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

Nineteen patients with primary aldosteronism due to surgically confirmed aldosterone-producing adenoma (APA) were examined to evaluate the response of aldosterone to upright posture and angiotensin II infusion. Upright posture reportedly decreases the plasma aldosterone concentration (PAC) in APA but raises it in idiopathic hyperaldosteronism. However, our findings showed the opposite result, in that the upright posture did not change or raised PAC in 15 of 19 cases (79%). Angiotensin II was infused i.v. at doses from 0.5-2 ng/min.kg body weight in six patients in whom the upright posture raised PAC, but did not raise PAC in all cases. This result supports the assumption that APA is functionally insensitive to angiotensin II. A concomitant rise of ACTH, pretreatment with calcium channel blockade, and other modulating factors may be involved in this PAC rise. Whatever the reason, such a high frequency of patients with increased PAC in APA raises some question about the clinical value of the upright posture test. We believe, then, there is reason to check any interpretation concerning increased PAC in the case of the upright posture test in distinguishing between APA and idiopathic hyperaldosteronism.

Abstract.A 76-year-old female patient who had been taking vitamin D2100,000 U/day for more than 14 years due to hypoparathyroidism following total thyroidectomy was admitted because of protracted hypercalcemia.On admission, the levels of serum vitamin D2 (99.8 ng/ml) and 25-OHD2 (356 ng/ml) were very high, and 1,25-(OH)2D2 was low (4.0-18.7 pg/ml). In addition, some bisphosphonates would certainly promote PTH-independent production of 1,25-(OH)2D2.

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.

A55-year-old patient with hypercalcemic crisis due to gastric carcinoma with bone marrow metastasis was treated with bisphosphonate (pamidronate) and calcitonin. Urinary excretion of parathyroid hormone-related protein (PTHrP) was increased. When normocalcemia had been attained, intravenous hyperalimentation was started, in which 1,000 U vitamin D2 was inadvertently supplemented on days 5-18, On days 15-18, hypercalcemia rapidly recurred, accompanied by markedly increased serum levels of 25-OHD2 (9.1 ng/dl) and 1,25-(OH)2D2 (161 pg/ml). This clinical course suggests that PTHrP, like PTH, stimulated loc-hydroxylase activity and produced excessive 1,25-(OH)2D2. Vitamin D should not be administered to patients with malignancyassociated hypercalcemia, particularly that due to PTHrP-producing tumors. (Internal Medicine 32: 886-890, 1993)