Present evidence indicates that proteinuria in patients with the nephrotic syndrome is the result of increased permeability of the glomerular capillary walls to proteins, particularly to albumin (1, 2). A rough indication of the permeability to albumin, relative to permeability to water, is provided by the ratio of the concentration of albumin in glomerular fluid to that in plasma. Assuming that no albumin is excreted by the tubules, the rate of albumin excretion (in mg. per min.) divided by the rate of glomerular filtration of water (GFR, in ml. per min.) represents the lowest possible concentration of albumin in glomerular fluid (in mg. per ml.) ; if some albumin is reabsorbed by the tubules, as seems likely, the actual concentration of albumin in glomerular fluid would be greater than this calculated value. If it is accepted that the clearance of inulin (CIN) is equivalent to GFR in children with the nephrotic syndrome (3), it follows that the renal clearance of albumin (CALB) divided by CIN, i.e., CALB/CIN, represents the minimum ratio of the albumin concentration in glomerular fluid to that in plasma. Chinard, Lauson, and Eder (4) showed that in patients with the nephrotic syndrome the renal clearance of the blue dye, T-1824 (CT_1824), was somewhat less than but approximately proportional to CALB. It would appear, therefore, that where large changes in permeability are expected CT_1824should be a satisfactory substitute for CALB. The
A study has been made of the relationship of antibody formation and the changes in amount of the nucleic acids in rabbit lymph nodes draining areas injected with typhoid vaccine.
The increase in DNA was found to parallel the increase in weight of the nodes, as might be expected from the active multiplication of cells.
The peak of PNA increase occurred between the 4th and 6th days after vaccine injection when antibody formation was at its maximum.
A histologic study of methyl green- and pyronine-stained sections of the nodes revealed that during the first 6 days of the experiment the cellular reaction was chiefly one of plasma cells. During the first 3 days plasmoblasts predominated; on the 5th and 6th days mature plasma cells were the prevailing cells. Most of the PNA was contained in the plasma cells.
The lymphocytes began to proliferate in significant numbers on the 3rd and 4th days, and germinal centers began to appear on the 4th and 5th days. They showed their greatest activity only on the 9th day when PNA and antibody formation had passed their peaks.
These results are interpreted as indicating that the plasma cell and not the lymphocyte is responsible for antibody formation.
The intravenous injection of one large dose of serum into rabbits caused a variety of changes of considerable complexity.
1. There was an immediate proliferation of mesenchymal cells, including plasma cells, particularly in heart, lungs, and spleen.
2. The signs of serum disease developed only at the time of abundant antibody formation, before significant quantities of antibody were laid down in the vascular connective tissue.
3. Allergic arteritis, marked glomerular nephritis, myocardial necrosis, and Aschoff body-like structures were seen only after hypersensitivity had developed. It appears that most, if not all, of these pathological alterations were true Arthus phenomena.
4. There were at least two distinct varieties of allergic arteritis and glomerular nephritis, namely a proliferative one, following the first injection, and a a necrotizing one, seen only after 2 injections. It appears that the first was a subacute Arthus phenomenon, while the latter was an acute Arthus phenomenon superimposed on a subacute one. The subacute experimental glomerular nephritis resembled the intracapillary glomerulonephritis in man, while the acute variety was like human extracapillary glomerular nephritis.
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