muramidase and Nephrotic-Syndrome

Topics: Adult; Animals; Bence Jones Protein; Blood Urea Nitrogen; Calcium; Carcinoma; Electrolytes; Fanconi Syndrome; Humans; Kidney; Kidney Diseases; Leukemia; Lymphoma; Multiple Myeloma; Muramidase; Neoplasms; Nephrotic Syndrome; Phosphorus; Potassium; Proteinuria; Sodium

Topics: Amyloidosis; Blood Vessels; Diabetes Insipidus; Humans; Hypercalcemia; Hyponatremia; Kidney; Kidney Diseases; Lactates; Leukemia; Lymphoma; Muramidase; Nephrotic Syndrome; Uric Acid; Urinary Tract

An attempt is made in this study to provide an answer to the question whether glomerular diseases are accompanied by tubular disorders. The urinary lysozyme activity was determined by means of a turbidimetric assay method in 10 healthy children as controls, 10 patients with glomerulonephritis, 8 patients with Alport's syndrome (hereditary glomerulonephritis with deafness) and 12 children with idiopathic nephrotic syndrome. In most of the cases a significant increase in urinary lysozyme excretion, indicative of tubular damage, was found and this finding correlates well with the tubular morphology of the patients.

Topics: Child; Child, Preschool; Clinical Trials as Topic; Glomerulonephritis; Humans; Infant; Kidney Diseases; Kidney Glomerulus; Kidney Tubules; Muramidase; Nephritis, Hereditary; Nephrotic Syndrome

1 In previous studies on the renal targeting of the ACE inhibitor captopril, we demonstrated that a 6 fold increased concentration of this drug could be obtained in the kidney after conjugation to the low-molecular-weight protein lysozyme. In this study, we investigated in unrestrained rats whether systemic administration of captopril-lysozyme also results in an enhanced effect on renal parameters, relative to the systemic effects. 2 Renal effects: intravenous infusion of captopril-lysozyme for 6 h resulted in a more pronounced increment of renal blood flow (31+/-2% vs 17+/-4% at 0.5 mg kg(-1) 6h(-1), P<0.01) and an approximately 5 fold enhanced natriuresis (167+/-17% vs 36+/-7% at 1 mg kg(-1) 6 h(-1), P<0.001) in comparison with equimolar amounts of captopril as a free drug. In correspondence with these findings, renal ACE inhibition was potentiated approximately 5 fold (-50+/-4% vs -22+/-3% at 1 mg kg(-1) 6 h(-1), P<0.001). 3 Systemic effects: conjugated captopril did not affect blood pressure in dosages up to 5 mg kg(-1) 6 h(-1). This effect coincided with a less pronounced inhibition of the pressor response to intravenously administered angiotensin I (-12+/-3% vs -66+/-5% at 1 mg kg(-1) 6 h(-1), P<0.001), and a markedly attenuated plasma ACE inhibition (-19+/-2% vs -37+/-3% at 1 mg kg(-1) 6 h(-1), P<0.001) compared to an equivalent dose of free captopril. 4 An experiment of continued intravenous administration of captopril-lysozyme for 7 days in nephrotic syndrome demonstrated that the conjugate is also active in renal disease: the antiproteinuric response was substantially augmented (-67+/-5% vs -15+/-7% at 4 mg kg(-1) 24 h(-1), P<0.001) compared to the free drug, in the absence of blood pressure reduction. 5 These data demonstrate that intravenous administration of a captopril-lysozyme conjugate leads to more selective renal ACE inhibition and enhanced renal effects as well as less systemic effects compared to captopril itself.

Topics: Angiotensin I; Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Pressure; Captopril; Dose-Response Relationship, Drug; Doxorubicin; Drug Carriers; Immunohistochemistry; Injections, Intravenous; Kidney; Male; Muramidase; Nephrotic Syndrome; Rats; Rats, Wistar; Regional Blood Flow

Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Biopsy; Bone Marrow; Diagnosis, Differential; Fatal Outcome; Humans; Leukemia, Monocytic, Acute; Male; Muramidase; Nephrotic Syndrome; Proteinuria; Remission Induction

Topics: Humans; Leukemia, Monocytic, Acute; Male; Middle Aged; Muramidase; Nephrotic Syndrome; Proteinuria

Topics: Albuminuria; Autoantigens; beta 2-Microglobulin; Diagnosis, Differential; Epithelium; Glomerulonephritis; Humans; Immunoglobulin G; Kidney Tubules; Muramidase; Nephritis, Interstitial; Nephrotic Syndrome; Proteinuria

In order to assess to what extent glomerular or tubular function is involved in the renal handling of amylase and the lysozyme to creatine clearance ratios (CAm/CCr and CLys/CCr) were evaluated in 22 healthy volunteers and in 71 patients with different renal diseases. In normal controls, the mean CAm/CCr was 2.55 +/-1.54 SD, with an upper normal limit of 5.56. A normal ratio was found in patients with glomerulonephritis, with or without a nephrotic syndrome, and in patients with pyelonephritis. A significantly elevated ratio (P less than 0.001) was instead found in patients with uremia and in patients with uremia and in patients with either chronic or acute tubular damage. The CLus/CCr ratio was elevated in all the groups, except in patients with glomerulonephritis and minimal proteinuria. These results show that in humans, as in animals, the amylase filtered load undergoes partial tubular reabsorption. In renal diseases, an increase of the CAm/CCr is caused by either a marked reduction of functioning nephrons or a severe tubular damage, while the glomerular permeability does not seem to be involved. Some other mechanism is probably involved in the elevation of the CAm/CCr during acute pancreatitis.

Topics: Acute Disease; Amylases; Creatinine; Glomerulonephritis; Humans; Kidney Diseases; Kidney Failure, Chronic; Kidney Glomerulus; Muramidase; Nephrotic Syndrome; Pancreatitis; Proteinuria; Pyelonephritis

Topics: Acute Kidney Injury; Alkaline Phosphatase; Arylsulfatases; Enzymes; gamma-Glutamyltransferase; Glomerulonephritis; Glucosidases; Glucuronidase; Humans; Kidney Transplantation; L-Lactate Dehydrogenase; Muramidase; Nephrotic Syndrome; Pyelonephritis; Transplantation, Homologous

Topics: Animals; Biological Transport; Blood Proteins; Capillaries; Chromatography, Gel; Cyanides; Dogs; Humans; Iodine Radioisotopes; Kidney; Kidney Cortex; Kidney Glomerulus; Kidney Tubules; Kinetics; Mathematics; Microscopy, Phase-Contrast; Models, Biological; Molecular Weight; Muramidase; Nephrotic Syndrome; Protein Binding; Proteinuria

On the assumption that increased urinary lysozyme concentration (;lysozymuria') indicates tubular proteinuria and therefore impaired tubular function, urinary lysozyme has been estimated in acute disorders where transient disturbances of renal function might be expected, in cases diagnosed clinically as extrarenal uraemia, and in a few examples of acute renal disease. Reversible lysozymuria occurred with hypokalaemia, postoperative ;collapse', electrolyte depletion, severe extrarenal infection, acute pyelonephritis, the nephrotic syndrome, after a few apparently uncomplicated surgical operations, and very transiently after ventricular fibrillation abolished by DC shock. There was no lysozymuria with severe uraemic heart failure, aspirin and paracetamol poisoning, or severe jaundice, nor in two cases of acute glomerulonephritis. Although lysozymuria may occasionally be useful in the clinical diagnosis of acutely disordered renal function, the results suggest that its value is limited; on the other hand, they have provided information on renal pathophysiology in acute disease.

Topics: Acetaminophen; Acute Disease; Aspirin; Electroshock; Glomerulonephritis; Heart Failure; Humans; Hypokalemia; Jaundice; Kidney; Kidney Diseases; Kidney Failure, Chronic; Kidney Tubules; Muramidase; Myocardial Infarction; Nephrotic Syndrome; Pneumonia; Postoperative Complications; Proteinuria; Pyelonephritis; Uremia; Ventricular Fibrillation

Topics: Adolescent; Adult; Aged; Animals; Chronic Disease; Dogs; Female; Glomerular Filtration Rate; Glomerulonephritis; Humans; Hypertension; Hypertension, Renal; Immunoelectrophoresis; Kidney Diseases; Male; Middle Aged; Muramidase; Myeloma Proteins; Nephritis, Interstitial; Nephrocalcinosis; Nephrotic Syndrome; Pyelonephritis; Rabbits; Vascular Diseases

The present study was directed toward determining the role of the kidney in the metabolism of various classes of serum proteins and to define the urinary protein excretion patterns and the pathogenesis of disorders of protein metabolism in patients with proteinuria. To this end, the metabolic fates of a small protein, lambda-L chain (mol wt 44,000), and a protein of intermediate size, IgG (mol wt 160,000), were studied in controls and patients with renal disease. Controls metabolized 0.28%/hr of circulating IgG and 22.3%/hr of circulating lambda-L chain. All the IgG and 99% of the lambda-L chain was catabolized with the remaining lambda-L chain lost intact into the urine. The kidney was shown to be the major site of catabolism for small serum proteins. Three distinct disorders of protein metabolism were noted in patients with renal tubular disease and tubular proteinuria, glomerular disease (the nephrotic syndrome), and disease involving the entire nephrons (uremia), respectively. Patients with renal tubular disease had a 50-fold increase in the daily urinary excretion of 15-40,000 molecular weight proteins such as lysozyme and lambda-L chains. Serum IgG and lambda-L chain survivals were normal; however, the fraction of the over-all lambda-L chain metabolism accounted for by proteinuria was increased 40-fold whereas endogenous catabolism was correspondingly decreased. Thus, tubular proteinuria results from a failure of proximal tubular uptake and catabolism of small proteins that are normally filtered through the glomerulus. Patients with the nephrotic syndrome had a slight increase in lambda-L chain survival whereas IgG survival was decreased and the fraction of IgG lost in the urine was markedly increased. Here, abnormal glomerular permeability to proteins of intermediate size is the basic abnormality. Patients with uremia had a normal IgG survival but a four to 10-fold prolongation of lambda-L chain survival due to loss of entire nephrons, the major site of metabolism of these proteins. This results in an increase (up to 10-fold) in the serum concentration of lambda-L chain, lysozyme, and other small biologically active proteins, a phenomenon that may be of importance in causing some of the manifestations of the uremic syndrome.

Topics: Adult; Blood Protein Disorders; Blood Protein Electrophoresis; Blood Proteins; Cell Membrane Permeability; Child; Electrophoresis, Disc; Humans; Immunoglobulin G; Iodine Radioisotopes; Kidney; Kidney Glomerulus; Molecular Weight; Muramidase; Nephrotic Syndrome; Proteinuria; Radioimmunoassay; Uremia

Topics: Adolescent; Adult; Albumins; Albuminuria; Child; Child, Preschool; Creatinine; Fanconi Syndrome; Female; Humans; Infant; Infant, Newborn; Kidney Tubules; Male; Muramidase; Nephrotic Syndrome; Pyuria

Topics: Adolescent; Adult; Age Factors; Asthma; Child; Child, Preschool; Female; Humans; Infant; Infant, Newborn; Leukemia; Liver Diseases; Male; Muramidase; Nephrotic Syndrome; Sex Factors

Topics: Acute Kidney Injury; Blood Urea Nitrogen; Glomerulonephritis; Humans; Kidney Diseases; Kidney Tubules; Leukemia; Muramidase; Nephritis; Nephrocalcinosis; Nephrotic Syndrome; Urinary Calculi

Topics: Child; Dermatologic Agents; Humans; Muramidase; Nephritis; Nephrotic Syndrome; Urine