The Excretion of Ammonia and Titratable Acid in Nephritis

Slyke, Donald D. Van; Linder, G. C.; Hiller, Alma; Leiter, Louis; McIntosh, John F.

doi:10.1172/jci100045

Cited by 76 publications

(33 citation statements)

References 4 publications

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“…Experiments on globulin precipitation In order to determine the solubility of globulin in 22 per cent sodium sulfate, globulin was prepared from horse serum according to the In order to test the optimum reaction for the precipitation of globulin with sodium sulfate, portions of urine were adjusted to pH 9, 7.4, 5.4, the isoelectric point of serum globulin, and 4.7, the iso-electric point of serum albumin. Figure 1 shows that between the isoelectric point of globulin and pH 9.0 the precipitation of protein is practically constant, while at the isoelectric point of albumin the amount of protein precipitated increases.…”

Section: Methods For the Determination Of Proteins In Urine1mentioning

confidence: 99%

The Excretion of Albumin and Globulin in Nephritis

Hiller¹,

McIntosh²,

Slyke³

1927

J. Clin. Invest.

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The present work was undertaken in order to ascertain whether the nature of the protein mixture excreted in the different types of nephritis is related to the type and severity of the disease. I. HISTORICALA summary of the early literature on the relation of albumiin to globulin excretion in the urine of nephritic patients has been given by Senator (1) and by Cloetta (2). A general survey of the literature has been given given more recently by Gemll (3). Hoffman was the first to take up the work in detail. Using the early gravimetric methods in 1882 (4) he reported that any albumin: globulin ratio may occur in any type of nephritis, and the value of the ratio is dependent not upon the type of change in the kidney, but on the intensity of the disease processes. A low ratio signified a severe condition, a high ratio a mild one. The ratio was found to rise with recovery in acute nephritis. Lecorche and Talamon (5) found the ratio to decrease with increased severity of the disease. CsatAry (6) found great fluctuations in the albumin: globulin ratio, but made a general statement that he found ratios below 1 in cases of amyloid kidney and above 10 in cases of contracted kidney. In severe cases the ratio fell. Cloetta (2) confirmed the work of Csatiry and reported low ratios in acute nephritis, with rise on recovery, and ratios usually over 10 in chronic nephritis. He found no relation between the albumin: globulin ratios in urine and in sernm. Joachim (7) reported a low ratio in amyloid kidney, a high ratio in contracted kidney. A rise in the ratio signified a good prognosis while a fall signified a poor prognosis. Paton (8) reported albumin fractions high in chronic nephritis and low in acute cases. He was unable to find high globulins in amyloid kidney, and was unable to form any conclusions on the relation of the urinary ratio to that of plasma. Dreser (9) reported that the ratio has no diagnostic importance. Gross (10) reported that the ratio varied and had no prognostic or diagnostic value. Strauss (11) reported that the ratio had no diagnostic value, and that it was mostly so different from that of serum that one would be led to believe that the protein excretion is a selective process of the glomerulus. Wallis (12) re-235

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Section: Methods For the Determination Of Proteins In Urine1mentioning

confidence: 99%

The Excretion of Albumin and Globulin in Nephritis

Hiller¹,

McIntosh²,

Slyke³

1927

J. Clin. Invest.

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“…An investigation of the role of the glycine molecule in uremia appears indicated.-It is not believed that a toxic effect of elevated plasma glycine levels in uremia is due to the increase in free plasma ammonia which has been observed following glycine infusions in dogs and patients (17). The plasma ammonia of uremic patients is not consistently elevated (19,20), and the symptomatology of uremia cannot be reproduced by infusion of ammonia and is not identical with other clinical conditions in which plasma ammonia is increased (21). The elevated plasma glycine content of uremic plasma could be caused by a deficient glycine excretion on the part of the failing kidney, by reduced glycine transformations, or by increased glycine production in the uremic state.…”

Section: Range Of Valuesmentioning

confidence: 99%

Apparent Free Amino Acids in Deproteinized Plasma of Normal and Uremic Persons1

Salisbury¹,

Dunn²,

Murphy³

1957

J. Clin. Invest.

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“…The second mechanism operative in the metabolic acidosis of uremia is the reduced excretion of ammonium (4,(10)(11)(12)(13). In humans (4,11,12) and in animals (14-17) with reduced renal mass, ammonium excretion does not increase appropriately when an acid load is administered chronically or when the substrate for ammonia production, glutamine, is given (13).…”

Section: Introductionmentioning

confidence: 99%

Effect of Reduced Renal Mass on Ammonium Handling and Net Acid Formation by the Superficial and Juxtamedullary Nephron of the Rat

Buerkert¹,

Martin²,

Trigg³

et al. 1983

J. Clin. Invest.

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A B S T R A C T Papillary and surface micropuncture were used to study the handling of ammonium and the formation of net acid by surface nephrons, deep nephrons, and the terminal segment of collecting duct (CD) after renal mass was reduced by two-thirds. Net acid excretion by the remnant kidney (RK) was significantly reduced, averaging 794±81 neq/min (SE) compared with 1,220±105 neq/min after sham operation (P < 0.001), due to a decrease in ammonium excretion (494±54 vs. 871±79 nmol/min in controls, P < 0.001). Urinary pH and titratable acid excretion were not different in the two groups of animals. After RK formation, ammonium delivery to the end of the proximal tubule increased nearly threefold and averaged 66.2±5.6 compared with 18.4±2.9 pmol/min in controls, (P < 0.001). This greater delivery of ammonium was primarily due to renal tubule entry rather than to changes in the filtered load and was only partially related to the differences in flow rate. Ammonium processing by deep nephrons was profoundly affected by a reduction in renal mass. Although absolute delivery of ammonium was greater to the bend of Henle's loop (BHL), the difference could be accounted for on the basis of an increase in nephron size. Received for publication I November 1982 and in revised form 23 February 1983. with the RK. Hydrogen secretion in the proximal segments of deep and surface nephrons did not increase in proportion to the decrease in renal mass and as a consequence bicarbonate delivery to the end of the proximal tubule of surface nephrons and to the BHL of deep nephrons was increased.When renal mass was reduced FDNH. to the base of the terminal CD doubled but did not change by the tip. In both groups FDNI4+ to the base of the CD was greater than to the end of the distal tubule. However, the increase was the same. On the other hand, the increase in the net acid index between the end of the distal tubule and the base of the CD was profoundly greater in rats with an RK. This difference was primarily due to bicarbonate reabsorption rather than enhanced ammonium reentry. Indeed, >400% of the fractional ammonium delivered to the end of the proximal tubule was lost from the tubule fluid. The data suggest that the decrease in acid excretion by the RK is due to two factors. First, hydrogen secretion in the proximal segments of both nephron populations fails to increase in the proportion to the reduction in renal mass. Second, a reduced reentrapment of ammonia, rather than its impaired production, causes ammonium excretion to decrease.

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The Excretion of Ammonia and Titratable Acid in Nephritis

Cited by 76 publications

References 4 publications

The Excretion of Albumin and Globulin in Nephritis

The Excretion of Albumin and Globulin in Nephritis

Apparent Free Amino Acids in Deproteinized Plasma of Normal and Uremic Persons1

Effect of Reduced Renal Mass on Ammonium Handling and Net Acid Formation by the Superficial and Juxtamedullary Nephron of the Rat

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