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The evaluation of accuracy and efficiency of the frequency-modulated simultaneous Atomic Absorption Spectrometry (FremsAAS) has been extended to an arrangement with EDL as light sources. Fundamental calibrations have been worked out for As, Se and Sb using a graphite furnace as well as hydride generation in combination with a heated quartz tube as atomization unit. The characteristic data are in good agreement with results obtained by conventional single-channel AAS instruments. Determinations in three standard reference materials with different complex matrices resulted in complete agreement with the certified values.

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Determination of marker proteins like albumin and alpha 1-microglobulin allows to differentiate various types of proteinuria in kidney diseases. In the present communication we calculate the degree of tubulointerstitial involvement by quantitation of the tubular marker alpha 1-microglobulin in urine in relation to albuminuria. A mathematical relation between minimal tubular proteinuria with the degree of albumin excretion was observed. Cases forming this line did not exhibit interstitial fibrosis when analyzed histologically. In contrast most cases exhibiting higher excretion rates of the tubular marker showed various degrees of tubulointerstitial involvement. In order to differentiate interstitial contribution from overload tubular proteinuria in patients with an albumin excretion rate above 3000 mg/g creatinine alpha 1-microglobulin (measured) is suggested to be corrected by the "glomerular" component of alpha 1-microglobulin using the following equation: "tubulo-interstitial alpha 1-microglobulin" = alpha 1-microglobulin (measured) -4.7 exp (2.2 x 10(-4)) [albumin]. Alternatively the correction can be performed graphically. This procedure may be of considerable help in preventing misinterpretations of urinary protein patterns in patients with nephrotic proteinuria.

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The traditional methods in urinalysis (visual microscopy, qualitative test strip screening) were compared with automated microscopy (UA-1000, TOA-medicals, Japan) and quantitative single protein analysis in 562 fresh morning urine samples. Albumin served as "glomerular" and alpha 1-microglobulin as "tubular" markers measured by turbidimetry. The test strip delivered at least one positive result in 60% of the urine for blood (21%), leukocytes (27%), or protein (34%). In only 4% casts or renal cells were found by traditional microscopy, whereas automated microscopy was positive for these findings in 28% of the urine. Quantitative urine protein analysis alone exhibited results outside the reference interval in 52% of the urine. Combination of the test strip procedure for blood and leukocytes with urine protein analysis increased the number of positives to 73%. Thirteen percent of these additional findings were classified as glomerular (64%) and tubular (72%) proteinurias. In 7% of the urine a false positive protein test strip result was confirmed by quantitative albumin determination. Of 157 urine samples, positive in mechanized video recorded screening, 60 (38%) were normal in single protein analysis. The results allow for the conclusion that the advanced techniques are superior to traditional screening procedures in detecting abnormal urine composition. It is suggested that traditional urinalysis should be supported or replaced by quantitative determination of albumin and alpha 1-microglobulin. This recommended strategy is able to exclude or detect tubulo-interstitial nephropathies or microalbuminuria in earlier phases of renal complications, such as in diabetes mellitus, hypertension or in nephrotoxic injury. A fully mechanized version is suggested to meet appropriate quality criteria and economic needs.(ABSTRACT TRUNCATED AT 250 WORDS)

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Prerenal, glomerular, tubulointerstitial and postrenal proteinurias and haematurias are usually differentiated by a number of non-invasive and invasive diagnostic procedures. We have applied a new analytical strategy based on the observation that different urine protein patterns are excreted in normal, prerenal, renal and postrenal proteinurias and haematurias. When analysed by turbidimetric procedures urine albumin, IgG, alpha 1-microglobulin and alpha 2-macroglobulin can be used as marker proteins to characterize the degree of glomerular permeability, tubular protein reabsorption and postrenal bleeding respectively. Primary glomerulopathies (selective and non-selective) and tubulointerstitial nephropathies can be differentiated by plotting the excretion rates of IgG or alpha 1-microglobulin against that of albumin. Postrenal contaminations are detected by quantitative turbidimetric assay of the high molecular weight proteins, alpha 2-macroglobulin and IgG. In postrenal bleeding, with albumin concentrations above 100 mg/l, the relative excretion rates of these proteins were proportional to their plasma concentrations. In glomerular haematurias, however, the ratios to albumin were much lower. The optimal discriminating ratio was found to be 2.0 x 10(-2) for alpha 2-macroglobulin/albumin and 2 x 10(-1) for IgG/albumin. Tubulointerstitial involvement in haematuria is characterized by elevated alpha 1-microglobulin excretion rates, with alpha 2-macroglobulin/albumin ratios below 2.0 x 10(-2) and IgG/albumin ratios above 2 x 10(-1). The reported procedure allows the exclusion and differentiation of clinically relevant proteinurias and haematurias in a single urine specimen.

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Appraisal of the long-term prognosis of primary glomerulonephritis at the time of diagnosis, i.e. when there are no longitudinal observations, is based on the constellation of clinical findings as well as on the morphological changes in glomeruli and interstitial renal tissue which can be detected in histological examinations of biopsy specimens. A favorable long-term prognosis is to be expected with reasonable probability when 1. an isolated proteinuria of less than 1 g/24 hour and/or erythrocyturia (no cell casts in the sediment) are present in normal kidney function (glomerular filtration rate) as well as normal blood pressure characteristics, and the renal parenchyma shows normal sonographic findings; 2. Only slight mesangial cell proliferations can be detected histologically, and interstitial lesions (cell infiltration, fibrosis) are absent.

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Hematuria caused by prerenal, glomerular, postglomerular, and postrenal causes is usually differentiated by a number of noninvasive and invasive diagnostic procedures. In the present study we have applied a new analytical strategy based on observations that the various forms of hematuria can be classified by their typical protein pattern. When analyzed by quantitative turbidimetric assays, urines from postrenal hematurias contained high-molecular-weight proteins (alpha 2-macroglobulin and IgG) in proportions found in plasma. Relating excretion rates (mg/mg) of these proteins to those of albumin, ratios for alpha 2-macroglobulin/albumin and IgG/albumin were 2.0-31 x 10(-2) and 20.0-180 x 10(-2), respectively. In contrast, glomerular hematurias exhibited ratios of 0.01-2.0 x 10(-2) (alpha 2-macroglobulin/albumin) and 2.0-20 x 10(-2) (IgG/albumin). Additional determination of alpha 1-microglobulin allowed us to differentiate postglomerular hematurias caused by interstitial nephropathies from glomerular and postrenal diseases. Critical evaluation of 93 cases diagnosed by independent clinical examination including histology, sonography, and cystoscopy revealed that the criteria derived from protein measurements resulted in correct classification when urine albumin exceeds 100 mg/l. This noninvasive procedure is expected to be of considerable help in the primary care of patients with unexplained hematuria.

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Auxin causes elongation growth of plant cells by increasing the plastic extensibility of the cell wall. Putative cellular events involved in this hormone action were studied using maize (Zea mays L.) coleoptiles with the following results: (i) Auxin enhances membrane flow from the endoplasmic reticulum to the plasma membrane (PM). This effect was demonstrated by pulse-labeling of the endoplasmic reticulum with myo-[(3)H]inositol in coleoptile segments and by measuring the distribution of the label within isolated and separated microsomal membrane fractions, (ii) Auxin rapidly increases the amount of antibody-detectable H(+)-ATPase in the PM. This augmentation is already significant 10 min after the addition of indole-3-acetic acid (IAA) and reaches a new higher steady-state level after about 30 min. (iii) Cycloheximide, a potent inhibitor of both protein synthesis and extension growth, quickly diminishes the auxin-enhanced level of the PM H(+)-ATPase, indicating an apparent half-life of the enzyme of around 12 min. (iv) Cordycepin, which blocks the synthesis of mRNAs, reduces the auxin-elevated level of the H(+)-ATPase similar to cycloheximide. (v) Changes in the growth rate of coleoptile segments in response to IAA, cycloheximide, and cordycepin exactly reflect the changes of the H(+)-ATPase level in the PM. (vi) The elongation growth induced by fusicoccin, or ester compounds, or by an elevated CO2 concentration in the incubation medium, is not related to an increased number of H(+)-ATPase molecules within the PM. (vii) The necessity of H(+) for cell-wall-loosening processes is again demonstrated by growth experiments with abraded coleoptile segments. The adjustment of the cell wall to a pH of ≥6.5 completely abolishes the auxin-induced elongation growth; no inhibition occurs with non-abraded segments. Buffer solutions of pH ≤6.0 induce "acid growth" of abraded segments for several hours. It is suggested that auxin activates a cluster of genes responsible (i) for the induction and acceleration of exocytotic processes (e.g. by the synthesis of either proteins, necessary for the fusion of membranes, or of other effectors); (ii) for the synthesis of PM H(+)-ATPases, increasing the capacity for H(+)-extrusion into the apoplast as a precondition for wall enlargement ("acid growth"); (iii) for a supposed synthesis and exocytosis of certain proteins, enzymes and wall precursors necessary for wall metabolism and the "repair" of the proton-loosened and turgor-stretched cell wall. Both, fusicoccin and auxin affect cell-wall plasticity according to the "acid-growth" theory. However, the mechanisms leading to this event are completely different; the auxinenhanced H(+)-extrusion is a gene-controlled process.

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A family showed a renal disturbance, characterized by an elevated urea plasma concentration while glomerular filtration was found to be normal. A detailed study of renal clearance was performed on two members of this family in order to define the nature and site of the disorder. Evidence points to an isolated impairment of urea elimination, giving rise to a reduced urea concentrating ability and thus to a decrease in maximum urine concentration and water conservation. The most probable site of this impairment seems to be the proximal tubule.

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In an open study three chronically schizophrenic patients with normal kidney function were treated by hemodialysis in an attempt to ameliorate their psychotic symptoms. Neuroleptic treatment was stopped at least four weeks prior to hemodialysis. The patients were dialysed once weekly for twelve (in one case eleven) weeks. Psychopathology was evaluated using the IMPS, BPRS and NOSIE. No patient showed any improvement during the course of dialysis, one patient showed a marked detrioration. These observations raise doubts about whether schizophrenic psychoses can be improved by means of hemodialysis as previously published by Wagemaker (1977).

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Therapeutic trials with hemodialysis have been performed in three cases of chronic schizophrenia. The severely ill patients had been hospitalized for more than ten years and had not responded to different types of conventional somatic treatment. Psychopathology was evaluated by use of the IMPS, BPRS, and NOSIE scales. No improvement could be observed as a consequence of 12 (11 in one case) hemodialysis treatments. Rather, some deterioration occurred in two of the patients. This result is not in accord with the markedly positive findings of Wagemaker and Cade (1977). However, further studies appear necessary to render final conclusions.

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