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Kidney International May 1972
Review
Topics: Acid-Base Equilibrium; Acidosis; Acidosis, Respiratory; Alkalosis; Alkalosis, Respiratory; Altitude; Animals; Bicarbonates; Blood Pressure; Blood Vessels; Calcium; Cardiac Output; Cardiovascular System; Cerebrovascular Circulation; Heart; Heart Rate; Humans; Hydrogen; Oxygen Inhalation Therapy; Oxyhemoglobins; Physical Exertion; Potassium; Protein Binding; Respiratory System; Vascular Resistance; Ventilation-Perfusion Ratio; Ventricular Function
PubMed: 4599247
DOI: 10.1038/ki.1972.48 -
British Medical Journal (Clinical... Feb 1982
Topics: Alkalosis; Carbon Dioxide; Humans; Hypercapnia
PubMed: 6800517
DOI: 10.1136/bmj.284.6314.507-a -
British Medical Journal (Clinical... Jan 1982
Topics: Adult; Alkalosis; Humans; Male; Sodium Chloride
PubMed: 6799138
DOI: No ID Found -
The Western Journal of Medicine Mar 1974
Topics: Adult; Alkalosis; Anorexia Nervosa; Diagnosis, Differential; Female; Humans; Hypertrophy; Parotid Gland; Psychophysiologic Disorders; Sjogren's Syndrome; Vomiting
PubMed: 4816403
DOI: No ID Found -
Canadian Medical Association Journal Jun 1969
Review
Topics: Acid-Base Equilibrium; Acidosis; Acidosis, Respiratory; Alkalosis; Carbon Dioxide; Humans; Hydrogen-Ion Concentration; Partial Pressure
PubMed: 4892611
DOI: No ID Found -
The Tohoku Journal of Experimental... Nov 2013Gitelman's syndrome is an autosomal recessive salt-losing tubulopathy showing hypokalemic hypomagnesemic hypocalciuria with metabolic alkalosis and hyperreninemic...
Gitelman's syndrome is an autosomal recessive salt-losing tubulopathy showing hypokalemic hypomagnesemic hypocalciuria with metabolic alkalosis and hyperreninemic hyperaldosteronism. This syndrome is caused by mutations in the SLC12A3 gene that encodes sodium-chloride cotransporter expressed at the apical membrane of renal distal convoluted tubule. Symptoms and renal outcomes of Gitelman's syndrome are, in general, mild and benign, and renal insufficiency from Gitelman's syndrome associated with long-standing hypokalemia and volume depletion is extremely rare. Herein, we report a 27-year-old male patient with Gitelman's syndrome who manifested renal failure, hypokalemia, severe metabolic alkalosis and altered mentality. About one year ago, the patient had been transferred to Seoul National University Hospital, because of unsolved hypokalemia, and was diagnosed as Gitelman's syndrome by clinical features and genetic analysis of the SLC12A3 gene. The patient carries a missense mutation at one allele of SLC12A3 gene (c.781C>T, p.Arg261Cys). His mother is also heterozygous for the same mutation and she had a history of hypokalemia. On this admission, the patient had recurrent bouts of vomiting induced by psychiatric eating disorder and showed severe volume depletion with hypotension, azotemia and metabolic alkalosis. Intense hydration therapy and emergency hemodialysis transiently improved his fluid-electrolyte imbalance and renal function. However, renal dysfunction progressively deteriorated despite the medical treatment. Our findings suggest that even in Gitelman's syndrome, constant monitoring for volume status and other comorbid conditions should be employed to prevent progressive renal injury.
Topics: Adult; Alkalosis; Base Sequence; Biopsy; DNA Mutational Analysis; Disease Progression; Gitelman Syndrome; Heterozygote; Humans; Kidney; Male; Molecular Sequence Data; Renal Insufficiency; Solute Carrier Family 12, Member 3; Vomiting
PubMed: 24162365
DOI: 10.1620/tjem.231.165 -
The Journal of Clinical Investigation Mar 1971The recent reports of the effect of 2,3-diphosphoglycerate (2,3-DPG) on hemoglobin affinity for oxygen suggested that this substance may play a role in man's adaptation...
The recent reports of the effect of 2,3-diphosphoglycerate (2,3-DPG) on hemoglobin affinity for oxygen suggested that this substance may play a role in man's adaptation to acidosis and alkalosis.A study of the effect of induced acidosis and alkalosis on the oxyhemoglobin dissociation curve of normal man was therefore carried out, and the mechanisms involved in the physiological regulation of hemoglobin oxygen affinity examined.In acute changes of plasma pH there was no alteration in red cell 2,3-DPG content. However, there were changes in hemoglobin oxygen affinity and these correlated with changes in mean corpuscular hemoglobin concentration (MCHC). With maintained acidosis and alkalosis, red cell 2,3-DPG content was altered and correlated with the changes in hemoglobin oxygen affinity. Both of these mechanisms shift the hemoglobin oxygen dissociation curve opposite to the direct pH (Bohr) effect, and providing the rate of pH change is neither too rapid nor too large, they counteract the direct pH effect and the in vivo hemoglobin oxygen affinity remains unchanged. It is also shown that approximately 35% of the change in hemoglobin oxygen affinity resulting from an alteration in red cell 2,3-DPG, is explained by effect of 2,3-DPG on the red cell pH.
Topics: Acidosis; Alkalosis; Arteries; Blood; Carbon Dioxide
PubMed: 5545127
DOI: 10.1172/JCI106540 -
British Medical Journal Nov 1968Hypokalaemia and metabolic alkalosis were seen in three patients and additionally hypernatraemia in two patients treated with 100 mega units of sodium penicillin G for...
Hypokalaemia and metabolic alkalosis were seen in three patients and additionally hypernatraemia in two patients treated with 100 mega units of sodium penicillin G for subacute bacterial endocarditis. The hypernatraemia was probably due to the administration of insufficient fluid, while urinary potassium loss was an important factor in producing hypokalaemia and metabolic alkalosis after. Penicillin may promote urinary potassium excretion by acting as a non-reabsorbable anion.Potassium depletion during treatment with massive doses of sodium penicillin G may be prevented by concurrently administering potassium-sparing diuretics or by using the potassium salt of penicillin.
Topics: Absorption; Adolescent; Adult; Aged; Alkalosis; Diuretics; Endocarditis, Subacute Bacterial; Female; Humans; Hypernatremia; Hypokalemia; Kidney; Male; Middle Aged; Penicillin G; Potassium; Sodium
PubMed: 5722316
DOI: 10.1136/bmj.4.5630.550 -
CMAJ : Canadian Medical Association... Jun 2024
Topics: Humans; Female; Hypokalemia; Alkalosis; Young Adult; Diagnosis, Differential
PubMed: 38857937
DOI: 10.1503/cmaj.240163 -
Kidney International Apr 2018Kir4.1 in the distal convoluted tubule plays a key role in sensing plasma potassium and in modulating the thiazide-sensitive sodium-chloride cotransporter (NCC). Here we...
Kir4.1 in the distal convoluted tubule plays a key role in sensing plasma potassium and in modulating the thiazide-sensitive sodium-chloride cotransporter (NCC). Here we tested whether dietary potassium intake modulates Kir4.1 and whether this is essential for mediating the effect of potassium diet on NCC. High potassium intake inhibited the basolateral 40 pS potassium channel (a Kir4.1/5.1 heterotetramer) in the distal convoluted tubule, decreased basolateral potassium conductance, and depolarized the distal convoluted tubule membrane in Kcnj10flox/flox mice, herein referred to as control mice. In contrast, low potassium intake activated Kir4.1, increased potassium currents, and hyperpolarized the distal convoluted tubule membrane. These effects of dietary potassium intake on the basolateral potassium conductance and membrane potential in the distal convoluted tubule were completely absent in inducible kidney-specific Kir4.1 knockout mice. Furthermore, high potassium intake decreased, whereas low potassium intake increased the abundance of NCC expression only in the control but not in kidney-specific Kir4.1 knockout mice. Renal clearance studies demonstrated that low potassium augmented, while high potassium diminished, hydrochlorothiazide-induced natriuresis in control mice. Disruption of Kir4.1 significantly increased basal urinary sodium excretion but it abolished the natriuretic effect of hydrochlorothiazide. Finally, hypokalemia and metabolic alkalosis in kidney-specific Kir4.1 knockout mice were exacerbated by potassium restriction and only partially corrected by a high-potassium diet. Thus, Kir4.1 plays an essential role in mediating the effect of dietary potassium intake on NCC activity and potassium homeostasis.
Topics: Alkalosis; Animals; Disease Models, Animal; Female; Homeostasis; Hydrochlorothiazide; Hypokalemia; Kidney Tubules, Distal; Male; Membrane Potentials; Mice, Knockout; Natriuresis; Potassium Channels, Inwardly Rectifying; Potassium, Dietary; Renal Elimination; Sodium; Sodium Chloride Symporter Inhibitors; Solute Carrier Family 12, Member 3; Kir5.1 Channel
PubMed: 29310825
DOI: 10.1016/j.kint.2017.10.023