Effect of acute metabolic acidemia on renal electrolyte transport in man

Rex Mahnensmith; Samuel O. Thier; C. Robert Cooke; Arthur Broadus; Ralph A. DeFronzo

doi:10.1016/0026-0495(79)90210-5

Effect of acute metabolic acidemia on renal electrolyte transport in man

Rex Mahnensmith, Samuel O. Thier, C. Robert Cooke, Arthur Broadus, Ralph A. DeFronzo

Research output: Contribution to journal › Article › peer-review

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Abstract

The effect of acute NH₄C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH₄C1, venous pH and bicarbonate concentration declined significantly (p < 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (U_NaV) increased from 142 ± 16 μeq/min (mean ± SEM) to 310 ± 49 μeq/min (p < 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while C_H₂O (C_H₂O + C_Cl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in U_NaV.U_KV fell acutely from 91 ± 13 to 45 ± 5 μeq/min (p < 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. U_CaV rose from 66 ± 15 to 143 ± 18 μg/min and fractional excretion of calcium increased from 0.55 ± 0.13 to 1.24 ± 0.21% (p < 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 ± 0.05 to 4.30 ± 0.03 mg/dl (p < 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independent of changes in parathyroid hormone (as reflected by urinary cAMP).

Original language	English (US)
Pages (from-to)	831-842
Number of pages	12
Journal	Metabolism
Volume	28
Issue number	8
DOIs	https://doi.org/10.1016/0026-0495(79)90210-5
State	Published - Aug 1979
Externally published	Yes

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism
Endocrinology

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10.1016/0026-0495(79)90210-5

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@article{a6a300ebac334e81bcb175898d872f33,

title = "Effect of acute metabolic acidemia on renal electrolyte transport in man",

abstract = "The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p < 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 ± 16 μeq/min (mean ± SEM) to 310 ± 49 μeq/min (p < 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O (CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV.UKV fell acutely from 91 ± 13 to 45 ± 5 μeq/min (p < 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 ± 15 to 143 ± 18 μg/min and fractional excretion of calcium increased from 0.55 ± 0.13 to 1.24 ± 0.21% (p < 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 ± 0.05 to 4.30 ± 0.03 mg/dl (p < 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independent of changes in parathyroid hormone (as reflected by urinary cAMP).",

author = "Rex Mahnensmith and Thier, {Samuel O.} and Cooke, {C. Robert} and Arthur Broadus and DeFronzo, {Ralph A.}",

note = "Funding Information: From the Yale University School of Medicine, Department of Medicine. New Haven, Conn. and The Johns Hopkins University School of Medicine. Department of Medicine, Baltimore. Md. Received for publication September 28, 1978. Supported in part by USIWS Grunt HL-03303. Address reprint requests to Ralph A. DeFronzo, M.D., 2074 LMP, Yale-New Haven Hospital, 333 Cedar Street, New Haven, Conn. 06510. o 1979 by Grune & Stratton, Inc. 0026-0495/79,f2808~006$02.00/0",

year = "1979",

month = aug,

doi = "10.1016/0026-0495(79)90210-5",

language = "English (US)",

volume = "28",

pages = "831--842",

journal = "Metabolism: Clinical and Experimental",

issn = "0026-0495",

publisher = "W.B. Saunders Ltd",

number = "8",

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T1 - Effect of acute metabolic acidemia on renal electrolyte transport in man

AU - Mahnensmith, Rex

AU - Thier, Samuel O.

AU - Cooke, C. Robert

AU - Broadus, Arthur

AU - DeFronzo, Ralph A.

N1 - Funding Information: From the Yale University School of Medicine, Department of Medicine. New Haven, Conn. and The Johns Hopkins University School of Medicine. Department of Medicine, Baltimore. Md. Received for publication September 28, 1978. Supported in part by USIWS Grunt HL-03303. Address reprint requests to Ralph A. DeFronzo, M.D., 2074 LMP, Yale-New Haven Hospital, 333 Cedar Street, New Haven, Conn. 06510. o 1979 by Grune & Stratton, Inc. 0026-0495/79,f2808~006$02.00/0

PY - 1979/8

Y1 - 1979/8

N2 - The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p < 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 ± 16 μeq/min (mean ± SEM) to 310 ± 49 μeq/min (p < 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O (CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV.UKV fell acutely from 91 ± 13 to 45 ± 5 μeq/min (p < 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 ± 15 to 143 ± 18 μg/min and fractional excretion of calcium increased from 0.55 ± 0.13 to 1.24 ± 0.21% (p < 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 ± 0.05 to 4.30 ± 0.03 mg/dl (p < 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independent of changes in parathyroid hormone (as reflected by urinary cAMP).

AB - The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p < 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 ± 16 μeq/min (mean ± SEM) to 310 ± 49 μeq/min (p < 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O (CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV.UKV fell acutely from 91 ± 13 to 45 ± 5 μeq/min (p < 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 ± 15 to 143 ± 18 μg/min and fractional excretion of calcium increased from 0.55 ± 0.13 to 1.24 ± 0.21% (p < 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 ± 0.05 to 4.30 ± 0.03 mg/dl (p < 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independent of changes in parathyroid hormone (as reflected by urinary cAMP).

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Effect of acute metabolic acidemia on renal electrolyte transport in man

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