The aim of the study was to compare under in vivo conditions the new polyamide (Polyflux 160, Gambro) and cuprammonium-rayon dialyzers (AM-FP-17, Asahi; Clirans SE15NL, Terumo) with the polysulfone dialyzer (F60, Fresenius) regarding their permeability for beta-2-microglobulin (11.8 kD), retinol binding protein (21 kD), alpha-1-microglobulin (26.7 kD), alpha-1-glycoprotein (41 kD), alpha-1-antitrypsin (54 kD), albumin (66.3 kD) and transferrin (90 kD). The marker substances were measured by nephelometry or radioimmunoassay. To evaluate the membrane permeability, sieving coefficients 20 min after the start of hemodialysis were calculated using the concentration in the afferent and efferent blood line and in the ultrafiltrate. To get an idea about convective protein loss during a hemofiltration session, the values were computed in milligrams per 20 liters ultrafiltrate. Concerning the permeability of beta-2-microglobulin, the F60, AM-FP-17 and the Polyflux 160 hemofilter were comparable. In the molecular weight range of 20-60 kD both synthetic hemofilters were nearly impermeable. However, the cuprammonium-rayon dialyzers showed in this range a higher cutoff. The calculated albumin and transferrin loss is lower than those of CAPD patients or patients with nephrotic syndrome.

No abstract

Ten cases of adrenal adenomas, one case with unilateral adrenal hyperplasia, and another case with apparent bilateral are reported, in whom an alternative pathway of aldosterone via 21-deoxyaldosterone is operative. They all manifested hypertension, low renin activity, low normal potassium values, as well as high urinary excretion rates of 21-deoxyaldosterone and its related metabolite Kelly's-M1 steroid. In all cases, urinary aldosterone metabolites (aldosterone-18-glucuronide and tetrahydroaldosterone) and aldosterone precursor 18-hydroxycorticosterone levels were normal. Hence, the adrenal lesions give rise to hyper-21-deoxyaldosteronism. 21-Deoxyaldosterone is a weak mineralocorticoid, and its elevated production in the presence of normal aldosterone can induce a pathological state of hypermineralocorticoidism. Adrenalectomy resulted in normalization of hypertension in six of eight and amelioration in two of eight cases. Six of seven adenoma cases examined as well as the case of unilateral adrenal hyperplasia were sensitive to ACTH. One of the seven adenomas and, as expected, the case with apparent bilateral hyperplasia were angiotensin responsive. Histologically and electron microscopically, the operated adenomas consisted predominantly of clear cells, characterized by mitochondria with tubulo-vesicular internal structure similar to those of the zona fasciculata (in contrast, our classical Conn's adenoma with normal 21-deoxyaldosterone excretion exhibited a more heterogenous histological appearance and were, in terms of ultrastructure, more similar to cells of the zona glomerulosa). Ultrastructurally and immunocytochemically, the clear cells of 21-deoxyaldosterone adenomas showed features of both the zona glomerulosa and the zona fasciculata and are, hence, considered to be hybrid cells. We conclude that the determination of 21-deoxyaldosterone and Kelly's-M1 should be considered in the diagnosis of mineralocorticoid-induced forms of hypertension, especially when an adrenal adenoma has been detected with an imaging procedure.

Lab.med. 18:275(1994) 275 Brought to you by | University of Arizona Authenticated Download Date | 7/13/15 5:36 AM Orlginalie Schlüsselwörter: 18-Hydroxycorticosteron -Tetrahydro-Aldosteron -primärer Hyperaldosteronismus -Nebennierenrinden-Adenom -Nebennierenrinden-Hyperplasie Summary:18 is considered to be the immediate precursor o f aldosterone. In vitro studies and few clinical observations show that adrenal adenomas (associated with primary aldosteronism), in contrast to adrenal hyperplasia, produce increased amounts of 18 OH-B. In this study the diagnostic value of 18 OH-B was compared with that ofthe aldosterone metabolites aldosterone-18-glucuronide (ALD-18-G) and tetrahydroaldosterone (TH-ALD) in regard to recognition of primary aldosteronism and differential diagnosis of adenomas and hyperplasia. 1,272 outpatients with hypertension were studied, whereby the diagnosis of primary aldosteronism could be confirmed, in 84 patients due to adrenal adenomas and in 1 10 patients due to adrenal hyperplasia. A diagnostic sensitivity of 99.2% and a diagnostic specificity of 95.2% was calculated for 18 OH-B when differentiating primary aldosteronism due to adenomas from essential hypertension. This was markedly Iower when differentiating between primary aldosteronism due to hyperplasia and essential hypertension; the diagnostic sensitivity here was 79.7% and the diagnostic specificity 60.9% Furthermore, in 1 1 ofthe 84 adenoma cases and in 5 ofthe 1 10 hyperplasia cases 18 OH-B was at first the only elevated steroid. Only over an observation period of up to two years could a slow increase in the aldosterone metabolites be observed in these patients. Thus, 18 OH-B is an "early maker" for primary aldosteronism.