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https://www.readbyqxmd.com/read/29649820/accuracy-of-acid-base-diagnoses-using-the-central-venous-blood-gas-in-the-medical-intensive-care-unit
#1
Sarah J Schrauben, Dan Negoianu, Cristiana Costa, Raphael M Cohen, Stanley Goldfarb, Barry D Fuchs, Jeffrey S Berns
BACKGROUND: Acid-base disturbances are frequent in critically ill patients. Arterial blood gas (ABG) is the gold standard in the diagnosis of these disturbances, but it is invasive with potential hazards. For patients with a central venous catheter, venous blood gas (VBG) sampling may be an alternative, less-invasive diagnostic tool. However, the accuracy of a central VBG-based acid-base disorder diagnosis compared to an ABG is unknown. The primary objective of this study was to assess the accuracy of a central VBG-based acid-base disorder diagnosis compared to the "gold standard" ABG in critically ill patients...
April 12, 2018: Nephron
https://www.readbyqxmd.com/read/29597222/clinical-complications-of-continuous-renal-replacement-therapy
#2
Florent Sigwalt, Axelle Bouteleux, François Dambricourt, Théo Asselborn, Florent Moriceau, Thomas Rimmelé
The various complications of continuous renal replacement therapy (CRRT) are mostly preventable. Hemodynamic disturbances are dominated by hypotension due to the modification of volume status, myocardial dysfunction, cardiac arrhythmia, or modification of systemic vascular resistances, which are correlated with body temperature changes. Metabolic complications remain at the forefront and have profoundly changed with the use of regional citrate anticoagulation (RCA). RCA may lead to two distinct situations: citrate overload and citrate accumulation, respectively, responsible for metabolic alkalosis and metabolic acidosis...
2018: Contributions to Nephrology
https://www.readbyqxmd.com/read/29568987/furosemide-induced-tubular-dysfunction-responding-to-prostaglandin-synthesis-inhibitor-therapy-in-a-child-with-nephrotic-syndrome
#3
T Harish Varma, Ashish Sharma, S Santhiya, Lesa Dawman, Karalanglin Tiewsoh
Furosemide is one of the most common drug used to treat anasarca in childhood nephrotic syndrome. It has minimal side effects on short-term usage, but prolonged use can result in polyuria, hypokalemia and metabolic alkalosis. This pseudo-bartter complication can be treated by discontinuation of the drug with adequate potassium replacement. We report a child who was given furosemide for 20 days elsewhere to treat the edema due to nephrotic syndrome and then presented to us with bartter-like syndrome. Furosemide was discontinued and potassium replacement was initiated...
March 22, 2018: CEN Case Reports
https://www.readbyqxmd.com/read/29564279/sporadic-hypothyroidism-related-hypokalemic-paralysis-diagnosis-in-a-resource-poor-setting
#4
Nadasha Kadeeja, Nivetha Senthilnathan, Stalin Viswanathan, Rajeswari Aghoram
Hypothyroidism and distal renal tubular acidosis causing hypokalemic paralysis (HP) have been described only in four female patients. HP as the initial manifestation of uncomplicated diabetes has been reported only in three young males. We report two middle-aged patients presenting with gradual-onset areflexic quadriparesis and neck flop, associated with urinary potassium losses, and recovering over 3 days. The male patient with alcohol abuse had urine pH >5.5 and hyperchloremic metabolic acidosis due to renal tubular acidosis and hypothyroidism...
October 2017: Journal of Family Medicine and Primary Care
https://www.readbyqxmd.com/read/29535093/an-unusual-manifestation-of-olfactory-neuroblastoma
#5
Zona Batacchi, Nicole K Andeen, Subbulaxmi Trikudanathan
A 62-year-old woman presented with an 11-month history of worsening nasal symptoms of rhinorrhoea, anosmia, nasal congestion and intermittent epistaxis. MRI revealed a large mass in the upper nasal vault. Biopsy of the mass revealed an olfactory neuroblastoma. While waiting resection, she acutely developed severe proximal muscle weakness, lethargy and lower extremity oedema. Blood glucose was elevated, and hypokalaemic metabolic alkalosis was noted. Elevated serum cortisol level of 95.7 µg/dL (8.7-22.4 µg/dL) and markedly elevated 24-hour urinary cortisol level of 6962...
March 13, 2018: BMJ Case Reports
https://www.readbyqxmd.com/read/29534496/liddle-syndrome-review-of-the-literature-and-description-of-a-new-case
#6
REVIEW
Martina Tetti, Silvia Monticone, Jacopo Burrello, Patrizia Matarazzo, Franco Veglio, Barbara Pasini, Xavier Jeunemaitre, Paolo Mulatero
Liddle syndrome is an inherited form of low-renin hypertension, transmitted with an autosomal dominant pattern. The molecular basis of Liddle syndrome resides in germline mutations of the SCNN1A , SCNN1B and SCNN1G genes, encoding the α, β, and γ-subunits of the epithelial Na⁺ channel (ENaC), respectively. To date, 31 different causative mutations have been reported in 72 families from four continents. The majority of the substitutions cause an increased expression of the channel at the distal nephron apical membrane, with subsequent enhanced renal sodium reabsorption...
March 11, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29527380/bartter-syndrome-type-1-presenting-as-nephrogenic-diabetes-insipidus
#7
Gianluca Vergine, Elena Fabbri, Annalisa Pedini, Silvana Tedeschi, Niccolò Borsa
Bartter syndrome (BS) type 1 (OMIM #601678) is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, polyuria, recurrent vomiting, and growth retardation. It is caused by loss-of-function mutations of the SLC12A1 gene, encoding the furosemide-sensitive Na-K-Cl cotransporter. Recently, a phenotypic variability has been observed in patients with genetically determined BS, including absence of nephrocalcinosis, hypokalemia, and/or metabolic alkalosis in the first year of life as well as persistent metabolic acidosis mimicking distal renal tubular acidosis...
2018: Case Reports in Pediatrics
https://www.readbyqxmd.com/read/29522710/vitamin-c-pharmacokinetics-in-critically-ill-patients-a-randomized-trial-of-four-intravenous-regimens
#8
Harm-Jan de Grooth, Wai-Ping Manubulu-Choo, Anthe S Zandvliet, Angélique M E Spoelstra-de Man, Armand R Girbes, Eleonora L Swart, Heleen M Oudemans-van Straaten
BACKGROUND: Early high-dose intravenous vitamin-C is being investigated as adjuvant therapy in critically ill patients, but the optimal dose and infusion method are unclear. The primary aim of this study was to describe the dose-plasma concentration relationship and safety of four different dosing regimens. METHODS: Four-group randomized pharmacokinetic trial. Critically ill patients with multiple organ dysfunction were randomized to receive 2g/day or 10g/day vitamin-C as a twice daily bolus infusion or continuous infusion for 48 hours...
March 6, 2018: Chest
https://www.readbyqxmd.com/read/29514039/a-young-patient-with-leg-weakness-and-hypokalemia-case-report
#9
Elias Andrawus, Irit Hochberg, Zaher S Azzam
A 20-year-old female patient was admitted to hospital because of bilateral leg weakness. Laboratory investigation showed metabolic alkalosis and severe hypokalemia. Differential diagnosis included mineralocorticoid or apparent mineralocorticoid excess diseases, with a high aldosterone-to-renin ratio (ARR) after correcting hypokalemia. After confirmatory tests, imaging studies revealed a unilateral adrenocortical adenoma consistent with Conn's disease. Surgery was curative.
February 1, 2018: Rambam Maimonides Medical Journal
https://www.readbyqxmd.com/read/29495132/acid-base-assessment-of-patients-receiving-hemodialysis-what-are-our-management-goals
#10
F John Gennari
Acid-base assessment of patients receiving conventional hemodialysis (HD) has been based solely on predialysis serum [total CO2 ], and treatment is currently driven by the KDOQI guideline from 2000. This guideline was directed solely at minimizing metabolic acidosis and thereby improving bone and muscle metabolism. In 2000, no data were available to assess the effects of acid-base status on morbidity and mortality. Since then, new data have emerged from several large cohort studies about the association between variations in predialysis serum [total CO2 ], as well as blood pH, and morbidity and mortality risk...
March 1, 2018: Seminars in Dialysis
https://www.readbyqxmd.com/read/29482189/downregulation-of-the-cl-hco3-exchanger-pendrin-in-kidneys-of-mice-with-cystic-fibrosis-role-in-the-pathogenesis-of-metabolic-alkalosis
#11
Mujan Varasteh Kia, Sharon Barone, Alicia A McDonough, Kamyar Zahedi, Jie Xu, Manoocher Soleimani
BACKGROUND/AIMS: Patients with cystic fibrosis (CF) are prone to the development of metabolic alkalosis; however, the pathogenesis of this life threatening derangement remains unknown. We hypothesized that altered acid base transport machinery in the kidney collecting duct underlies the mechanism of impaired bicarbonate elimination in the CF kidney. METHODS: Balance studies in metabolic cages were performed in WT and CFTR knockout (CF) mice with the intestinal rescue in response to bicarbonate loading or salt restriction, and the expression levels and cellular distribution of acid base and electrolyte transporters in the proximal tubule, collecting duct and small intestine were examined by western blots, northern blots and/or immunofluorescence labeling...
February 21, 2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29465034/-hypercalcaemia-due-to-the-milk-alkali-syndrome
#12
Tamina Rokai Etemadi, Helle Skovmand Bosselmann
This case report is about an 87-year-old woman with Alzheimer's disease and the milk-alkali syndrome, who took calcium carbonate as osteoporosis prophylaxis. We describe, how the milk-alkali syndrome can result in a triad of hypercalcaemia, metabolic alkalosis, and renal insufficiency. The syndrome is now the third most common cause of hypercalcaemia because of the use of calcium carbonate in osteoporosis prophylaxis and treatment, and the syndrome should be considered in patients with hypercalcaemia, as it may result in permanent renal impairment...
February 12, 2018: Ugeskrift for Laeger
https://www.readbyqxmd.com/read/29459793/consequences-of-spak-inactivation-on-hyperkalemic-hypertension-caused-by-wnk1-mutations-evidence-for-differential-roles-of-wnk1-and-wnk4
#13
Chloé Rafael, Christelle Soukaseum, Véronique Baudrie, Perrine Frère, Juliette Hadchouel
Mutations of the gene encoding WNK1 [With No lysine (K) kinase 1] or WNK4 cause Familial Hyperkalemic Hypertension (FHHt). Previous studies have shown that the activation of SPAK (Ste20-related Proline/Alanine-rich Kinase) plays a dominant role in the development of FHHt caused by WNK4 mutations. The implication of SPAK in FHHt caused by WNK1 mutation has never been investigated. To clarify this issue, we crossed WNK1+/FHHt mice with SPAK knock-in mice in which the T-loop Thr243 residue was mutated to alanine to prevent activation by WNK kinases...
February 19, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29442545/novel-compound-heterozygous-clcnkb-gene-mutations-c-1755a-g-c-848_850deltct-cause-classic-bartter-syndrome
#14
Chunli Wang, Ying Chen, Bixia Zheng, Mengshu Zhu, Jia Fan, Juejin Wang, Zhanjun Jia, Songming Huang, Aihua Zhang
Inactivated variants in CLCNKB gene encoding the basolateral chloride channel ClC-Kb cause classic Bartter syndrome characterized by hypokalemic metabolic alkalosis and hyperreninemic hyperaldosteronism. Here we identified two cBS siblings presenting hypokalemia in a Chinese family due to novel compound heterozygous CLCNKB mutations (c.848_850delTCT/c.1755A>G). Compound heterozygosity was confirmed by amplifying and sequencing the patient's genomic DNA. The synonymous mutation c.1755A>G (Thr585Thr) was located at +2bp from the 5' splice donor site in exon 15, further transcript analysis demonstrated that this single nucleotide mutation causes exclusion of exon 15 in the cDNA from the proband and his mother...
February 14, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/29442351/milk-alkali-syndrome-mas-as-a-complication-of-the-treatment-of-hypoparathyroidism
#15
Agata Skwarek, Janusz Pachucki, Tomasz Bednarczuk, Zuzanna Żurecka, Michał Popow
Milk-alkali syndrome (MAS), characterized by renal failure, metabolic alkalosis and hypercalcemia, is a severe and life-threatening complication of the treatment of hypoparathyroidism. The clinical course is often sudden and is not preceded by any prodromal symptoms. Occurrence does not depend on the duration of hypoparathyroidism treatment, although it is closely related to the applied therapy, especially the dose of calcium carbonate and active vitamin D preparations. Drugs influencing the glomerular filtration rate (angiotensin receptor blockers, sartans, aldosterone receptor antagonists, thiazide diuretics), lack of adequate routine control, changing the calcium carbonate supplementation, dehydration, a diet rich in pH-basic foods (i...
February 14, 2018: Endokrynologia Polska
https://www.readbyqxmd.com/read/29421779/nephropathic-cystinosis-mimicking-bartter-syndrome-a-novel-mutation
#16
Funda Bastug, Hulya Nalcacioglu, Fatih Ozaltin, Emine Korkmaz, Sibel Yel
Cystinosis is a rare autosomal recessive disorder resulting from defective lysosomal transport of cystine due to mutations in the cystinosin lysosomal cystine transporter (CTNS) gene. The clinical phenotype of nephropathic cystinosis is characterized by renal tubular Fanconi syndrome and development of end-stage renal disease during the first decade. Although metabolic acidosis is the classically prominent finding of the disease, a few cases may present with hypokalemic metabolic alkalosis mimicking Bartter syndrome...
January 2018: Iranian Journal of Kidney Diseases
https://www.readbyqxmd.com/read/29417593/medical-findings-in-1-026-consecutive-adult-inpatient-residential-eating-disordered-patients
#17
Philip S Mehler, Dan V Blalock, Keegan Walden, Simrat Kaur, Jennifer McBride, Kristine Walsh, Jennifer Watts
OBJECTIVE: Eating disorders are associated with multiple medical complications. We report contemporary medical data, for newly admitted adult inpatient and residential level of care patients. METHOD: Medical records of a transdiagnostic sample of 1,026 patients, with eating disorders, were retrospectively reviewed for the presence of a broad array of medical complications at time of admission. The prevalence of physiologically relevant medical complications was assessed across major eating disorder categories...
February 8, 2018: International Journal of Eating Disorders
https://www.readbyqxmd.com/read/29403282/two-mutations-in-the-thiazide-sensitive-nacl-co-transporter-gene-in-a-romanian-gitelman-syndrome-patient-case-report
#18
Cristina Gug, Adelina Mihaescu, Ioana Mozos
Background: Gitelman syndrome (GS) is considered as the most common renal tubular disorder, and we report the first Romanian patient with GS confirmed at molecular level and diagnosed according to genetic testing. Patient and methods: This paper describes the case of a 27-year-old woman admitted with severe hypokalemia, slight hypomagnesemia, hypocalcemia, hypocalciuria, metabolic alkalosis, hyperreninemia, low blood pressure, limb muscle weakness, marked fatigue and palpitations...
2018: Therapeutics and Clinical Risk Management
https://www.readbyqxmd.com/read/29385285/itraconazole-induced-hypertension-and-hypokalemia-mechanistic-evaluation
#19
Wesley J Hoffmann, Ian McHardy, George R Thompson
We describe a case of apparent mineralocorticoid excess (hypertension, hypokalemia, metabolic alkalosis, and low plasma renin activity) secondary to itraconazole therapy. Inhibition of 11β-hydroxysteroid dehydrogenase 2 was demonstrated, and withholding itraconazole led to resolution of adverse effects that did not recur with voriconazole. This report adds to a growing body of evidence linking apparent mineralocorticoid excess with certain triazoles. This article is protected by copyright. All rights reserved...
January 31, 2018: Mycoses
https://www.readbyqxmd.com/read/29378538/a-novel-compound-heterozygous-variant-of-the-slc12a3-gene-in-gitelman-syndrome-pedigree
#20
Yixin Chen, Ziyi Zhang, Xihua Lin, Qianqian Pan, Fenping Zheng, Hong Li
BACKGROUND: Gitelman syndrome (GS) is an autosomal recessive disorder caused by genic mutations of SLC12A3 (Solute carrier family 12 member 3), which encodes the Na-Cl cotransporter (NCC), and presents with characteristic metabolic abnormalities, including hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. In this study, we report a case of a GS pedigree, including analysis of GS-associated gene mutations. METHODS: We performed next-generation sequencing analysis and Sanger sequencing to explore the SLC12A3 mutations in a GS pedigree that included a 35-year-old female patient with GS and five family members within three generations...
January 29, 2018: BMC Medical Genetics
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