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  1. Article: Transient Hyperkalemia Following Treatment of Chronic Hypokalemia: A Case Report and Review of Distal Tubule Physiology.

    Breeggemann, Matthew C / Gluck, Stephen L

    Case reports in nephrology and dialysis

    2022  Volume 12, Issue 1, Page(s) 1–4

    Abstract: Hypokalemia is a relatively common electrolyte disorder usually resulting from gastrointestinal wasting. Transient hyperkalemia in those treated for hypokalemia has been previously described to occur in 16% of hospitalized patients. The majority of those ...

    Abstract Hypokalemia is a relatively common electrolyte disorder usually resulting from gastrointestinal wasting. Transient hyperkalemia in those treated for hypokalemia has been previously described to occur in 16% of hospitalized patients. The majority of those patients had acute, hospital-acquired hypokalemia. Here, we report a case of a young man with alcohol use disorder and chronic hypokalemia who was hospitalized for muscle weakness, abdominal pain, and intractable emesis. His potassium was 2.5 mEq/L on the day of admission. Four days later, with a creatinine at baseline (0.9 mg/dL), potassium abruptly increased to 6.7 mEq/L. He did not have evidence of hyperaldosteronism. In cases of chronic hypokalemia, we propose that the adaptive mechanisms of the distal tubule with total body potassium deficits require time to revert back to a nonactive state and that transient hyperkalemia may be observed during these "refractory" periods during which potassium supplementation is continued. The time required for disassembly of with no lysine kinases following resolution of hypokalemia is unknown. Hyperkalemia is an important consideration when treating patients with chronic hypokalemia.
    Language English
    Publishing date 2022-01-31
    Publishing country Switzerland
    Document type Case Reports
    ZDB-ID 2809879-1
    ISSN 2296-9705
    ISSN 2296-9705
    DOI 10.1159/000521477
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: How We Treat Primary Hyperoxaluria Type 1.

    Breeggemann, Matthew C / Harris, Peter C / Lieske, John C / Tasian, Gregory E / Wood, Kyle D

    Clinical journal of the American Society of Nephrology : CJASN

    2024  

    Language English
    Publishing date 2024-03-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2226665-3
    ISSN 1555-905X ; 1555-9041
    ISSN (online) 1555-905X
    ISSN 1555-9041
    DOI 10.2215/CJN.0000000000000460
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: A Case Report of Kidney-Only Transplantation in Primary Hyperoxaluria Type 1: A Novel Approach with the Use of Nedosiran.

    Breeggemann, Matthew C / Gluck, Stephen L / Stoller, Marshall L / Lee, Marsha M

    Case reports in nephrology and dialysis

    2023  Volume 13, Issue 1, Page(s) 63–69

    Abstract: The primary hyperoxalurias (PHs) are a group of diseases characterized by kidney stones, nephrocalcinosis, and chronic kidney disease. At stages of advanced kidney disease, glomerular filtration of oxalate becomes insufficient, plasma levels increase, ... ...

    Abstract The primary hyperoxalurias (PHs) are a group of diseases characterized by kidney stones, nephrocalcinosis, and chronic kidney disease. At stages of advanced kidney disease, glomerular filtration of oxalate becomes insufficient, plasma levels increase, and tissue deposition may occur. Hemodialysis is often unable to overcome the excess hepatic oxalate production. The current surgical management of primary hyperoxaluria type 1 (PH1) is combined liver kidney transplantation. In a subset of PH1 patients who respond to pyridoxine, kidney-only transplantation has been successfully performed. Recently, kidney-only transplantation has also been performed in PH1 patients receiving a small interfering RNA therapy called lumasiran. This drug targets the hepatic overproduction of oxalate, making kidney-only transplantation a potentially practical novel approach for managing PH1 patients with advanced kidney disease. It is unknown if similar effects could be seen with a different small interfering RNA agent called nedosiran. This article will briefly review PH1, describe the small interfering RNA therapies being used to treat PH, summarize the reported cases of kidney-only transplantation performed with lumasiran, and detail a case of kidney-only transplantation performed in a PH1 patient receiving nedosiran.
    Language English
    Publishing date 2023-07-07
    Publishing country Switzerland
    Document type Case Reports
    ZDB-ID 2809879-1
    ISSN 2296-9705
    ISSN 2296-9705
    DOI 10.1159/000531053
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Proximal tubule-derived colony stimulating factor-1 mediates polarization of renal macrophages and dendritic cells, and recovery in acute kidney injury.

    Wang, Yinqiu / Chang, Jian / Yao, Bing / Niu, Aolei / Kelly, Emily / Breeggemann, Matthew C / Abboud Werner, Sherry L / Harris, Raymond C / Zhang, Ming-Zhi

    Kidney international

    2015  Volume 88, Issue 6, Page(s) 1274–1282

    Abstract: Infiltrating cells play an important role in both the development of and recovery from acute kidney injury (AKI). Macrophages and renal dendritic cells are of particular interest because they can exhibit distinctly different functional phenotypes, ... ...

    Abstract Infiltrating cells play an important role in both the development of and recovery from acute kidney injury (AKI). Macrophages and renal dendritic cells are of particular interest because they can exhibit distinctly different functional phenotypes, broadly characterized as proinflammatory (M1) or tissue reparative (M2). Resident renal macrophages and dendritic cells participate in recovery from AKI in response to either ischemia/reperfusion or a model of selective proximal tubule injury induced by diphtheria-toxin-induced apoptosis in transgenic mice expressing the human diphtheria toxin receptor on proximal tubule cells. Colony-stimulating factor-1 (CSF-1) is an important factor mediating the recovery from AKI, and CSF-1 can stimulate macrophage and dendritic cell proliferation and polarization during the recovery phase of AKI. The kidney, and specifically the proximal tubule, is a major source of intrarenal CSF-1 production in response to AKI. We induced selective deletion of proximal tubule CSF-1 to determine its role in expansion and proliferation of renal macrophages and dendritic cells and in recovery from AKI. In both models of AKI, there was decreased M2 polarization, delayed functional and structural recovery, and increased tubulointerstitial fibrosis. Thus, intrarenal CSF-1 is an important mediator of macrophage/dendritic cell polarization and recovery from AKI.
    Language English
    Publishing date 2015-09-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1038/ki.2015.295
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Gut microbiome-derived phenyl sulfate contributes to albuminuria in diabetic kidney disease.

    Kikuchi, Koichi / Saigusa, Daisuke / Kanemitsu, Yoshitomi / Matsumoto, Yotaro / Thanai, Paxton / Suzuki, Naoto / Mise, Koki / Yamaguchi, Hiroaki / Nakamura, Tomohiro / Asaji, Kei / Mukawa, Chikahisa / Tsukamoto, Hiroki / Sato, Toshihiro / Oikawa, Yoshitsugu / Iwasaki, Tomoyuki / Oe, Yuji / Tsukimi, Tomoya / Fukuda, Noriko N / Ho, Hsin-Jung /
    Nanto-Hara, Fumika / Ogura, Jiro / Saito, Ritsumi / Nagao, Shizuko / Ohsaki, Yusuke / Shimada, Satoshi / Suzuki, Takehiro / Toyohara, Takafumi / Mishima, Eikan / Shima, Hisato / Akiyama, Yasutoshi / Akiyama, Yukako / Ichijo, Mariko / Matsuhashi, Tetsuro / Matsuo, Akihiro / Ogata, Yoshiaki / Yang, Ching-Chin / Suzuki, Chitose / Breeggemann, Matthew C / Heymann, Jurgen / Shimizu, Miho / Ogawa, Susumu / Takahashi, Nobuyuki / Suzuki, Takashi / Owada, Yuji / Kure, Shigeo / Mano, Nariyasu / Soga, Tomoyoshi / Wada, Takashi / Kopp, Jeffrey B / Fukuda, Shinji / Hozawa, Atsushi / Yamamoto, Masayuki / Ito, Sadayoshi / Wada, Jun / Tomioka, Yoshihisa / Abe, Takaaki

    Nature communications

    2019  Volume 10, Issue 1, Page(s) 1835

    Abstract: Diabetic kidney disease is a major cause of renal failure that urgently necessitates a breakthrough in disease management. Here we show using untargeted metabolomics that levels of phenyl sulfate, a gut microbiota-derived metabolite, increase with the ... ...

    Abstract Diabetic kidney disease is a major cause of renal failure that urgently necessitates a breakthrough in disease management. Here we show using untargeted metabolomics that levels of phenyl sulfate, a gut microbiota-derived metabolite, increase with the progression of diabetes in rats overexpressing human uremic toxin transporter SLCO4C1 in the kidney, and are decreased in rats with limited proteinuria. In experimental models of diabetes, phenyl sulfate administration induces albuminuria and podocyte damage. In a diabetic patient cohort, phenyl sulfate levels significantly correlate with basal and predicted 2-year progression of albuminuria in patients with microalbuminuria. Inhibition of tyrosine phenol-lyase, a bacterial enzyme responsible for the synthesis of phenol from dietary tyrosine before it is metabolized into phenyl sulfate in the liver, reduces albuminuria in diabetic mice. Together, our results suggest that phenyl sulfate contributes to albuminuria and could be used as a disease marker and future therapeutic target in diabetic kidney disease.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Albuminuria/blood ; Albuminuria/drug therapy ; Albuminuria/etiology ; Albuminuria/pathology ; Animals ; Animals, Genetically Modified ; Cohort Studies ; Diabetes Mellitus, Experimental/blood ; Diabetes Mellitus, Experimental/chemically induced ; Diabetes Mellitus, Experimental/complications ; Diabetes Mellitus, Experimental/urine ; Diabetes Mellitus, Type 1/blood ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/complications ; Diabetic Nephropathies/blood ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/pathology ; Dogs ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Female ; Gastrointestinal Microbiome/physiology ; Humans ; Madin Darby Canine Kidney Cells ; Male ; Metabolomics/methods ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Organic Anion Transporters/genetics ; Podocytes/metabolism ; Podocytes/pathology ; Rats ; Streptozocin/toxicity ; Sulfuric Acid Esters/blood ; Sulfuric Acid Esters/metabolism ; Tyrosine Phenol-Lyase/antagonists & inhibitors ; Tyrosine Phenol-Lyase/metabolism ; Young Adult
    Chemical Substances Enzyme Inhibitors ; Organic Anion Transporters ; SLCO4C1 protein, human ; Sulfuric Acid Esters ; Streptozocin (5W494URQ81) ; phenylsulfate (937-34-8) ; Tyrosine Phenol-Lyase (EC 4.1.99.2)
    Language English
    Publishing date 2019-04-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-019-09735-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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