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Felix Beuschlein - One of the best experts on this subject based on the ideXlab platform.
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Hypokalemia and the Prevalence of Primary Aldosteronism.
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2020Co-Authors: Sven Gruber, Felix BeuschleinAbstract:Hypokalemia is closely linked with the pathophysiology of primary aldosteronism (PA). Although hypokalemic PA is less common than the normokalemic course of the disease, Hypokalemia is of particular importance for the manifestation and development of comorbidities. Specifically, a growing body of evidence demonstrates that Hypokalemia in PA patients is associated with a more severe disease course regarding cardiovascular and metabolic morbidity and mortality. It is also well appreciated that low potassium levels per se can promote or exacerbate hypertension. The spectrum of Hypokalemia-related symptoms ranges from asymptomatic courses to life-threatening conditions. Hypokalemia is found in 9-37% of all cases of PA with a predominance in patients with aldosterone producing adenoma. Conversely, Hypokalemia resolves in almost 100% of cases after both, specific medical or surgical treatment of the disease. However, to date, high-level evidence about the prevalence of primary aldosteronism in a hypokalemic population is missing. Epidemiological data are expected from the recently launched IPAHK+study ("Incidence of Primary Aldosteronism in Patients with Hypokalemia").
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cardiovascular and cerebrovascular comorbidities of hypokalemic and normokalemic primary aldosteronism results of the german conn s registry
The Journal of Clinical Endocrinology and Metabolism, 2009Co-Authors: E Bornfrontsberg, Martin Reincke, Lars Christian Rump, Stefanie Hahner, S Diederich, R Lorenz, Bruno Allolio, Jochen Seufert, Caroline Schirpenbach, Felix BeuschleinAbstract:Context: Primary aldosteronism (PA) is associated with vascular end-organ damage. Objective: Our objective was to evaluate differences regarding comorbidities between the hypokalemic and normokalemic form of PA. Design and Setting: This was a retrospective cross-sectional study collected from six German centers (German Conn’s registry) between 1990 and 2007. Patients: Of 640 registered patients with PA, 553 patients were analyzed. Main Outcome Measures: Comorbidities depending on Hypokalemia or normokalemia were examined. Results: Of the 553 patients (61 ± 13 yr, range 13–96), 56.1% had hypokalemic PA. The systolic (164 ± 29 vs. 155 ± 27 mm Hg; P < 0.01) and diastolic (96 ± 18 vs. 93 ± 15 mm Hg; P < 0.05) blood pressures were significantly higher in hypokalemic patients than in those with the normokalemic variant. The prevalence of cardiovascular events (angina pectoris, myocardial infarction, chronic cardiac insufficiency, coronary angioplasty) was 16.3%. Atrial fibrillation occurred in 7.1% and other at...
S Usha - One of the best experts on this subject based on the ideXlab platform.
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Two cases of Hypokalemic Paralysis due to Distal Renal Tubular Acidosis
Kerala Medical Journal, 2012Co-Authors: Anoop John, Santhosh Sp Kumar, K B Rojith, D K Sivakumar, S Avudiappan, Isaac Christian Moses, S UshaAbstract:Hypokalemic periodic paralysis is a rare disorder characterized by transient attacks of flaccid paralysis of varying intensity and frequency. Although mostly familial in etiology, several sporadic cases have been reported, including some resulting from renal tubular acidosis. Here we present two cases, first of a 55 yr. old woman with recurrent attacks of flaccid paralysis, and the second, of a 16 yr. Old girl who presented with flaccid quadriparesis with no similar history in the past, both of whom on evaluation turned out to be secondary hypokalemic periodic paralysis caused by Distal Renal Tubular Acidosis (RTA). As the clinical appearance of hypokalemic paralysis distal RTA is quite similar to Familial Hypokalemic Periodic Paralysis (FPP), and because the emergent and prophylactic treatment of the two disorders is quite different, we discuss the diagnostic evaluation and the treatment of distal renal tubular acidosis. Keywords: Paralysis, Acidosis, Hypokalemia, Renal tubular acidosis, Hypokalemic periodic paralysis
Junebum Kim - One of the best experts on this subject based on the ideXlab platform.
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the large conductance calcium activated potassium channel holds the key to the conundrum of familial hypokalemic periodic paralysis
Korean Journal of Pediatrics, 2014Co-Authors: Junebum Kim, Sungjo Kim, Sunyang Kang, Seungmin KimAbstract:Purpose Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant channelopathy characterized by episodic attacks of muscle weakness and Hypokalemia. Mutations in the calcium channel gene, CACNA1S, or the sodium channel gene, SCN4A, have been found to be responsible for HOKPP; however, the mechanism that causes Hypokalemia remains to be determined. The aim of this study was to improve the understanding of this mechanism by investigating the expression of calcium-activated potassium (KCa) channel genes in HOKPP patients.
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An atypical phenotype of hypokalemic periodic paralysis caused by a mutation in the sodium channel gene SCN4A
Korean Journal of Pediatrics, 2010Co-Authors: Yang Hee Park, Junebum KimAbstract:Familial hypokalemic periodic paralysis is an autosomal-dominant channelopathy characterized by episodic muscle weakness with Hypokalemia. The respiratory and cardiac muscles typically remain unaffected, but we report an atypical case of a family with hypokalemic periodic paralysis in which the affected members presented with frequent respiratory insufficiency during severe attacks. Molecular analysis revealed a heterozygous c.664 C>T transition in the sodium channel gene SCN4A, leading to an Arg222Trp mutation in the channel protein. The patients described here presented unusual clinical characteristics that included a severe respiratory phenotype, an incomplete penetrance in female carriers, and a different response to medications.
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An atypical phenotype of hypokalemic periodic paralysis caused by a mutation in the sodium channel gene
Korean Pediatric Society, 2010Co-Authors: Yang Hee Park, Junebum KimAbstract:Familial hypokalemic periodic paralysis is an autosomal-dominant channelopathy characterized by episodic muscle weakness with Hypokalemia. The respiratory and cardiac muscles typically remain unaffected, but we report an atypical case of a family with hypokalemic periodic paralysis in which the affected members presented with frequent respiratory insufficiency during severe attacks. Molecular analysis revealed a heterozygous c.664 C>T transition in the sodium channel gene SCN4A, leading to an Arg222Trp mutation in the channel protein. The patients described here presented unusual clinical characteristics that included a severe respiratory phenotype, an incomplete penetrance in female carriers, and a different response to medications
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effect of extracellular potassium on delayed rectifier potassium channel proteins of kcnq3 and kcnq5 in familial hypokalemic periodic paralysis
Journal of Life Science, 2009Co-Authors: Sungjo Kim, Dae Yong Kim, Junebum KimAbstract:Familial hypokalemic periodic paralysis (HOKPP) is an autosomal dominant muscle disorder characterized by episodic attacks of muscle weakness with concomitant Hypokalemia. Mutations in either a calcium channel gene (CACNA1S) or a sodium channel gene (SCN4A) have been shown to be responsible for this disease. The combination of sarcolemmal depolarization and Hypokalemia has been attributed to abnormalities of the potassium conductance governing the resting membrane potential. To understand the pathophysiology of this disorder, we examined both mRNA and protein levels of delayed rectifier potassium channel genes, KCNQ3 and KCNQ5, in skeletal muscle fibers biopsied from patients with HOKOur results showed an increase in the cytoplasmic level of KCNQ3 protein in patients` cells exposed to 50 mM external concentration of potassium. However, mRNA levels of both channel genes did not show significant change in the same condition. Our results suggest that long term exposure of skeletal muscle cells in HOKPP patients to high extracellular potassium alters the KCNQ3 localization, which could possibly hinder the normal function of this channel protein. These findings may provide an important clue to understanding the molecular mechanism of familial hypokalemic periodic paralysis.
Anoop John - One of the best experts on this subject based on the ideXlab platform.
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Two cases of Hypokalemic Paralysis due to Distal Renal Tubular Acidosis
Kerala Medical Journal, 2012Co-Authors: Anoop John, Santhosh Sp Kumar, K B Rojith, D K Sivakumar, S Avudiappan, Isaac Christian Moses, S UshaAbstract:Hypokalemic periodic paralysis is a rare disorder characterized by transient attacks of flaccid paralysis of varying intensity and frequency. Although mostly familial in etiology, several sporadic cases have been reported, including some resulting from renal tubular acidosis. Here we present two cases, first of a 55 yr. old woman with recurrent attacks of flaccid paralysis, and the second, of a 16 yr. Old girl who presented with flaccid quadriparesis with no similar history in the past, both of whom on evaluation turned out to be secondary hypokalemic periodic paralysis caused by Distal Renal Tubular Acidosis (RTA). As the clinical appearance of hypokalemic paralysis distal RTA is quite similar to Familial Hypokalemic Periodic Paralysis (FPP), and because the emergent and prophylactic treatment of the two disorders is quite different, we discuss the diagnostic evaluation and the treatment of distal renal tubular acidosis. Keywords: Paralysis, Acidosis, Hypokalemia, Renal tubular acidosis, Hypokalemic periodic paralysis
Visith Sitprija - One of the best experts on this subject based on the ideXlab platform.
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thiazide induced subtle renal injury not observed in states of equivalent Hypokalemia
Kidney International, 2007Co-Authors: Sirirat Reungjui, Carlos Roncal, Byron P Croker, J M Patel, Takahiko Nakagawa, Titte R Srinivas, Karen J Byer, Jan S Simoni, David E Wesson, Visith SitprijaAbstract:Hydrochlorothiazide (HCTZ) is used to manage hypertension and heart failure; however, its side effects include mild Hypokalemia, metabolic abnormalities, and volume depletion, which might have deleterious effects on renal and endothelial function. We studied whether HCTZ cause renal injury and/or altered vasoreactivity and if these changes are Hypokalemia-dependent. Rats were given a normal diet or a diet moderately low in potassium (K + ) with or without HCTZ. Animals fed either a low K + diet alone or HCTZ developed mild Hypokalemia. There was no significant difference in systolic blood pressure in the different treatment groups. All three groups with Hypokalemia had mild proteinuria; low K + -HCTZ rats had reduced creatinine clearance. HCTZ-treated rats displayed hypomagnesemia, hypertriglyceridemia, hyperglycemia, insulin resistance, and hyperaldosteronism. No renal injury was observed in the groups without HCTZ; however, increased kidney weight, glomerular ischemia, medullary injury, and cortical oxidative stress were seen with HCTZ treatment. Endothelium-dependent vasorelaxation was reduced in all hypokalemic groups and correlated with reduced serum K + , serum, and urine nitric oxide. Our results show that HCTZ is associated with greater renal injury for the same degree of Hypokalemia as the low K + diet, suggesting that factors such as chronic ischemia and hyperaldosteronism due to volume depletion may be responsible agents. We also found impaired endothelium-dependent vasorelaxation was linked to mild Hypokalemia.