Experimental Hyposthenuria 12

Hayman, J. M.; Shumway, Norman P.; Dumke, P.; Miller, Max

doi:10.1172/jci101035

Cited by 66 publications

(13 citation statements)

References 52 publications

(30 reference statements)

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“…The urate clearance data of Berglund and Frisk (33) The second interpretation utilizes the hypothesis advanced by Hayman et al (13). They have suggested that the failure of reabsorption of urea in dogs with damaged kidneys may be attributed to increased urine flow through the tubules.…”

Section: Action Of Drugsmentioning

confidence: 98%

Renal Function in Patients With Gout 1

Coombs¹,

Pecora²,

Thorogood³

et al. 1940

J. Clin. Invest.

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There are several theories of the pathogenesis of urate 2 accumulation in patients with gout. A disturbance of elimination of this substance by the kidneys is probably the most popular. This has been challenged, however, in a previous communication from this laboratory (1), since it appears to be inconsistent with certain experimental data. Whether or not this theory is valid, it deserves serious consideration because urates as naturally occurring end-products of purine metabolism are disposed of by the body largely by excretion through the kidneys. If one pursues the hypothesis to a logical conclusion, any defect of elimination might be inherited or it might be an acquired phenomenon following damage to the functioning units of the kidneys.The accepted theory (2, 3) of renal physiology in man assumes that urates are present in glomerular urine as are other ultrafiltrable substances and reabsorbed in part by the cells lining the tubules. If the kidneys were primarily at fault in the gouty diathesis, accumulation of urate might be attributed either to (a) a reduction of the number of functioning glomeruli or (b) an increased reabsorption by the tubules. Both of these phenomena are partially susceptible of quantitative analysis now that improved methods for the study of kidney function are available.A presentation and discussion of kidney function data, as determined by five experimental procedures, are contained in this communication. These include tests for the excretion of substances normally present in the body such as urea, creatinine, urate, sodium and chloride and for the excretion of foreign substances introduced parenterally such as phenolsulphonphthalein, neo-iopax 1 This investigation was supported in part by a grant from the Corn Industries Research Foundation.2 The term urate is preferable to uric acid in a consideration of acid-base equilibrium of biological media just as chloride is preferable to hydrochloric acid and phosphate is preferable to phosphoric acid. and inulin. Studies were made of normal persons and of patients suffering from diseases other than gout, as well as of patients with classical gout. The action of drugs used therapeutically in the treatment of acute and chronic gouty arthritis was investigated. SUBJECTSThirty-one persons acted as experimental subjects. Twenty-two were afflicted with gout; six were patients with diseases other than gout; three were normal persons. The patients with gout were selected without regard to extent of disease or duration of symptoms. It was necessary only that the criteria for the diagnosis of gout were satisfied (1, 4, 5) and that the patients consented to hospital admission for study. All except K. He. were males. Their ages varied from 28 to 81 years. Each patient had had two or more attacks of acute arthritis, and on two or more occasions the concentration of fasting serum urate had been greater than 6.0 mgm. per 100 cc. Osseous or cartilagenous tophi were suspected from the roentgenogram in thirteen. Subcutaneous tophi were present in seventeen....

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Section: Action Of Drugsmentioning

confidence: 98%

Renal Function in Patients With Gout 1

Coombs¹,

Pecora²,

Thorogood³

et al. 1940

J. Clin. Invest.

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“…The possible effect of anemia and hemoglobinemia on formation of concentrated urine. It has been suggested that anemia, which in some instances is associated with reduced renal clearances of inulin and PAH (10), may result in hyposthenuria but this apparently is not always the case (3,4,11). The maximum urine specific gravity value recorded in the hospital record of patients with various types of anemia, including some with chronic anemia, is seen in Figure 5.…”

Section: Cell Trait Subjects and (C) Sicklementioning

confidence: 99%

Hyposthenuria in Sickle Cell Anemia: A Reversible Renal Defect

Keitel¹,

Thompson²,

Itano³

1956

J. Clin. Invest.

142

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“…It has not been clear whether the capacity of the kidneys to concentrate urine is selectively impaired by hypercalcemia or whether it is depressed together with many other renal functions as a result of substantial injury to and encroachment upon active renal parenchyma (9). In the present experiments the effects of hypercalcemia on renal function and morphology were studied in rats given large doses of calciferol (vitamin D2) for several days.…”

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confidence: 95%

The Effect of Hypercalcemia Induced by Calciferol Upon Renal Concentrating Ability1

Epstein¹,

Rivera²,

Carone³

1958

J. Clin. Invest.

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Polyuria and loss of renal concentrating ability have frequently been observed in patients with hypercalcemia (1-8). It has not been clear whether the capacity of the kidneys to concentrate urine is selectively impaired by hypercalcemia or whether it is depressed together with many other renal functions as a result of substantial injury to and encroachment upon active renal parenchyma (9). In the present experiments the effects of hypercalcemia on renal function and morphology were studied in rats given large doses of calciferol (vitamin D2) for several days. The results suggest that hypercalcemia and renal damage produced in this manner specifically impair renal concentrating ability. This functional defect is associated with alterations in the structure of the collecting tubules of the renal medulla. METHODSEighteen male albino rats of the Sprague-Dawley strain, weighing about 300 Gm., were maintained on a measured diet of Purina Lab Chow and allowed to drink tap water ad libitum. Following initial determinations of blood urea nitrogen, urea clearance, phenolsulfonphthalein (PSP) excretion and maximum urinary osmolality, 200,-000 units or 400,000 units of vitamin D2 in peanut oil was injected subcutaneously daily for four days. At the end of this time, the same tests were repeated. The animals were then sacrificed by exsanguination from the abdominal aorta during pentobarbital anesthesia and the kidneys removed for morphologic examination. Eight rats served as controls, receiving only peanut oil for four days, with food intake limited to that taken by matched animals receiving vitamin D2.For the measurement of urea clearance, 0.2 to 0.3 ml. of heparinized blood was obtained from the tail. Rats

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Experimental Hyposthenuria 12

Cited by 66 publications

References 52 publications

Renal Function in Patients With Gout 1

Renal Function in Patients With Gout 1

Hyposthenuria in Sickle Cell Anemia: A Reversible Renal Defect

The Effect of Hypercalcemia Induced by Calciferol Upon Renal Concentrating Ability1

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