Acid-Base Homeostasis

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I. David Weiner - One of the best experts on this subject based on the ideXlab platform.

  • Sex differences in renal ammonia metabolism
    American journal of physiology. Renal physiology, 2020
    Co-Authors: Autumn N. Harris, I. David Weiner
    Abstract:

    Sexual dimorphic variations are present in many aspects of biology and involve the structure and/or function of nearly every organ system. Acid-Base Homeostasis is critical for optimal health, and ...

  • Differences in acidosis-stimulated renal ammonia metabolism in the male and female kidney
    American Journal of Physiology-Renal Physiology, 2019
    Co-Authors: Autumn N. Harris, Jill W. Verlander, Hyun-wook Lee, Lijuan Fang, I. David Weiner
    Abstract:

    Renal ammonia excretion is a critical component of Acid-Base Homeostasis, and changes in ammonia excretion are the predominant component of increased net acid excretion in response to metabolic aci...

  • Differences in renal ammonia metabolism in male and female kidney
    American journal of physiology. Renal physiology, 2018
    Co-Authors: Autumn N. Harris, Hyun-wook Lee, Jill W. Verlander, Lijuan Fang, Gunars Osis, Kierstin L. Webster, I. David Weiner
    Abstract:

    Renal ammonia metabolism has a major role in the maintenance of Acid-Base Homeostasis. Sex differences are well recognized as an important biological variable in many aspects of renal function, inc...

  • Roles of renal ammonia metabolism other than in acid–base Homeostasis
    Pediatric Nephrology, 2017
    Co-Authors: I. David Weiner
    Abstract:

    The importance of renal ammonia metabolism in acid–base Homeostasis is well known. However, the effects of renal ammonia metabolism other than in acid–base Homeostasis are not as widely recognized. First, ammonia differs from almost all other solutes in the urine in that it does not result from arterial delivery. Instead, ammonia is produced by the kidney, and only a portion of the ammonia produced is excreted in the urine, with the remainder returned to the systemic circulation through the renal veins. In normal individuals, systemic ammonia addition is metabolized efficiently by the liver, but in patients with either acute or chronic liver disease, conditions that increase the addition of ammonia of renal origin to the systemic circulation can result in precipitation and/or worsening of hyperammonemia. Second, ammonia appears to serve as an intrarenal paracrine signaling molecule. Hypokalemia increases proximal tubule ammonia production and secretion as well as reabsorption in the thick ascending limb of the loop of Henle, thereby increasing delivery to the renal interstitium and the collecting duct. In the collecting duct, ammonia decreases potassium secretion and stimulates potassium reabsorption, thereby decreasing urinary potassium excretion and enabling feedback correction of the initiating hypokalemia. Finally, the stimulation of renal ammonia metabolism by hypokalemia may contribute to the development of metabolic alkalosis, which in turn can stimulate NaCl reabsorption and contribute to the intravascular volume expansion, increased blood pressure and diuretic resistance that can develop with hypokalemia. The evidence supporting these novel non-acid–base roles of renal ammonia metabolism is discussed in this review.

  • Ammonia Transporters and Their Role in Acid-Base Balance
    Physiological Reviews, 2017
    Co-Authors: I. David Weiner, Jill W. Verlander
    Abstract:

    Acid-Base Homeostasis is critical to maintenance of normal health. Renal ammonia excretion is the quantitatively predominant component of renal net acid excretion, both under basal conditions and i...

Jill W. Verlander - One of the best experts on this subject based on the ideXlab platform.

Hyun-wook Lee - One of the best experts on this subject based on the ideXlab platform.

Autumn N. Harris - One of the best experts on this subject based on the ideXlab platform.

Nathalie Godefroid - One of the best experts on this subject based on the ideXlab platform.

  • Defects in KCNJ16 Cause a Novel Tubulopathy with Hypokalemia, Salt Wasting, Disturbed Acid-Base Homeostasis, and Sensorineural Deafness
    Journal of the American Society of Nephrology, 2021
    Co-Authors: Karl P. Schlingmann, Aparna Renigunta, Ewout J. Hoorn, Anna-lena Forst, Vijay Renigunta, Velko Atanasov, Sinthura Mahendran, Tahsin Stefan Barakat, Valentine Gillion, Nathalie Godefroid
    Abstract:

    BackgroundThe transepithelial transport of electrolytes, solutes, and water in the kidney is a well-orchestrated process involving numerous membrane transport systems. Basolateral potassium channels in tubular cells not only mediate potassium recycling for proper Na+,K+-ATPase function but are also involved in potassium and pH sensing. Genetic defects in KCNJ10 cause EAST/SeSAME syndrome, characterized by renal salt wasting with hypokalemic alkalosis associated with epilepsy, ataxia, and sensorineural deafness.MethodsA candidate gene approach and whole-exome sequencing determined the underlying genetic defect in eight patients with a novel disease phenotype comprising a hypokalemic tubulopathy with renal salt wasting, disturbed Acid-Base Homeostasis, and sensorineural deafness. Electrophysiologic studies and surface expression experiments investigated the functional consequences of newly identified gene variants.ResultsWe identified mutations in the KCNJ16 gene encoding KCNJ16, which along with KCNJ15 and KCNJ10, constitutes the major basolateral potassium channel of the proximal and distal tubules, respectively. Coexpression of mutant KCNJ16 together with KCNJ15 or KCNJ10 in Xenopus oocytes significantly reduced currents.ConclusionsBiallelic variants in KCNJ16 were identified in patients with a novel disease phenotype comprising a variable proximal and distal tubulopathy associated with deafness. Variants affect the function of heteromeric potassium channels, disturbing proximal tubular bicarbonate handling as well as distal tubular salt reabsorption.

  • Defects in KCNJ16 Cause a Novel Tubulopathy with Hypokalemia, Salt Wasting, Disturbed Acid-Base Homeostasis, and Sensorineural Deafness.
    Journal of the American Society of Nephrology : JASN, 2021
    Co-Authors: Karl P. Schlingmann, Aparna Renigunta, Ewout J. Hoorn, Anna-lena Forst, Vijay Renigunta, Velko Atanasov, Sinthura Mahendran, Tahsin Stefan Barakat, Valentine Gillion, Nathalie Godefroid
    Abstract:

    The transepithelial transport of electrolytes, solutes, and water in the kidney is a well-orchestrated process involving numerous membrane transport systems. Basolateral potassium channels in tubular cells not only mediate potassium recycling for proper Na+,K+-ATPase function but are also involved in potassium and pH sensing. Genetic defects in KCNJ10 cause EAST/SeSAME syndrome, characterized by renal salt wasting with hypokalemic alkalosis associated with epilepsy, ataxia, and sensorineural deafness. A candidate gene approach and whole-exome sequencing determined the underlying genetic defect in eight patients with a novel disease phenotype comprising a hypokalemic tubulopathy with renal salt wasting, disturbed Acid-Base Homeostasis, and sensorineural deafness. Electrophysiologic studies and surface expression experiments investigated the functional consequences of newly identified gene variants. We identified mutations in the KCNJ16 gene encoding KCNJ16, which along with KCNJ15 and KCNJ10, constitutes the major basolateral potassium channel of the proximal and distal tubules, respectively. Coexpression of mutant KCNJ16 together with KCNJ15 or KCNJ10 in Xenopus oocytes significantly reduced currents. Biallelic variants in KCNJ16 were identified in patients with a novel disease phenotype comprising a variable proximal and distal tubulopathy associated with deafness. Variants affect the function of heteromeric potassium channels, disturbing proximal tubular bicarbonate handling as well as distal tubular salt reabsorption. Copyright © 2021 by the American Society of Nephrology.

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