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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2009, Volume 106, Issue 14, pp. 5842 - 5847
Journal Article
Pharmacogenomics Journal, ISSN 1470-269X, 04/2015, Volume 15, Issue 2, pp. 153 - 157
Journal Article
Kidney International, ISSN 0085-2538, 01/2017, Volume 91, Issue 1, pp. 24 - 33
Gitelman syndrome (GS) is a rare, salt-losing tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. The disease... 
hypokalemic metabolic alkalosis | hypomagnesemia | SLC12A3 | thiazide-sensitive sodium-chloride cotransporter | salt-losing tubulopathy | Hypokalemia/blood | Angiotensin-Converting Enzyme Inhibitors/therapeutic use | Diagnosis, Differential | Anti-Inflammatory Agents, Non-Steroidal/therapeutic use | Genetic Testing | Bartter Syndrome/blood | Chloride Channels/genetics | Potassium/administration & dosage | Humans | Consensus Development Conferences as Topic | Rare Diseases/genetics | Sodium Chloride, Dietary/therapeutic use | Gitelman Syndrome/complications | Phenotype | Solute Carrier Family 12, Member 3/genetics | Ultrasonography | Calcium/urine | Quality of Life | Magnesium/administration & dosage | Angiotensin Receptor Antagonists/therapeutic use | Mutation | Chondrocalcinosis/etiology | Dietary Supplements | Practice Guidelines as Topic | SERUM POTASSIUM | FOLLOW-UP | HYPOKALEMIC ALKALOSIS | THERAPEUTIC APPROACH | BARTTERS-SYNDROME | BLOOD-PRESSURE | NCC GENE | GLUCOSE-METABOLISM | UROLOGY & NEPHROLOGY | CHANNEL GENE | SODIUM-CHLORIDE COTRANSPORTER | Rare Diseases - genetics | Gitelman Syndrome - drug therapy | Hypokalemia - blood | Magnesium - administration & dosage | Bartter Syndrome - diagnosis | Chloride Channels - genetics | Bartter Syndrome - urine | Angiotensin-Converting Enzyme Inhibitors - therapeutic use | Bartter Syndrome - genetics | Solute Carrier Family 12, Member 3 - genetics | Bartter Syndrome - blood | Chondrocalcinosis - prevention & control | Sodium Chloride, Dietary - therapeutic use | Calcium - urine | Magnesium - therapeutic use | Anti-Inflammatory Agents, Non-Steroidal - therapeutic use | Potassium - administration & dosage | Chondrocalcinosis - etiology | Potassium - therapeutic use | Gitelman Syndrome - complications | Gitelman Syndrome - diagnosis | Potassium - blood | Gitelman Syndrome - genetics | Angiotensin Receptor Antagonists - therapeutic use | Hypokalemia - genetics | Magnesium - blood
Journal Article
Kidney International, ISSN 0085-2538, 08/2016, Volume 90, Issue 2, pp. 430 - 439
Journal Article
Journal of Molecular Endocrinology, ISSN 0952-5041, 07/2017, Volume 59, Issue 1, pp. R47 - R63
Primary aldosteronism (PA), the most common form of secondary hypertension, is caused in the majority of cases by unilateral aldosterone-producing adenoma... 
Calcium channels | Familial hyperaldosteronism | Primary aldosteronism | Somatic mutations | Aldosterone-producing adenoma | ATPase | Germline mutations | Potassium channels | Wnt/β-catenin pathway | aldosterone-producing adenoma | HYPERALDOSTERONISM TYPE-II | MEMBRANE CA2+ ATPASE | familial hyperaldosteronism | calcium channels | Wnt/beta-catenin pathway | germline mutations | PCR-SSCP ANALYSIS | somatic mutations | MOUSE ADRENAL-CORTEX | GLUCOCORTICOID-REMEDIABLE ALDOSTERONISM | potassium channels | K+ CHANNEL MUTATIONS | primary aldosteronism | ENDOCRINOLOGY & METABOLISM | CLINICAL-PRACTICE GUIDELINE | KCNJ5 MUTATIONS | POTASSIUM CHANNEL | Adrenal Glands - pathology | Sodium-Potassium-Exchanging ATPase - genetics | Plasma Membrane Calcium-Transporting ATPases - genetics | Adenoma - genetics | Humans | Hyperaldosteronism - pathology | Hyperaldosteronism - metabolism | Adrenal Hyperplasia, Congenital - genetics | Adenoma - metabolism | Plasma Membrane Calcium-Transporting ATPases - metabolism | Hyperaldosteronism - diagnosis | Adrenal Hyperplasia, Congenital - diagnosis | Hypokalemia - metabolism | Adrenal Hyperplasia, Congenital - pathology | G Protein-Coupled Inwardly-Rectifying Potassium Channels - metabolism | Hypertension - genetics | Hypertension - diagnosis | Hypokalemia - pathology | Adenoma - diagnosis | Gene Expression | Genetic Predisposition to Disease | Adrenal Hyperplasia, Congenital - metabolism | Hyperaldosteronism - genetics | G Protein-Coupled Inwardly-Rectifying Potassium Channels - genetics | beta Catenin - metabolism | Hypertension - pathology | beta Catenin - genetics | Hypertension - metabolism | Hypokalemia - diagnosis | Sodium-Potassium-Exchanging ATPase - metabolism | Calcium Channels, L-Type - genetics | Adrenal Glands - metabolism | Adenoma - pathology | Calcium Channels, L-Type - metabolism | Mutation | Hypokalemia - genetics
Journal Article
Pediatric Nephrology, ISSN 0931-041X, 2017, Volume 32, Issue 7, pp. 1123 - 1135
Magnesium is essential to the proper functioning of numerous cellular processes. Magnesium ion (Mg2+) deficits, as reflected in hypomagnesemia, can cause... 
Homeostasis | Thick ascending limb of Henle’s loop | Magnesium | Hereditary | Distal convoluted tubule | Kidney | PCBD1 CAUSE | FAMILIAL HYPOMAGNESEMIA | SENSORINEURAL DEAFNESS | ATAXIA | CALCIUM-SENSING RECEPTOR | HYPOPARATHYROIDISM | UROLOGY & NEPHROLOGY | Thick ascending limb of Henle's loop | PEDIATRICS | MUTATIONS | KENNY-CAFFEY-SYNDROME | BARTTER-SYNDROME | Seizures - blood | Hypokalemia - blood | Kidney Tubules, Distal - physiology | Humans | Renal Tubular Transport, Inborn Errors - genetics | Renal Reabsorption - genetics | Nephrocalcinosis - complications | Renal Tubular Transport, Inborn Errors - blood | Hypercalciuria - blood | Magnesium Deficiency - genetics | Magnesium Deficiency - complications | Renal Reabsorption - drug effects | Hypokalemia - drug therapy | Magnesium - physiology | Magnesium Deficiency - drug therapy | Hypercalciuria - genetics | Membrane Proteins - metabolism | Child | Hypokalemia - etiology | Renal Tubular Transport, Inborn Errors - drug therapy | Membrane Proteins - genetics | Nephrocalcinosis - drug therapy | Arrhythmias, Cardiac - etiology | Mitochondria - metabolism | Loop of Henle - physiology | Renal Tubular Transport, Inborn Errors - complications | Magnesium - therapeutic use | Mineralocorticoid Receptor Antagonists - therapeutic use | Hypercalciuria - complications | Hypercalciuria - drug therapy | Phenotype | Renal Elimination - genetics | Nephrocalcinosis - genetics | Epithelial Sodium Channel Blockers - therapeutic use | Seizures - etiology | Nephrocalcinosis - blood | Arrhythmias, Cardiac - blood | Mutation | Recommended Dietary Allowances | Hypokalemia - genetics | Magnesium - blood | Homeostasis - genetics | Complications and side effects | Care and treatment | Kidney failure | Arrhythmia | Gene mutations | Research | Magnesium deficiency diseases | Review
Journal Article
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 11/2016, Volume 480, Issue 4, pp. 745 - 751
Kelch-like 3 (KLHL3) is a component of an E3 ubiquitin ligase complex that regulates blood pressure by targeting With-No-Lysine (WNK) kinases for degradation.... 
Post-translational modification | Hypokalemia | Distal nephron | Ubiquitin proteasome pathway | SPAK | PROTEIN-KINASE-C | BIOCHEMISTRY & MOLECULAR BIOLOGY | WNK4 | KLHL3 | BLOOD-PRESSURE | TRANSPORT | BIOPHYSICS | DEGRADATION | MUTATIONS | HYPERKALEMIC HYPERTENSION | CHLORIDE | Potassium Deficiency - genetics | Protein Kinase C - genetics | Phosphorylation | Kidney - pathology | Humans | Male | Potassium, Dietary - administration & dosage | Sodium - metabolism | Kidney - metabolism | WNK Lysine-Deficient Protein Kinase 1 | Protein Kinase C - metabolism | Potassium Deficiency - pathology | Potassium, Dietary - metabolism | Solute Carrier Family 12, Member 3 - genetics | HEK293 Cells | Hypokalemia - metabolism | Minor Histocompatibility Antigens - genetics | Microfilament Proteins - metabolism | Hypertension - genetics | Hypokalemia - pathology | Microfilament Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Protein-Serine-Threonine Kinases - genetics | Hypertension - pathology | Hypertension - metabolism | Minor Histocompatibility Antigens - metabolism | Animals | Diet | Potassium Deficiency - metabolism | Mice | Hypokalemia - genetics | Solute Carrier Family 12, Member 3 - metabolism | Hypertension | Ubiquitin | Medical colleges | Lysine | Ligases | Protein kinases | hypokalemia | distal nephron | post-translational modification | ubiquitin proteasome pathway
Journal Article
Journal Article
Journal Article
Seminars in Nephrology, ISSN 0270-9295, 2013, Volume 33, Issue 3, pp. 300 - 309
Summary Hereditary disorders of potassium homeostasis are an interesting group of disorders, affecting people from the newborn period to adults of all ages.... 
Nephrology | Liddle | aldosteronism | Genetic disorders of potassium | Gitelman | Bartter | Aldosteronism | APPARENT MINERALOCORTICOID EXCESS | EPITHELIAL NA+ CHANNEL | SENSORINEURAL DEAFNESS | HUMAN HYPERTENSION | BARTTERS-SYNDROME | CHLORIDE CHANNEL GENE | CALCIUM-SENSING RECEPTOR | GLUCOCORTICOID-REMEDIABLE ALDOSTERONISM | TUBULAR HYPOKALEMIC DISORDERS | PSEUDOHYPOALDOSTERONISM TYPE-1 | UROLOGY & NEPHROLOGY | Potassium - metabolism | Pseudohypoaldosteronism - therapy | Bartter Syndrome - therapy | Mineralocorticoid Excess Syndrome, Apparent - genetics | Humans | Bartter Syndrome - diagnosis | Adrenal Hyperplasia, Congenital - genetics | Mineralocorticoid Excess Syndrome, Apparent - therapy | Hyperaldosteronism - diagnosis | Hyperkalemia - genetics | Liddle Syndrome - diagnosis | Bartter Syndrome - genetics | Pseudohypoaldosteronism - diagnosis | Adrenal Hyperplasia, Congenital - diagnosis | Gitelman Syndrome - therapy | Hypoaldosteronism - diagnosis | Hypoaldosteronism - genetics | Liddle Syndrome - genetics | Adrenal Hyperplasia, Congenital - therapy | Pseudohypoaldosteronism - genetics | Hyperaldosteronism - genetics | Liddle Syndrome - therapy | Mineralocorticoid Excess Syndrome, Apparent - diagnosis | Gitelman Syndrome - diagnosis | Gitelman Syndrome - genetics | Hypokalemia - genetics | Hyperaldosteronism - therapy | Hypoaldosteronism - therapy
Journal Article