Refeeding syndrome refers to a life-threatening shift of electrolytes and fluid with metabolic abnormalities in malnourished patients undergoing refeeding, whether orally, enterally, or parenterally. Clinical findings are fluid-balance abnormalities, abnormal glucose metabolism, hypophosphatemia, hypomagnesemia, hypokalemia and deficiencies of vitamin and trace element. Multiple organ systems including cardiac, respiratory, neurologic, renal, hematologic, and gastrointestinal can be affected. When recognized in a timely manner, these complications can be easily and successfully prevented and treated. Four factors appear fundamental: early identification of patients at risk, correction of abnormalities before refeeding, close monitoring during refeeding, and an appropriate feeding regimen.
Electrolytes ; Glucose ; Humans ; Hypokalemia ; Hypophosphatemia ; Metabolism ; Nutritional Support ; Refeeding Syndrome* ; Vitamins

In order to explore the reason why hypokalemia could increase the vulnerable window (VW) for unidirectional conduction block in Long QT Syndromes (LQTS), we observed the effect of hypokalemia on the spatial gradients of Na channel conductance (G(Na)) and gating factors by using the LR91 1-dimensional heterogeneous virtual cardiac ventricular tissue model quatitively. The computer simulation experiments were divided into two groups, namely control and LQTS groups. The action potential was elicited after the basic stimulus S1 (-70 microA/microF, 1.5 ms) was given 10 times with basic cycle length (BCL) 500, 1000 and 2000 ms. To test the VW in unit of time (VWtime), the S1-S2 programmed stimuli were used with shortening S1S2 interval at the decrement of 1 ms. At the same time, the spatial gradients of Na channel conductance (G(Na)) and gating factors, m, h, j, were investigated. The APD and ionic channel currents were also detected under the conditions of normal and lower concentration of K+ outside of cell. We found that hypokalemia, LQTS and slow pacing rate enhanced the spatial gradient of G(Na) by increasing the spatial gradient of inactive gating factors h x j. The results also showed that hypokalemia deduced the peak values of I(K) and I(K1), which prolonged the action potential duration and enlarged the repolarization dispersion in this 1-D tissue cable model. Possibly these are the important factors to cause the spatial gradient of h x j and G(Na). enlargement. These changes increase the incidence of unidirectional conduction block of VW, and are vital reasons to increase the possibility of ventricular arrhythmia generation.
Computer Simulation ; Extracellular Space ; metabolism ; Humans ; Hypokalemia ; metabolism ; Long QT Syndrome ; etiology ; metabolism ; physiopathology ; Models, Biological ; Myocardium ; metabolism ; Sodium Channels ; metabolism

Virtually all of the dietary potassium intake is absorbed in the intestine, over 90% of which is excreted by the kidneys regarded as the most important organ of potassium excretion in the body. The renal excretion of potassium results primarily from the secretion of potassium by the principal cells in the aldosterone-sensitive distal nephron (ASDN), which is coupled to the reabsorption of Na⁺ by the epithelial Na⁺ channel (ENaC) located at the apical membrane of principal cells. When Na⁺ is transferred from the lumen into the cell by ENaC, the negativity in the lumen is relatively increased. K⁺ efflux, H⁺ efflux, and Cl^- influx are the 3 pathways that respond to Na⁺ influx, that is, all these 3 pathways are coupled to Na⁺ influx. In general, Na⁺ influx is equal to the sum of K⁺ efflux, H⁺ efflux, and Cl^- influx. Therefore, any alteration in Na⁺ influx, H⁺ efflux, or Cl^- influx can affect K⁺ efflux, thereby affecting the renal K⁺ excretion. Firstly, Na⁺ influx is affected by the expression level of ENaC, which is mainly regulated by the aldosterone-mineralocorticoid receptor (MR) pathway. ENaC gain-of-function mutations (Liddle syndrome, also known as pseudohyperaldosteronism), MR gain-of-function mutations (Geller syndrome), increased aldosterone levels (primary/secondary hyperaldosteronism), and increased cortisol (Cushing syndrome) or deoxycorticosterone (hypercortisolism) which also activate MR, can lead to up-regulation of ENaC expression, and increased Na⁺ reabsorption, K⁺ excretion, as well as H⁺ excretion, clinically manifested as hypertension, hypokalemia and alkalosis. Conversely, ENaC inactivating mutations (pseudohypoaldosteronism type 1b), MR inactivating mutations (pseudohypoaldosteronism type 1a), or decreased aldosterone levels (hypoaldosteronism) can cause decreased reabsorption of Na⁺ and decreased excretion of both K⁺ and H⁺, clinically manifested as hypotension, hyperkalemia, and acidosis. The ENaC inhibitors amiloride and Triamterene can cause manifestations resembling pseudohypoaldosteronism type 1b; MR antagonist spironolactone causes manifestations similar to pseudohypoaldosteronism type 1a. Secondly, Na⁺ influx is regulated by the distal delivery of water and sodium. Therefore, when loss-of-function mutations in Na⁺-K⁺-2Cl^- cotransporter (NKCC) expressed in the thick ascending limb of the loop and in Na⁺-Cl^- cotransporter (NCC) expressed in the distal convoluted tubule (Bartter syndrome and Gitelman syndrome, respectively) occur, the distal delivery of water and sodium increases, followed by an increase in the reabsorption of Na⁺ by ENaC at the collecting duct, as well as increased excretion of K⁺ and H⁺, clinically manifested as hypokalemia and alkalosis. Loop diuretics acting as NKCC inhibitors and thiazide diuretics acting as NCC inhibitors can cause manifestations resembling Bartter syndrome and Gitelman syndrome, respectively. Conversely, when the distal delivery of water and sodium is reduced (e.g., Gordon syndrome, also known as pseudohypoaldosteronism type 2), it is manifested as hypertension, hyperkalemia, and acidosis. Finally, when the distal delivery of non-chloride anions increases (e.g., proximal renal tubular acidosis and congenital chloride-losing diarrhea), the influx of Cl^- in the collecting duct decreases; or when the excretion of hydrogen ions by collecting duct intercalated cells is impaired (e.g., distal renal tubular acidosis), the efflux of H⁺ decreases. Both above conditions can lead to increased K⁺ secretion and hypokalemia. In this review, we focus on the regulatory mechanisms of renal potassium excretion and the corresponding diseases arising from dysregulation.
Humans ; Bartter Syndrome/metabolism* ; Pseudohypoaldosteronism/metabolism* ; Potassium/metabolism* ; Aldosterone/metabolism* ; Hypokalemia/metabolism* ; Gitelman Syndrome/metabolism* ; Hyperkalemia/metabolism* ; Clinical Relevance ; Epithelial Sodium Channels/metabolism* ; Kidney Tubules, Distal/metabolism* ; Sodium/metabolism* ; Hypertension ; Alkalosis/metabolism* ; Water/metabolism* ; Kidney/metabolism*

In end-stage renal disease (ESRD) patients regardless of dialysis modes, i.e. maintenance hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD), potassium (K) homeostasis is regulated primarily via dialysis and extrarenal K regulation in the diverse daily K intake. However, K metabolism has been known to differ greatly between the two main methods of dialysis. Hyperkalemia is a common complication (10-24%) and the most common cause of the death (3-5%) among electrolyte disorders in patients on maintenance HD. On the contrary, hypokalemia (10-36%) is responsible for a rather common complication and independent prognostic factor on CAPD. Although excessive K intake or inadequate dialysis on maintenance HD and poor nutritional K intake on CAPD are accused without doubts upto 50% of ESRD patients as a primary cause of the K-imbalance, i.e. hyperkalemia on HD and hypokalemia on CAPD, other contributory factors including certain medications and unknown causes remain still to be resolved. Accordingly, the effects of medications as another source of K-imbalance on HD with RAS blockades and beta blockers as well as those of conventional and glucose-free dialysates (Icodextrin) for internal K-redistribution on CAPD were evaluated with reviewing the literatures and our data. Furthermore, new developments in the clinical managements of hyperkalemia on HD following the exclusion of pseudohyperkalemia before the initiation of dialysis were suggested, especially, by the comparison of the effects between mono- and dual-therapy with medications for transcellular K shifting in the emergent situation. Also, the intraperitoneal K administration via conventional glucose-containing (2.5%) and glucose-free dialysates (Icodextrin) as a specific route of K-supplementation for hypokalemia on CAPD was examined for its efficiency and the degree of intracellular K shift between these two different types of dialysates.
Dialysis ; Dialysis Solutions ; Homeostasis ; Humans ; Hyperkalemia ; Hypokalemia ; Kidney Failure, Chronic ; Metabolism ; Peritoneal Dialysis, Continuous Ambulatory* ; Potassium ; Renal Dialysis*

OBJECTIVETo investigate the effect of potassium deficiency on glucose and insulin metabolism in primary hyperaldosteronism, including aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA).

METHODSTotally 178 patients who were diagnosed as primary hyperaldosteronism (103 patients with APA and 75 with IHA) were divided into hypokalemia group and normal potassium group according to their serum potassium levels. All patients received 3 hours of oral glucose tolerance test and aldosterone test to observe the relationship among glucose, insulin and serum potassium.

RESULTSArea under curve of serum potassium, area under curve of plasma insulin, and fasting serum insulin were significantly lower in the hypokalemia group than in the normal potassium group (P <0. 05, P <0. 01); area under curve of glucose and aldosterone level were significantly higher in the hypokalemia group than in the normal potassium group ( P < 0. 05 ) . The prevalence of metabolic syndrome was significantly higher in IHA than in APA (57. 3% vs 38. 8% ; P < 0. 05).

CONCLUSIONHypokalemia may play an important role in inhibiting insulin secretion in primary hyperaldosteronism.

Adult ; Blood Glucose ; metabolism ; Female ; Glucose Tolerance Test ; Humans ; Hyperaldosteronism ; complications ; metabolism ; Hypokalemia ; complications ; Insulin ; metabolism ; Male ; Metabolic Syndrome ; etiology ; Middle Aged

In order to determine the relationship between acid-base balance and K+ metabolism in patients whi controlled respiration during surgery, 20 patients under general anesthesia were studied. Anesthesia was induced with 2% thiopental and was maintained with halothane. Suxamethonium was used for intubation. During surgery, the respiration of the patient was controlled by a volume controlled respirator with tidal volume of 800ml and a rate of 12/min. Blood and urine samples were collected before anesthesia, and 30 and 60 minutes thereafter. REsults were as follows: Hyperventilation induced by artificial respiration during surgical anesthesia produced a significant decrease in PaCO2 from 36.1+/-1.3mmHg to 19.9+/-1.5mmHg at 30 min, and to 20.1+/-1.7mmHg at 60 min. Hyperventilation increased arterial pH from 7.41+/-0.008 to 7.49+/-0.028 at 30 min, and 7.47+/-0.011 at 60 min. Hyperventilation produced a significant decrease in serum concentration of K+ from 4.04+/-0.12 to 3.75+/-0.08mEq/l at 30min, and 3.62+/-0.05 mEq/l at 60min. Urinary excrets of K+ was not significantly altered during the hour of the hyperventilation. These results suggest that hypokalemia followed by respiratory alkasisis mainly due to the movement of K+ from extracellular to intracellular compartments rather than a change in renal excretion of K+.
Acid-Base Equilibrium ; Anesthesia ; Anesthesia, General ; Halothane ; Humans ; Hydrogen-Ion Concentration* ; Hyperventilation* ; Hypokalemia ; Intubation ; Metabolism* ; Potassium* ; Respiration ; Respiration, Artificial ; Succinylcholine ; Thiopental ; Tidal Volume ; Ventilators, Mechanical

Congenital adrenal hyperplasia is an uncommon diagnosis in routine clinical practice. 21-hydroxylase deficiency, which is its most common subtype, may be diagnosed at birth in a female infant by virilisation or by features of salt wasting in both genders. However, other uncommon subtypes of this condition such as 17-alpha-hydroxylase deficiency, 11-beta-hydroxylase deficiency may present much later in adolescence or adulthood. A high index of suspicion is necessary when evaluating children with hypertension, hypokalaemia, metabolic alkalosis or sexual infantilism.
Adolescent ; Adrenal Hyperplasia, Congenital ; diagnosis ; genetics ; Alkalosis ; diagnosis ; Diagnosis, Differential ; Female ; Humans ; Hypertension ; diagnosis ; Hypokalemia ; diagnosis ; Models, Biological ; Paralysis ; diagnosis ; Sexual Infantilism ; diagnosis ; Steroid 21-Hydroxylase ; metabolism

Hypokalemic periodic paralysis (HOPP) is a rare disease characterized by reversible attacks of muscle weakness accompanied by episodic hypokalemia. Recent molecular work has revealed that the majority of familial HOPP is due to mutations in a skeletal muscle voltage-dependent calcium-channel: the dihydropyridine receptor. We report a 13-yr old boy with HOPP from a family in which 6 members are affected in three generations. Genetic examination identified a nucleotide 3705 C to G mutation in exon 30 of the calcium channel gene, CACNA1S. This mutation predicts a codon change from arginine to glycine at the amino acid position #1239 (R1239G). Among the three known mutations of the CACNA1S gene, the R1239G mutation was rarely reported. This boy and the other family members who did not respond to acetazolamide, showed a marked improvement of the paralytic symptoms after spironolactone treatment.
Acetazolamide/pharmacology ; Adolescent ; Arginine/chemistry ; Calcium Channels/chemistry/*genetics ; Codon ; Exons ; Family Health ; Female ; Glycine/chemistry ; Humans ; Hypokalemia/metabolism ; Hypokalemic Periodic Paralysis/*diagnosis/*genetics ; Korea ; Male ; Muscle, Skeletal/metabolism ; Mutation ; Pedigree ; Protein Structure, Tertiary ; Sequence Analysis, DNA ; Spironolactone/pharmacology

OBJECTIVETo investigate the clinical and genetic characteristics of 7 patients from 5 families with 17a-hydroxylase/17,20 lyase deficiency (17OHD) and the CYP17A1 mutation in Chinese.

METHODSClinical features and laboratory data were collected from 5 families with 17OHD. PCR direct sequencing was performed to screen the mutation of CYP17A1 gene of the patients. Polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) and sequencing were performed to screen the mutations of CYP17A1 gene in 288 healthy individuals from Shandong province.

RESULTSSeven patients (5 of them were 46,XX; 2 were 46,XY) had typical clinical presentation of sexual infantilism, hypertension and hypokalemia. Hormone profile indicated decreased plasma cortisol and sex hormones, and elevated blood adrenocorticotrophic hormone (ACTH). TAC329AA and H373L in exon 6 and D487_F489del in exon 8 were identified from the patients. One heterozygote for D487_F489del was identified in 288 healthy controls.

CONCLUSIONThe TAC329AA and D487_F489del of the CYP17A1 gene were the most frequent mutations in Chinese with 17OHD.There might be certain frequency of heterozygotes for D487_F489del in Chinese population.

Adolescent ; Adult ; Asian Continental Ancestry Group ; genetics ; Exons ; Female ; Gene Frequency ; Humans ; Hypertension ; genetics ; Hypokalemia ; genetics ; Male ; Middle Aged ; Molecular Sequence Data ; Mutation ; Pedigree ; Polymerase Chain Reaction ; Sequence Analysis, DNA ; Sexual Infantilism ; genetics ; metabolism ; Steroid 17-alpha-Hydroxylase ; genetics ; metabolism ; Steroid 21-Hydroxylase ; genetics ; metabolism ; Young Adult

BACKGROUND/AIMS: To investigate abnormalities in blood electrolyte levels during severe hypoglycemia in Korean patients with type 2 diabetes mellitus (T2DM) in a clinical setting. METHODS: Blood electrolyte levels in adult T2DM patients during severe hypoglycemia were collected from January 1, 2008 to December 31, 2012. Patients who maintained normal serum creatinine and blood urea nitrogen levels were utilized in the study. Severe hypoglycemia was defined as a condition requiring medical assistance, such as administering carbohydrates when serum glucose levels less than 70 mg/dL were observed, in conjunction with other symptoms of hypoglycemia. RESULTS: A total of 1,068 patients who visited the emergency room with severe hypoglycemia were screened, of which 219 patients were included in this study. The incidence of abnormal levels for any electrolyte was 47%. Hypokalemia (< 3.5 mmol/L) was the most common type of electrolyte disturbance observed at 21.9%. A decrease in serum potassium levels was associated with decreases in blood glucose levels (r = 0.151, p = 0.025). During severe hypoglycemia, median blood glucose levels, incidence of tachycardia (> 100 beats per minute) and severe hypertension (> or = 180/120 mmHg) were 30 mg/dL (range, 14 to 62) and 35 mg/dL (range, 10 to 69; p = 0.04), 18.8% and 7.2% (p = 0.02), and 20.8% and 10.2% (p = 0.05) in the hypokalemia and normokalemia groups, respectively. CONCLUSIONS: During severe hypoglycemia, hypokalemia occurred in 21.9% of T2DM patients and was associated with tachycardia and severe hypertension. Therefore, the results suggest that severe hypoglycemia may increase cardiovascular events in T2DM.
Aged ; Aged, 80 and over ; Biomarkers/blood ; Blood Glucose/drug effects/*metabolism ; Diabetes Mellitus, Type 2/blood/diagnosis/drug therapy/*epidemiology ; Emergency Service, Hospital ; Female ; Humans ; Hypertension/chemically induced/epidemiology ; Hypoglycemia/blood/chemically induced/diagnosis/*epidemiology/therapy ; Hypoglycemic Agents/adverse effects ; Hypokalemia/blood/chemically induced/diagnosis/*epidemiology ; Male ; Middle Aged ; Potassium/*blood ; Republic of Korea/epidemiology ; Risk Factors ; Severity of Illness Index ; Tachycardia/chemically induced/epidemiology ; *Water-Electrolyte Balance/drug effects