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Biff F Palmer - One of the best experts on this subject based on the ideXlab platform.
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regulation of Potassium homeostasis
Clinical Journal of The American Society of Nephrology, 2015Co-Authors: Biff F PalmerAbstract:Potassium is the most abundant cation in the intracellular fluid, and maintaining the proper distribution of Potassium across the cell membrane is critical for normal cell function. Long-term maintenance of Potassium homeostasis is achieved by alterations in renal excretion of Potassium in response to variations in intake. Understanding the mechanism and regulatory influences governing the internal distribution and renal clearance of Potassium under normal circumstances can provide a framework for approaching disorders of Potassium commonly encountered in clinical practice. This paper reviews key aspects of the normal regulation of Potassium Metabolism and is designed to serve as a readily accessible review for the well informed clinician as well as a resource for teaching trainees and medical students.
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Potassium Metabolism in chronic kidney disease
Chronic Renal Disease, 2015Co-Authors: Biff F PalmerAbstract:Adaptive increases in renal and gastrointestinal excretion of K+ help to prevent hyperkalemia in patients with CKD as long as the GFR remains greater than 15–20 mL/min. In these patients K+ balance is maintained by increased K+ secretion per functioning nephron, which is mediated in part by elevated plasma K+ concentration, aldosterone, increased flow rate, and enhanced Na+-K+-ATPase activity. Fecal losses of Potassium also increase in CKD. These adaptive mechanisms are effective in preventing hyperkalemia provided that urine output is in excess of 600 mL/day. However, limits of adaptation render the CKD patient susceptible to hyperkalemia with even minor perturbations in these factors. Such is the case in patients with diabetes, where decreased mineralocorticoid activity is often an early finding, caused by hyporeninemic hypoaldosteronism, or in patients with renal injury primarily directed toward the tubule, as in tubulointerstitial renal disease. In these settings, hyperkalemia often develops with only mild or moderate reductions in GFR. Once the GFR falls to less than 15 mL/min an inflection point is reached whereby small incremental losses in renal function require progressively steeper rises in steady state serum K+ concentration in order to maintain total body K+ balance. At this level of renal function the impact of factors known to adversely affect K+ homeostasis is significantly magnified. In clinical practice hyperkalemia is usually the result of a combination of factors superimposed on renal dysfunction.
G Giebisch - One of the best experts on this subject based on the ideXlab platform.
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challenges to Potassium Metabolism internal distribution and external balance
Wiener Klinische Wochenschrift, 2004Co-Authors: G GiebischAbstract:A complex pump-leak system involving both active and passive transport mechanisms is responsible for the appropriate distribution of Potassium (K) between the intra- and extracellular fluid compartments. In addition, the kidneys, and to a lesser extent the colon, safeguard maintenance of the narrow range of low K concentrations in the extracellular fluid. Early renal clearance studies showed that K is normally both reabsorbed and secreted by renal tubules, and that regulated secretion is the major source of K excretion. Net K secretion occurs mainly in principal cells while K absorption takes place in intercalated cells. Studies on single tubules and principal and intercalated cells have defined the determinants of K secretion and reabsorption including the electrochemical driving forces, specific carriers, ATPases, and K channels. Recent studies on the properties and molecular identity of renal K channels have also contributed significantly to understanding the renal mechanisms that transport and regulate K excretion.
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renal Potassium transport mechanisms and regulation
American Journal of Physiology-renal Physiology, 1998Co-Authors: G GiebischAbstract:The regulation of Potassium Metabolism involves mechanisms for the appropriate distribution between the intra- and extracellular fluid compartments and for the excretion by the kidney. Clearance and single-nephron studies show that renal excretion is determined by regulated Potassium secretion and Potassium reabsorption, respectively, in principal and intercalated cells of the distal nephron. Measurement of the electrochemical driving forces acting on Potassium transport across individual cell membranes and characterization of several ATPases and Potassium channels provide insights into the transport and regulation of renal Potassium excretion.
Gedske Daugaard - One of the best experts on this subject based on the ideXlab platform.
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magnesium and Potassium homeostasis during cisplatin treatment
Cancer Chemotherapy and Pharmacology, 2005Co-Authors: H Lajer, M Kristensen, H H Hansen, Sten Christensen, Ten Jonassen, Gedske DaugaardAbstract:Administration of cisplatin causes changes in magnesium and Potassium Metabolism. The purpose of this study was to investigate day-to-day changes in renal and intestinal homeostasis of magnesium (Mg) and Potassium (K) during repeated cisplatin treatments in rats to provide guidelines for human supplementation studies. Rats were housed in metabolic cages with access to a diet containing excess Mg and K. Treatment was administered once a week for 3 weeks and comprised either cisplatin 2.5 mg/kg body weight i.p or, as sham treatment, isotonic NaCl 2.5 ml/kg body weight i.p. Urine and feces were collected every 24 h. Blood samples for measurement of plasma Mg and K were obtained from a permanent arterial catheter prior to each treatment cycle and at the termination of the study. Cisplatin exerted a significant negative effect on total Mg balance. This effect was cumulative with repeated doses of cisplatin. The observed difference was mainly due to the difference in Mg balance between the treatment day and the following 2–3 days. The cumulated urinary excretion of Mg did not differ significantly between the two groups at the end of follow-up. A significant decrease was observed in cumulated intestinal absorption in treated rats compared to control rats at the end of follow-up. Lowered intestinal absorption accounted for 90% of the difference in total Mg balance between the two groups as compared to the renal loss. Cisplatin treatment also exerted a negative effect on total K balance, although the difference between cisplatin-treated and control rats was not significant at the end of follow-up. The Mg loss associated with cisplatin treatment was mainly the result of lowered intestinal absorption and not, as presently thought, the result of increased renal elimination. Instead, an increased renal reabsorption capacity was observed in response to decreased intestinal absorption. The study further showed that Mg and K Metabolism are subject to predictable changes in intestinal absorption and renal excretion with each cisplatin treatment, and that knowledge of these changes can be used in planning supplementation. Thus, the experimental observations support intravenous supplementation on the day of treatment and 2–3 days after treatment followed by oral supplementation until the next treatment.
Jurgen Goldschmidt - One of the best experts on this subject based on the ideXlab platform.
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the use of thallium diethyldithiocarbamate for mapping cns Potassium Metabolism and neuronal activity tl redistribution tl kinetics and tl equilibrium distribution
Journal of Neurochemistry, 2012Co-Authors: Tim Wanger, Henning Scheich, Frank W Ohl, Jurgen GoldschmidtAbstract:J. Neurochem. (2012) 122, 106–114. Abstract The Potassium (K+) analogue thallium (Tl+) can be used as a tracer for mapping neuronal activity. However, because of the poor blood–brain barrier (BBB) K+-permeability, only minute amounts of Tl+ enter the brain after systemic injection of Tl+-salts like thallium acetate (TlAc). We have recently shown that it is possible to overcome this limitation by injecting animals with the lipophilic chelate complex thallium diethyldithiocarbamate (TlDDC), that crosses the BBB and releases Tl+ prior to neuronal or glial uptake. TlDDC can thus be used for mapping CNS K+ Metabolism and neuronal activity. Here, we analyze Tl+-kinetics in the rodent brain both experimentally and using simple mathematical models. We systemically injected animals either with TlAc or with TlDDC. Using an autometallographic method we mapped the brain Tl+-distribution at various time points after injection. We show that the patterns and kinetics of Tl+-redistribution in the brain are essentially the same irrespective of whether animals have been injected with TlAc or TlDDC. Data from modeling and experiments indicate that transmembrane Tl+-fluxes in cells within the CNS in vivo equilibrate at similar rates as K+-fluxes in vitro. This equilibration is much faster than and largely independent of the equilibration of Tl+-fluxes across the BBB. The study provides further proof-of-concept for the use of TlDDC for mapping neuronal activity and CNS K+-Metabolism. A theoretical guideline is given for the use of K+-analogues for imaging neuronal activity with general implications for the use of metal ions in neuroimaging.
Manching Law - One of the best experts on this subject based on the ideXlab platform.
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hypokalemia in chinese peritoneal dialysis patients prevalence and prognostic implication
American Journal of Kidney Diseases, 2005Co-Authors: Cheukchun Szeto, Kaiming Chow, Bonnie Chingha Kwan, Chibon Leung, Kwokyi Chung, Manching LawAbstract:Background: Abnormal Potassium Metabolism may contribute to the increased cardiac morbidity and mortality seen in dialysis patients. We studied the pattern of serum Potassium levels in a cohort of Chinese peritoneal dialysis (PD) patients. Methods: We studied serum Potassium levels of 266 PD patients during 3 consecutive clinic visits. Dialysis adequacy, residual renal function, and nutritional status also were assessed. Patients were followed up for 33.7 ± 20.7 months. Results: Mean serum Potassium level was 3.9 ± 0.5 mEq/L (mmol/L). Five patients (1.9%) had an average serum Potassium level less than 3 mEq/L (mmol/L), whereas 54 patients (20.3%) had a serum Potassium level less than 3.5 mEq/L (mmol/L). Serum Potassium levels correlated with overall Subjective Global Assessment score ( r = 0.276; P r = 0.173; P = 0.005) and inversely with Charlson comorbidity score ( r = −0.155; P = 0.011). There was no correlation between serum Potassium level and daily PD exchange volume, total Kt/V, urine volume, or residual glomerular filtration rate. By means of multivariate analysis with Cox proportional hazard model to adjust for confounders, serum Potassium level was an independent predictor of actuarial patient survival. PD patients with hypokalemia (serum Potassium P = 0.015) than those without hypokalemia after adjusting for confounding factors. Conclusion: Hypokalemia is common in Chinese PD patients. Serum Potassium level was associated with nutritional status and severity of coexisting comorbid condition. Furthermore, hypokalemia was an independent predictor of survival in PD patients. Additional studies may be needed to investigate the benefit of Potassium supplementation for PD patients with hypokalemia.