism activated the preventive and defensive mechanisms that protect the kidney through both decreased plasma testosterone and high or even normal plasma LH.
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