The Renal Clearance of Endogenous “Creatinine” in Man

Brod, J; Sirota, Jonas H.

doi:10.1172/jci102012

Cited by 365 publications

(123 citation statements)

References 20 publications

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“…Table III shows the data we have collected re-TABLE I Nude, fasting body weights of subjectsfor the three days before, the three days of sodium administration and the three following days garding glomerular filtration rate and sodium and chloride excretion in these normal subjects. In subject E. W. the glomerular filtration rate is estimated from the 24 hour endogenous creatinine clearance (2,3). In our other two subjects, glomerular filtration rate was determined by inulin clearances (4).…”

Section: Resultsmentioning

confidence: 99%

“…Because our studies involved very low and very high rates of sodium and chloride excretion resulting from the marked variations in sodium intake, observations were made to determine, if possible, how glomerular filtration and tubular reabsorption of sodium affected the excretion of sodium by normal subjects. Table III shows the simultaneous 24 hour endogenous creatinine clearance taken as a measure of glomerular filtration rate (2,3) and the simultaneous 24 hour urine sodium and chloride content. Simultaneous inulin clearances and sodium excretions for subjects M. L. and W. C. are also recorded.…”

Section: Displacement Of Intracellular Potassium By Sodiummentioning

confidence: 99%

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Some Effects of Variation in Sodium Intake and of Different Sodium Salts in Normal Subjects 1

Leaf

Couter²,

Newburgh³

1949

J. Clin. Invest.

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In a separate paper ( 1 ) we have described effects resulting from variation of sodium intake in normal subjects, which we attribute to changes in adrenal cortical activity. It is the purpose of this paper to describe some additional effects of considerable physiological interest that were observed in the course of that study. METHODSThree normal young adults were maintained throughout the study on a constant diet adequate in calories and protein with a very low sodium (about 9 mEq.) and chloride (about 25 mEq.) content. At definite periods 480 mEq. of sodium were administered orally daily either as sodium chloride or as sodium citrate. The analytical methods and diet are described in detail in the previous report (1). RESULTSThe complete data of this study were presented in a separate paper (1). Only data pertinent to the present discussions will be presented here. Table I shows the weights of our three normal subjects for the three days before, during and following sodium administration. It is evident that with sodium chloride administration a much more marked gain of weight occurred than with sodium citrate. Each subject was on a maintenance caloric intake so that practically all weight changes occurring over such short periods as these are due to change in body fluid content. Table II shows the changes in urinary sodium, chloride and potassium excretion that occurred before, during and following each period of sodium administration. No significant changes in fecal sodium, chloride, and potassium were noted and these are not recorded here. It is seen that with administration of sodium chloride there is in each case a parallel increase in both urinary sodium and chloride as would be expected. Following the 1 This study was aided by a grant from the United States Public Health Service. sodium citrate administration a similar increase in sodium excretion is noted; however, chloride excretion remains unchanged, or if anything, slightly decreases. Table II shows further that with the sodium chloride administration no significant increase in potassium excretion occurred except in the case of M. L., whose urine potassium content rose from about 40 mEq. in 24 hours to 88 mEq. the first day of sodium chloride administration. In subjects W. C. and E. W. a significant decrease in potassium excretion occurred after cessation of sodium chloride administration. On the first day of sodium citrate administration, a very definite increase in potassium excretion took place in all subjects. This was followed, after omission of sodium citrate, by a decrease to unusually low levels of potassium excretion. Table III shows the data we have collected re-

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Section: Resultsmentioning

confidence: 99%

Section: Displacement Of Intracellular Potassium By Sodiummentioning

confidence: 99%

Some Effects of Variation in Sodium Intake and of Different Sodium Salts in Normal Subjects 1

Leaf

Couter²,

Newburgh³

1949

J. Clin. Invest.

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“…The clear serum was separated and used for biochemical assays. Renal function was assessed by measurement of serum urea (Natelson et al 1951) and serum creatinine levels (Brod and Sirota 1948).…”

Section: Serum Kidney Marker Analysismentioning

confidence: 99%

Fish oil rich in eicosapentaenoic acid protects against oxidative stress-related renal dysfunction induced by TCDD in Wistar rats

Palaniswamy

Vishwanadha

Singaravelu

2014

Cell Stress and Chaperones

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Humans are systemically exposed to persistent organic pollutants, of which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has become a major environmental concern. Exposure to TCDD results in a wide variety of adverse health effects which is mediated by oxidative stress through CYP1A1 activation and arachidonic acid metabolites. Eicosapentaenoic acid (EPA) exhibits antioxidant property and competes with arachidonic acid in membrane phospholipids and produces anti-inflammatory EPA derivatives. Since both EPA and its derivatives have been reported to enhance the antioxidant mechanism, the present study aimed at studying whether EPA could offer protection against TCDDinduced oxidative stress and nephrotoxicity in Wistar rats. Estimation of kidney markers (serum urea and creatinine) and histopathological studies revealed that EPA treatment significantly reduced TCDD-induced renal damage. TCDDinduced oxidative damage was reflected in a significant increase in CYP1A1 activity and lipid peroxide levels with a concomitant decline in non-enzymic antioxidant (GSH) and various enzymic antioxidants such catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), and glutathione peroxidase (GPx). In addition, TCDD-induced oxidative stress also resulted in decline in Na + -K + and Mg 2+ATPases activities with increase in Ca 2+ ATPases activity. Oral treatment with EPA showed a significant cytoprotection against TCDD-induced renal oxidative stress by decreased CYP1A1 activity and enhanced antioxidant status. TCDD-induced alterations in ATPase enzyme activities were also prevented by EPA treatment. Our results show clear evidence that EPA ameliorates TCDD-induced oxidative stress and kidney damage; thus suggest the potential of EPA as an effective therapeutic agent against toxic effects mediated through redox imbalance.

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“…Creatinine clearance in man has therefore usually been found to be higher than inulin clearance, both in health (Miller and Winkler, 1938;Brod and Sirota, 1948;Hare et al, 1949;Smith, 1951 ;Mattar et al, 1952) and in disease (Miller and Winkler, 1938;Brod and Sirota, 1948;Hare et al, 1949;Smith, 1951 ; Mattar et al, Miller et al, 1952 ;Berlyne et al, 1964;Vere and Walduck, 1964 (1938) found that endogenous creatinine clearance was equal to inulin clearance in several normal subjects. In four patients with renal disease, however, the creatinine clearance was greater than inulin clearance (Miller and Winkler, 1938).…”

Section: Introductionmentioning

confidence: 99%