The APS Journal Legacy Content is the corpus of 100 years of historical scientific research from the American Physiological Society research journals. This package goes back to the first issue of each of the APS journals including the American Journal of Physiology, first published in 1898. The full text scanned images of the printed pages are easily searchable. Downloads quickly in PDF format.

The renal mechanisms by which urate is excreted have not yet been defined and there still is disagreement on several major points.Previous studies are in accord on one point, that the normal urate clearance in man is only a small fraction of the glomerular filtration rate, usually of the order of 8-10o. Differing explanations for the relatively low clearance have been offered. Patently, the difference between the clearance of urate and the clearance of inulin must be due either to non-filterability of a large fraction of the plasma urate, to tubular reabsorption of a major fraction of the filtered urate, or to some combination of these two.Some observers have reported non-filterability of the plasma urate, presumably due to proteinbinding or polymerization, but the magnitude of the bound fraction, 4-24%o (1), and 23% (2) has not been nearly sufficient to account for the difference between the clearances of urate and inulin. In a number of other studies (3)(4)(5) Despite this evidence of filterability in sitro and, at least in lower vertebrates, in s'ivo, several investigators have held that this is not the situation in man and that the actual amount filtered at the glomerulus is close to the amount excreted. Berglund and Frisk (9) advanced this theory to explain the fairly constant clearance of urate over a moderate range of plasma urate concentrations and a fairly constant ratio of urate to creatinine clearance in a series of patients with a wide range of renal functional impairment. The same hypothesis has been more recently supported by Wolfson and his associates (2, 10, 11), for reasons similar to those of Berglund and Frisk. In addition, it was suggested that the very low cerebro-spinal fluid urate concentration was due to non-filterability in vivo. The latter position, however, is not tenable since the composition of spinal fluid departs in several respects from that of a plasma ultrafiltrate, the concentration of a number of filterable substances in the spinal fluid being appreciably lower than that in plasma water (12, 13). These authors hypothesize that non-filterability of urate is due to polymerization and that urate is excreted by filtration only or by filtration with a small amount diffusing back passively.The most extensive work on the mechanism of uric acid excretion is probably that of Talbott (14) who reported a number of simultaneous determinations of inulin and urate clearances and the effect of various agents on the clearance ratio. Benedict's method (17). No correction for non-uric acid chromogen was made in any of these experiments since all critical data were obtained at times when the plasma concentration and urinary excretion of urate had been greatly increased by the administration of solutions of pure urate. At such times the non-uric acid chromogen is a negligible fraction of the total. Complete diffusibility of the plasma urate has been assumed in all calculations. Toxic reactionsNausea and vomiting occurred in about half of the patients who received infusions of the lithium carbon...

Synopsis Initial reporting suggested that kidney involvement following COVID-19 infection was uncommon but this is now known not to be the case. Acute kidney injury (AKI) may arise through several mechanisms and complicate up to a quarter of patients hospitalised with COVID-19 infection being associated with an increased risk for both morbidity and death. Mechanisms of injury include direct kidney damage predominantly through tubular injury, although glomerular injury has been reported; the consequences of the treatment of patients with severe hypoxic respiratory failure; secondary infection; and exposure to nephrotoxic drugs. The mainstay of treatment remains prevention of worsening kidney damage and in some cases the need for renal replacement therapies (RRT). Although the use of other blood purification techniques has been proposed as potential treatments, results to-date have not been definitive.

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The appearance of proteinuria in patients suffering from congestive heart failure is a common clinical occurrence. Since such patients, without any intrinsic renal disease, frequently have both an elevated renal venous pressure and a reduced renal blood flow (1), it would seem that either one or both of these factors may lead to proteinuria.Proteinuria has been produced experimentally by partial obstruction either of the renal artery or of the renal vein (2-5). In most of this work, however, studies of renal hemodynamics were incomplete, or when adequate pressure and blood flow measurements were made (6, 7), the experiments were such that it was impossible to determine specifically which hemodynamic factor was responsible for the appearance of the proteinuria.The present study was The estimations of renal plasma flow (RPF) and glomerular filtration rate (GFR) for each kidney were made by determining the clearances of para-aminohippurate (PAH) and exogenous creatinine, respectively. Blood samples were drawn at the midpoint of each clearance period from the right femoral artery through an indwelling needle. During the operative procedure the animal was given intravenously a priming d.nse of 1.5 grams of creatinine dissolved in 30 ml. of water. This was followed by a sustaining infusion of an 0.85 per cent NaCl solution delivered at a constant rate of 3 or 5 ml. per minute by a Bowman Pump for the remainder of the experiment. This sustaining infusion contained sufficient amoants of creatinine and PAH so that these substances were delivered at rates of 20 mg. of creatinine per minute and 3 mg. of PAH per minute. In some instances an additional infusion of NaCl solution (0.85 or 1.5 per cent) was given during the course of the experiment. The reason for this will be discussed later.After completion of the operative procedure the animal was allowed to recover for about 30 minutes. One or more control urine samples were then collected in order to measure the clearances and determine the presence of proteinuria. The clamp was then tightened until the pressure in the left renal vein rose to the desired level. After the pressure had been elevated for 15 to 30 minutes, con-secutive urine samples were collected until proteinuria appeared or until the pressure had been elevated for 1 to approximately 3 hours without the occurrence of proteinuria. The clamp was then released allowing the pressure in the left renal vein to fall freely.After an interval of time at least sufficient to allow the renal dead space to be cleared, one or more recovery samples were collected.Creatinine concentration in urine and plasma was determined by the method of Kennedy, Hilton, and Berliner (9). PAH concentration in urine and plasma was determined by the method of Smith, Finkelstein, Aliminosa, Crawford, and Graber (10).The method used to determine the concentration of protein in urine was a modification of the method of 737