A B S T R A C T A low molecular weight 82-globulin (,82-microglobulin), albumin, and total protein were measured in concentrated 24-hr urine specimens from 20 healthy subjects and 30 patients with clinical proteinuria of glomerular or tubular type. Classification of proteinuria was made on the basis of clinical diagnosis and size distribution of urinary proteins after gel chromatography. The molecular radii (Stokes' radii) of /2-microglobulin and albumin, estimated by gel chromatography, were 15 A and 35 A.The average 24-hr urinary excretion in healthy subjects was 0.12 mg for 82-microglobulin, 10 METHODSUrine and blood collection. 24-hr urine specimens were collected from 20 healthy male and female volunteers and from 30 patients with manifest or suspected clinical proteinuria. The females delivered urine between menstruations. Collections were carried out as described previously (12). Blood sera were obtained at the end of the urine collections from four normal subjects and 13 of the patients. Sera were also obtained from four patients with renal failure and from a patient whose kidneys were removed by operation after renal failure.15 patients were classified as having glomerular proteinuria on the basis of gel chromatography of urinary proteins, as described below. These patients had the following diagnoses: nephrotic syndrome, glomerulonephritis, Alport's syndrome, and orthostatic proteinuria. The patients with the nephrotic syndrome had edema, decreased albumin, and total protein in plasma (cf . Table III), and elevated concentrations of blood cholesterol. Hematuria and somewhat raised blood pressure was observed in two patients with chronic glomerulonephritis (N. N. and L. L.). Hematuria was also noted in a third patient with glomerulonephritis (C. S.). Proteinuria in the erect position had been observed in the subjects with orthostatic proteinuria.15 patients had diseases affecting the renal tubules, i.e., chronic cadmium poisoning, Wilson's disease, cystinosis, lower urinary tract obstruction, oculo-cerebro-renal syndrome, renal tubular acidosis, tyrosinemia, and Laurence-Moon-Biedl syndrome with renal malfunction. Urinary proteins from these patients, with the exception of L. K., A. G., and A. W., vere submitted to gel chromatography. All patients were classified in the category of tubular proteinuria on the basis of the observed size distribution of urinary proteins (see below). Slightly or moderately increased excretion of glucose was noted in all patients belonging to this group, except in K. L., P. Z., and A. G. Increased phosphaturia had been found in patients E. J., L. K., A. G., and A. WV.; increased aminoaciduria had been observed in patients G. N., A. W., and I. W. Glomerular filtration rate and serum creatinine (13) was determined in a number of the subjects (Table III and Fig. 2). Glomerular filtration rate was measured as endogenous creatinine clearance, and, in two patients, as inulin clearance (Table III) Concentration of proteins. The proteins in filtered urine specimens were concentrat...

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The microvascular permeability to small and large molecules was studied during good and poor metabolic regulation in ten short duration juvenile diabetics. The following variables were measured; daily urinary albumin and beta2-microglobulin-excretion rates, whole body transcapillary escape rate of albumin (TER), glomerular filtration rate (GFR), capillary filtration coefficient (CFC), and capillary diffusion capacity (CDC). The urinary albumin and beta2-microglobulin concentration were measured by sensitive radioimmunoassays; TER was detemined from the initial disappearance of intravenously injected 125I-labelled human serum albumin; GFR was measured on the forearm by straingauge plethysmography and CDS for 51Cr-EDTA clearance; CFC was measured on the forearm by straingauge plethysmography and CDC, for 51Cr-EDTA was determined in the jyperaemic anterio tibial muscle by the local clearance technique. All the above mentioned variables, except CDC, were significantly increased during poor metabolic regulation, indicating a functional microangiopathy. The mechanisms of these alterations appear to be increased filtration pressure in the microcirculation and/or increased porosity of the microvasculature. The findings of increased microvascular albumin passage are compatible with the hypothesis that the organic - histologicallly demonstrated - diabetic microangiopathy is a long-term effect of periods of increased extravasation of plasma proteins, with subsequent protein deposition in the microvascular wall, i.e. the concept to plasmatic vasculosis.