Current problems in clinical biochemistry最新文献

Human urine may inhibit or activate the phagocytosis by normal human blood of latex, zymosan and inuline. No specific difference was found between the urine of normals and patients with moderate, severe or end stage renal failure. The inhibiting effect was not due to urea or creatinine; the assumption is made that a middle molecular fraction D, which can be isolated by Sephadex G 15 columnchromatography from uraemic ultrafiltrate, is responsible for the observed inhibition. Urines of patients with significant bacteriuria were more frequently activating.

An increase in urinary enzyme activities reflected biopsy confirmed aminoglycoside nephrotoxicity (proximal tubular injury) before changes in blood urea nitrogen, serum creatinine, urinary osmolality and urinary protein excretion. Netilmicin, a semisynthetic derivative of gentamicin, was less nephrotoxic than gentamicin.

Previously reported experiments with animals suggested that reduced renal arterial flow might be the actual cause for the pathogenicity of nephroptosis. Clinical studies now give evidence that measurements of urinary LDH may be a criterion equal to the isotope nephrogram (ING) in considering this disease. Patients with a "mobile" kidney verified by i.v. pyelography were examined by an ING and a 1-day test for urinary LDH. In accordance with periodic kidney displacement total urinary LDH activities were measured in a 8-h urine volume in the supine position and a 8-h urine volume in the erect position of the patients. Evaluations were all expressed as percentage increase of LDH activity of the patient in the erect versus supine position and correlated with his ING-pattern. Among 45 nephroptotic individuals 34 showed, in accordance with a pathological ING, a mean LDH increase of more than a 100%. Eleven individuals had normal INGs and less than 20% increase equal to a group of 16 normal controls. We postulated a 30% increase as the upper limit between normal and pathological urinary LDH. The percentage distribution of isoenzymes was also altered within the pathological LDH range: LDH-I, which increases in normal controls, now decreased in nephroptotic patients. LDH-IV and V, which decrease in controls, now increased. Homomeric isoenzymes obviously show reciprocal behavior. The degree of kidney descent in cm does not correlate with percentage increase of urinary LDH, i.e. it is not a criterion for pathogenicity. Biopsies taken during nephropexy revealed that from an anamnestic duration of 50 weeks onwards the kidney is significantly affected and tissue damages become evident. If patients were re-investigated after nephropexy they showed normal i.v. pyelograms and normal LDH and no longer had clinical symptoms.

Physico-chemical characteristics of urokinase in urine were studied by immunological and chemical methods. By agar zone electrophoresis, commercial urokinase preparations could be separated into an anodic and cathodic fraction. The latter reacted with urokinase antibodies with two precipitation bands. Band I displayed the major part of urokinase activity and migrated as a beta-globulin with a molecular weight of 32,000 daltons. Band II showed immunological identity with human serum, human albumin, alpha-2-macroglobulin and alpha-2-HS-glycoprotein. The specific activity of the cathodic fractions was up to 80,000 ploug units/mg protein. The ratio esterase/fibrinolytic activity did not change during the purification procedure. Further purification of the fractions with higher specific activity by affinity chromatography was unable to eliminate material cross reacting with human antisera (Band II). These findings permit the conclusion, that urokinase activity in urine is not confined to a homogeneous protein fraction. Activity is found both in a low molecular weight fraction and in a high molecular weight complex which contains serum proteins. These cannot be removed by exhaustive purification procedures and may play an important role in stabilizing and/or protecting urinary urokinase against proteolytic degradation. With Todd's technique diffuse fibrinolytic activity could be demonstrated in the kidney in the iuxtamedullary border region, (venae arcuatae, venae interlobulares, vasa recta) and in the epithelium of the calyces. Urokinase activity was specifically blocked by highly purified urokinase antibodies and could thus be distinguished from nonspecific proteolytic activity. The topographic relationship to medulla and uroepithelium may point to a role of urokinase in maintaining patency in slow flow systems.

We describe the biochemical findings concerning five different types of mucolipidosis which have been defined as sialidosis on the basis of the specific enzyme deficiency and the nature of the storage material.

The goal of our study was: 1. To determine the urinary enzyme pattern from urine, taken by ureteral catheterization from the side of the renal disorder, and to compare it with the pattern from the healthy side of the same patient. 2. To compare the enzyme patterns of normal and tumor tissues with the corresponding urinary enzyme patterns.