Renal Bicarbonate Reabsorption and Hydrogen Ion Excretion in Normal Infants*

Edelmann, Chester M.; Soriano, Juan Rodríguez; Boichis, H; Gruskin, Alan B.; Acosta, Melinda I.

doi:10.1172/jci105623

Cited by 205 publications

(102 citation statements)

References 23 publications

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“…In both patients the renal contribution to acid-base balance was evaluated according to the methods described by EDELMANN et al [4].…”

Section: Methodsmentioning

confidence: 99%

“…The renal contribution to acid-base balance can be quantitatively documented by means of two standardized tests [4]. With an acute loading test using ammonium chloride administered per os, quantitation of renal hydrogen ion excretion is possible [5], whereas by means of a bicarbonate titration test, the renal handling of bicarbonate can be described.…”

Section: Introductionmentioning

confidence: 99%

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The Influence of Extracellular Fluid Volume on the Renal Bicarbonate Threshold. A Study of Two Children with Lowe's Syndrome

Oetliker

Rossi

1969

Pediatr Res

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ExtractThis study on the renal acid-base balance in two slightly acidotic patients with Lowe's syndrome was undertaken to demonstrate the influence of extracellular fluid volume on the renal bicarbonate threshold. The clinical observation of chronic dehydration in both patients lead to the hypothesis that a low plasma volume might account for a relative compensation of metabolic acidosis in these patients and, conversely, that volume expansion might unmask a more severe acidosis.The ability to excrete an acid urine was established by measuring the response to acute NH,Cl loading. Optimal response was seen three to four hours after NH,C1 was given. Both patients were able to excrete acid urine with a p H of 5.5 at blood total CO, content below 18.5 mmoles/l. The excretion rates for titratable acidity (TA) and for ammonium rose after NH,C1 administration to values within normal range (table I). The excretion rate of T A in one patient attained normal limits after correction for the low GFR, which on repeated examinations was 25-30 % of normal.The renal bicarbonate threshold was determined by infusions of increasing amounts of NaHCO,. The infusion rates were kept constant a t 1.4 ml/min/m2 during the first study undertaken in each patient, and 5.6 ml/min/m2 during the second. With low infusion rates, plasma volume, determined by the radioisotope dilution technique, was 57.8 ml/kg in Patient C.St. and 54.5 ml/kg in Patient M. B.; during high infusion rates it was 63.6 ml/kg in Patient C. St. and 64.9 ml/kg in Patient M. B.Plasma volume was thus expanded 10 and 19 %, respectively, from one study to the next. During low rates of infusion, the renal bicarbonate threshold in both patients was 21 mmoles/l (tables I1 and I11 and fig. 2) ; during high infusion rates it was 17.5 mmoles/l (tables I V and V and fig. 2). During low infusion rates, the bicarbonate thresholds were decreased, in comparison with the normal for age, 22-24 mmoles/l, and with the normal for weight, 21.5-22.5 mmoles/l. After expansion of extracellular fluid volume, the renal bicarbonate threshold decreased by 3.5 mmoles/l. SpeculationThe renal bicarbonate threshold can be decreased by volume expansion. In patients with Lowe's syndrome, chronic dehydration may compensate in part for the decreased renal bicarbonate threshold.

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“…In both patients the renal contribution to acid-base balance was evaluated according to the methods described by EDELMANN et al [4].…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Influence of Extracellular Fluid Volume on the Renal Bicarbonate Threshold. A Study of Two Children with Lowe's Syndrome

Oetliker

Rossi

1969

Pediatr Res

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“…In both humans and corresponding animal models, infants have lower plasma bicarbonate concentrations than adults, [1][2][3] and the levels of bicarbonate increase progressively after birth. 4 -6 The proximal tubule is responsible for the reabsorption of approximately 80% of filtered bicarbonate.…”

mentioning

confidence: 99%

Origin and Fate of Pendrin-Positive Intercalated Cells in Developing Mouse Kidney

Song

Kim

Lee

et al. 2007

Journal of the American Society of Nephrology

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Pendrin is an apical anion exchanger found in type B and nonA-nonB intercalated cells that is involved in bicarbonate secretion. The purpose of this study was to establish the origin and fate of pendrinpositive intercalated cells in the mouse kidney. Using immunohistochemistry, we found that pendrinpositive cells first appeared in the connecting tubule at embryonic day 14 (E14) and subsequently in the medullary collecting duct at E18. Most of the pendrin-positive cells in the connecting tubule were nonA-nonB intercalated cells, wheras those in the medullary collecting duct were type B intercalated cells. In the cortical collecting duct, pendrin-positive cells appeared in the inner part at day 4 after birth and in the outer part at day 7. Pendrin-positive cells gradually disappeared by apoptosis from the inner part of the medullary collecting duct two weeks after birth. Using 5-bromo-2Јdeoxy-uridine (BrdU) to follow cell proliferation, we determined that selective proliferation of pendrin-positive intercalated cells does not occur; instead, these cells may arise from undifferentiated precursor cells from separate foci, one in the connecting tubule and one in the collecting duct.

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“…The test must be validated by confirming that the NH 4 Cl dose induces metabolic acidosis: tCO 2 in blood at least <18 mmol/l in infants and <21 mmol/l in older children. In normal individuals urine pH drops below 5.5 and urinary NH 4 + increases up to 57±14 (mean±SD) μEq/min/1.73 m 2 in infants aged 1-16 months and 80±12 μEq/min/1.73 m 2 in children aged 7-12 years [22]. The capacity of urinary acidification is blunted in patients with distal RTA and preserved in patients with proximal RTA, when the plasma HCO 3 − is below the renal threshold, and patients with type 4 RTA.…”

Section: Functional Testsmentioning

confidence: 97%

Clinical and laboratory approaches in the diagnosis of renal tubular acidosis

et al. 2015

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In the absence of a gastrointestinal origin, a maintained hyperchloremic metabolic acidosis must raise the diagnostic suspicion of renal tubular acidosis (RTA). Unlike adults, in whom RTA is usually secondary to acquired causes, children most often have primary forms of RTA resulting from an inherited genetic defect in the tubular proteins involved in the renal regulation of acid-base homeostasis. According to their pathophysiological basis, four types of RTA are distinguished. Distal type 1 RTA, proximal type 2 RTA, mixed-type 3 RTA, and type 4 RTA can be differentiated based on the family history, the presenting manifestations, the biochemical profile, and the radiological findings. Functional tests to explore the proximal wasting of bicarbonate and the urinary acidification capacity are also useful diagnostic tools. Although currently the molecular basis of the disease can frequently be discovered by gene analysis, patients with RTA must undergo a detailed clinical study and laboratory work-up in order to understand the pathophysiology of the disease and to warrant a correct and accurate diagnosis.

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Renal Bicarbonate Reabsorption and Hydrogen Ion Excretion in Normal Infants*

Cited by 205 publications

References 23 publications

The Influence of Extracellular Fluid Volume on the Renal Bicarbonate Threshold. A Study of Two Children with Lowe's Syndrome

The Influence of Extracellular Fluid Volume on the Renal Bicarbonate Threshold. A Study of Two Children with Lowe's Syndrome

Origin and Fate of Pendrin-Positive Intercalated Cells in Developing Mouse Kidney

Clinical and laboratory approaches in the diagnosis of renal tubular acidosis

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