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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.

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.

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.

Micropuncture experiments were carried out in 20 rats with bilat. experimental chronic pyelonephritis. Inulin and urea concentrations were estimated in the late proximal, early distal and latte distal nephron segment. Proximal urea reabsorption did not differ from that in control animals. Fractional amount of filtered urea in the early distal segment was significantly lower in the pyelonephritic rats, urea reabsorption in the distal tubule approcimated zero. The data indicate that intrarenal urea recirculation is abolished by the experimental lesion, thus determining maximal urine urea concentration. It is suggested that the concentrating defect of experimental pyelonephritis is not only a result of an adaptational increase in individual nephron GFR; an additional intrinsic lesion seems to be present, located in the renal medulla.

From repeat biopsies of 291 patients with glomerulonephritis, the clinical and morphological course of the individual forms of glomerulonephritis were compared with one another. From these results we concluded that: 1. Every form of glomerulonephritis has in all probability its individual course and prognosis, which can only be very slightly influenced by therapy. 2. The prognosis is considerably worsened, when either hypertension develops or tubular lesions in the morphological sense of an acute renal failure.

Comparative morphological and clinical studies of 2,500 patients suffering from glomerulonephritis, enabled us to divide the different forms of diffuse glomerulonephritis into 3 distinct groups and to separate these groups from the focal glomerulonephritides. The different forms of diffuse glomerulonephritis in group I are: 1. endocapillary (acute) glomeruloenphritis (of the post-streptococcal type), 2. mesangioproliferative glomerulonephritis, 3. mesangioproliferative glomerulonephritis with focal crescents, 4. mesangioproliferative glomerulonephritis with focal scarring, 5. minimal proliferating intercapillary glomerulonephritis without nephrotic syndrome. It is emphasised that these forms can transform into one another, that they seldom occur with nephrotic syndrome, and with varying frequency with hypertension. Group II consists of: 1. minimal proliferating intercapillary glomerulonephritis with nephrotic syndrome, 2. focal sclerosing glomerulonephritis, 3. perimembranous glomerulonephritis, 4. membranoproliferative glomerulonephritis, 5. lobular glomerulonephritis. It is stressed that these glomerulonephritis forms usually do not develop out of group I type glomerulonephritis forms, and that in this group a nephrotic syndrome is the most prominent clinical syndrome. In the third group are 1. mesangioproliferative glomerulonephritis with diffuse crescents, 2. necrotising glomerulonephritis. It is shown that this form of glomerulonephritis does not usually develop from either group I of II forms. The fourth group of focal glomerulonephritis is uncommon. This disease is characterized by a necrotising and proliferative inflammatory lesion found segmentally and focally in the glomeruli. Most of the other glomeruli appearing normal. It is emphasised that in the literature the diagnosis focal glomerulonephritis is made far too often. This is because glomeruli in which the inflammatory process in a few lobules is of varying prominence, are included in the focal glomerulonephritis group. The classification of the different forms of glomerulonephritis into 3 groups here described, is thought of as a basic classification. It is compared with Ellis' classification (1942), with which it has much in common.

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).

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.