Hisashi Oda

NEPHROTIC SYNDROME ASSOCIATED WITH MALIGNANT MESOTHELIOMA

Sumi Tanaka, MD, 2nd Department of Internal Medicine, Urafune Hospital, 3-46 Urafune-cho, Minami-ku, Yokohama 232 (Japan) Discharge Admission Total protein ‘Albumin November 1991 Dear Sir, The association between nephrotic syndrome and malignancy has been well documented [1-3]. Several types of glomerular injury have been noted in patients with cancer [2], and the neoplasms that have been implicated include a variety of histological types from different primary sites [3]. We present a case with nephrotic syndrome associated with malignant mesothelioma. A 77-year-old man was admitted to our hospital with systemic edema, generalized weakness, and fatigue. Two years previously he had a pneumonia, at which time urinalysis showed no protein. He had not been receiving any medications. He had been working as an engineer on a ship and had been exposed to asbestos approximately 40 years prior to admission. Physical examination: On auscultation of his lungs, there were decreased breath sounds and some moist rales on the left. Heart sounds and abdomen were normal, and there was no lymphadenopathy. There was pitting edema of the whole body. Laboratory values included the following: total serum protein 5.4 g/dl, serum albumin 1.3 g/dl, total serum bilirubin 0.2 mg/ dl, serum glutamic-oxaloacetic transaminase 32 IU/1, serum glutamic-pyruvic transaminase 22, alkaline phosphatase 556IU/1, blood urea nitrogen 14 mg/dl, serum creatinine 0.8 mg/dl, Na 130 mEq/1, K 3.7 mEq/1, Ca 6.4 mg/dl, P 2.8, serum glucose 141, total cholesterol 184, triglycerides 107 mg/dl, eryth-rocyte sedimentation rate 50 mm/h, hemoglobin 8.9 g/dl, hematocrit 27.4%, white blood cell count 11.1 × lOVμl (with an increase in

Functional atrial natriuretic peptide receptor in human adrenal tumor.

&NA; The effects of synthetic human atrial natriuretic peptide (ANP) on the release of catecholamines, aldosterone, or cortisol were observed in human adrenal tumors obtained surgically from patients with pheochromocytoma, primary aldosteronism, or Cushings syndrome, respectively. Each tumor tissue or adjacent normal cortical tissue was sectioned into slices, which were incubated in medium‐199 in the presence or absence of adrenocorticotrophin (ACTH) and ANP. The amounts of epinephrine, norepinephrine, aldosterone, or cortisol released into the medium were measured. Existence of ANP receptors on the adrenal tissues was examined by binding assays, affinity labeling, and immunohistochemistry. Release of catecholamines from pheochromocytoma tissues was inhibited by ANP, and the presence of the ANP receptor on pheochromocytoma was further demonstrated by both binding assays and affinity labeling; Scatchard analysis revealed a single class of binding sites for ANP with a Kd of 1.0 nM and a Bmax of 0.4 pmol/mg of protein and the molecular size was estimated as 140 and a 70 kDa under nonreducing and reducing conditions, respectively. The presence of ANP receptors in pheochromocytoma was demonstrated by immunohistochemistry. ANP inhibited both basal and ACTH‐stimulated aldosterone secretion in the slices of normal cortex, and localization of ANP receptors in zona glomerulosa cells was also demonstrated. However, ANP did not inhibit basal and ACTH‐stimulated aldosterone and cortisol secretion in both tissue slices from aldosteronoma and Cushings adenoma. Consistent with these observations, the absence of ANP receptors in adenoma tissues was determined by binding assays, affinity labeling, and immunohistochemistry. In conclusion, we identified the functional ANP receptors in pheochromocytoma and normal zona glomerulosa cells, but not in aldosteronoma and Cushings adenoma.

Human Atrial Natriuretic Peptide in Aortic and Coronary Sinus Blood During Atrial Pacing in Patients with Ischemic Heart Disease

Summary: This study investigated the plasma concentrations of human atrial natriuretic peptide (hANP) of blood samples obtained from the aorta and coronary sinus (CS) in 19 male patients (mean age of 52.8 ± 2.1 years) with ischemic heart disease before and during atrial pacing. The plasma concentrations of hANP were measured by radioimmunoassay, and the secretion rate of hANP was calculated on the basis of the CS-aorta difference in plasma hANP concentration and the CS flow rate recorded at blood sampling. Before atrial pacing, aortic plasma hANP concentration showed a significant positive correlation with mean pulmonary capillary wedge pressure (r = 0.67, p < 0.002) or mean pulmonary artery pressure (r – 0.71, p < 0.001), and a significant negative correlation with left ventricular ejection fraction (r = −0.50, p < 0.05). During atrial pacing, aortic plasma hANP concentration increased from 67 ± 13 (SEM) to 151 + 33 pg/ml (p < 0.01), CS plasma hANP concentration from 727 ± 121 to 1205 ± 228 pg/ml (p < 0.01), and the hANP secretion rate from 45.4 ± 14.8 to 86.8 ± 28.2 ng/min (p < 0.05, n = 12). The aortic plasma hANP concentration was significantly correlated with the CS plasma hANP concentration (r = 0.81. p < 0.001) or the hANP secretion rate (r = 0.70, p < 0.001). When the patients were divided into the old myocardial infarction group (n = 10) and the angina pectoris group (n = 9), the aortic plasma hANP concentration was significantly higher in the former than in the latter before pacing (p < 0.05). The change in aortic plasma hANP concentration during pacing was significantly smaller in the infarction group than in the angina group (p < 0.05). These results suggest that the secretion rate of hANP determines the circulating level of hANP at rest and during atrial pacing and that the secretion of hANP is influenced by cardiac function.