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Magnesium homeostasis
Published in Kupetsky A. Erine, Magnesium, 2019
Ravi Sunderkrishnan, Maria P. Martinez Cantarin
Hypomagnesemia is frequently accompanied by other electrolyte abnormalities. Hypomagnesemia with simultaneous hypokalemia is seen with loop diuretics, Bartter and Gitelman syndromes, diarrhea, and aminoglycoside toxicity. The proposed mechanism by which hypomagnesemia alters K transport is via the ROMK channel. A deficiency of intracellular magnesium causes an alteration in the membrane potential of the ROMK channel, causing a K+ efflux into the tubular lumen. The resultant simultaneous loss of potassium and magnesium also results in an increase in the distal sodium (Na+) delivery and stimulates the ENaC channels, thus maintaining the potassium loss.17 Hence, unless magnesium is corrected, hypokalemia will not easily improve with potassium repletion alone.
Fluid and electrolyte disorders
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
Ploutarchos Tzoulis, Pierre-Marc G. Bouloux
Mg deficiency contributes to hypokalemia mainly by enhancing renal K secretion as a result of reduction of Mg-dependent inhibition of ROMK channels. In the cortical collecting duct cells, K is secreted into luminal fluid via apical (ROMK and BK) channels. At the physiologic intracellular Mg concentration, ROMK conducts more K ions inward than outward (inward rectifying). This is because intracellular Mg binds ROMK and blocks K efflux and secretion and in this way limits K efflux. This unique inward-rectifying property of ROMK renders intracellular Mg levels a critical determinant of ROMK-mediated K secretion in the distal nephron. Changes in intracellular Mg concentration over the physiologic-pathophysiologic range would significantly affect K secretion.117
The Nature of Renal Function
Published in Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George, The Scientific Basis of Urology, 2010
About 25% of filtered sodium is reabsorbed in the loop of Henle, all of it in the TAL. Entry into the cell here is effected by the transporter NKCC2 (the corresponding gene is SLC12A2; see above), which as its name suggests transports 1 Na+, 1 K+, and 2Cl−. Since the number of positively and negatively charged ions transported is equal, transport is electroneutral. Ammonium (NH4+), if present in the tubular fluid, can substitute for K+. NKCC2 is inhibited by bumetanide and furosemide (frusemide), a fact that accounts for the diuretic action of these drugs. The gene is located on chromosome 15q, and mutations of it cause one form of Bartter’s syndrome of hypokalemia, alkalosis, hypercalciuria and hyper-reninaemia with normal blood pressure, (56) as had been predicted from the close similarity between Bartter’s syndrome and the effect of chronic administration of loop diuretics. The very large amount of sodium reabsorbed by this transport system, and its relatively distal location, accounts for the great pharmacological power of the loop diuretics. The activity of NKCC2 causes large amounts of potassium and chloride, as well as sodium, to enter the cell from the tubular fluid. The absorbed potassium is recycled back into the tubule lumen via another apical membrane transporter, ROMK, and the chloride leaves the cell across the basolateral membrane via a chloride channel, ClC-Kb. Mutations in both ROMK and ClC-Kb can also cause forms of Bartter’s syndrome (57,58) since NKCC2 can operate efficiently only if the absorbed potassium and chloride are prevented from accumulating within the cell. The relationship between the various transporters in the TAL cell is shown in Figure 9.
Relationship between renal dysfunction and electrolyte abnormalities in hematopoietic stem cell transplant patients treated with foscarnet
Published in Journal of Chemotherapy, 2021
Generally, calcium in the blood is known to be distributed as follows: approximately 40% of the calcium in blood is bound to proteins consisting mainly of albumin; 10% is bound to complexes with anions; the remaining 50% is present in the form of ionized calcium.22 Castelli et al.23 reported that the plasma foscarnet and ionized calcium concentrations are strongly inversely proportional. Beaufils et al.15 reported that foscarnet crystals were found in the kidneys of patients with renal dysfunction caused by foscarnet administration. These findings suggest that foscarnet, which is a strong chelating agent of divalent cations, can result in hypocalcemia and renal dysfunction by forming a complex with blood calcium and depositing it in the kidney. Generally, calcium-sensing receptors (CaSR) expressed in tissues such as the kidney regulate calcium homeostasis.24 When calcium stimulates and activates CaSR, it is known to suppress the renal outer medullary potassium channel (ROMK), which has been defined as a potassium excretion channel from the intracellular space to the lumen.25 Calcium reduction relieves ROMK suppression by CaSR. As a result, potassium excretion increases. This present study showed an inverse correlation between the creatinine and calcium and potassium levels. These findings may explain that the complex of foscarnet and calcium caused a decrease in calcium levels and renal dysfunction, resulting in the relaxation of ROMK suppression by CaSR, which in turn led to decreased potassium levels. However, the clear mechanism of the relationship between foscarnet-induced renal dysfunction and hypokalemia remains unclear.
An infant presenting with failure to thrive and hyperkalaemia owing to transient pseudohypoaldosteronism: case report
Published in Paediatrics and International Child Health, 2018
Marieke De Clerck, Johan Vande Walle, Evelyn Dhont, Joke Dehoorne, Werner Keenswijk
At this stage, the differential diagnosis included adrenal insufficiency (owing to, for example, congenital hypoplasia, infection, tumour, haemorrhage), pseudohypoaldosteronsim (PHA) (pseudohypoaldosteronism type 1/2, TPHA), congenital adrenal hyperplasia (CAH) owing to 21-hydroxylase deficiency, chronic kidney disease and Bartter syndrome associated with ROMK mutations.
A novel nonsense mutation in the β-subunit of the epithelial sodium channel causing Liddle syndrome
Published in Blood Pressure, 2021
Štěpán Mareš, Jan Filipovský, Kateřina Vlková, Martin Pešta, Václava Černá, Jaroslav Hrabák, Jitka Mlíková Seidlerová, Otto Mayer
Increased activity of ENaC leads to excessive reabsorbtion of sodium ions resulting in volume expansion and hypertension. Consequently, hyporeninemia and hypoaldosteronemia develop. Hypokalaemia is a result of potassium excretion via ROMK channels, which is driven by transepithelial lumen-negative voltage generated by increased sodium reabsorption [7,8].