Journal Detail Information

1

Cite

Share

Icodextrin Improves the Serum Potassium Profile with the Enhancement of Nutritional Status in Continuous Ambulatory Peritoneal Dialysis Patients.

Joo Hark YI ; Jae Il PARK ; Hoon Young CHOI ; Ho Yung LEE ; Sang Woong HAN ; Ho Jung KIM

Electrolytes & Blood Pressure.2009;7(2):79-86. doi:10.5049/EBP.2009.7.2.79

The impact of glucose-free icodextrin (ID) for overnight dwell as compared to conventional glucose-containing dialysate (GD) on potassium (K+) metabolism in continuous ambulatory peritoneal dialysis (CAPD) patients has not yet been investigated. Serum K+ in a total of 255 stable patients (116 on GD and 139 on ID) on CAPD for more than 6 months and in 139 patients on ID before and after ID use (Pre-ID and Post-ID) were observed along with nutritional markers in a 2-year study period (Jan. 2006 to Dec. 2007). The prevalence of hypokalemia was similar between patients on GD and ID (16.7% vs 17.3%), but was lower on Post-ID than Pre-ID (17.3% vs 20.5%) without statistic significance. The mean serum K+ level was higher on ID than on GD (P<0.05) as well as Post-ID than Pre-ID (P<0.001). In the multivariate analysis, serum K+ levels were positively correlated with serum albumin, and creatinine in all patients (P<0.05), and ID-use in younger patients (age< or =56, P<0.001). Serum albumin, creatinine, total CO2, and body mass index were significantly higher on Post-ID than Pre-ID. Icodextrin dialysate for chronic overnight dwell could increase serum K+ levels and lower the prevalence of hypokalemia compared to conventional glucose-containing dialysate. The improved chronic K+ balance in CAPD patients on icodextrin could be related to enhanced nutritional status rather than its impact on acute intracellular K+ redistribution.
Body Mass Index ; Creatinine ; Glucans ; Glucose ; Humans ; Hypokalemia ; Multivariate Analysis ; Nutritional Status ; Peritoneal Dialysis ; Peritoneal Dialysis, Continuous Ambulatory ; Potassium ; Prevalence ; Serum Albumin

2

Cite

Share

De Novo Hypokalemia in Incident Peritoneal Dialysis Patients: A 1-Year Observational Study.

Ji Yong JUNG ; Jae Hyun CHANG ; Hyun Hee LEE ; Wookyung CHUNG ; Sejoong KIM

Electrolytes & Blood Pressure.2009;7(2):73-78. doi:10.5049/EBP.2009.7.2.73

Hypokalemia occurs frequently in patients undergoing peritoneal dialysis (PD). However, the therapeutic strategy may differ from that of non-PD-related hypokalemia. We investigated clinical features and related factors of de novo hypokalemia in incident PD patients. We retrospectively enrolled 82 normokalemic patients starting PD at Gachon University Gil Hospital, Korea. The patients were divided into hypokalemia (K+<3.5 mEq/L) and normokalemia (3.5 mEq/L< or =K+<5.5 mEq/L) groups based on the plasma potassium levels at month 13, and then clinical parameters including peritoneal function and adequacy tests and biochemical parameters were compared. Eight patients who showed hyperkalemia (K+> or =5.5 mEq/L) at month 13 were excluded from our analyses. The incidence of hypokalemia in PD patients was 7.3% in a year. The de novo hypokalemia (n=6) and normokalemia (n=68) groups had no significant differences in baseline characteristics. The serum albumin levels and normalized protein equivalent of nitrogen appearance (nPNA) at month 1 were not significantly different between the two groups. At month 13, on the other hand, serum albumin levels and nPNA were significantly lower in the hypokalemia group (P=0.014; P=0.006, respectively). Kt/Vurea, residual renal function, dialysate-peritoneal creatinine ratio, and glucose load were not significantly different between the two groups. Hypokalemia occurring after initiation of PD may largely be associated with poor nutritional status.
Creatinine ; Glucose ; Hand ; Humans ; Hyperkalemia ; Hypokalemia ; Incidence ; Korea ; Nitrogen ; Nutritional Status ; Peritoneal Dialysis ; Plasma ; Potassium ; Retrospective Studies ; Serum Albumin

3

Cite

Share

Aldosterone Synthase Gene (CYP11B2) Polymorphism in Korean End-Stage Renal Disease Patients on Hemodialysis.

Ji Eun LEE ; So Yon BAE ; Jeong Yup KIM ; Heui Jung PYO ; Young Joo KWON

Electrolytes & Blood Pressure.2009;7(2):67-72. doi:10.5049/EBP.2009.7.2.67

Aldosterone synthase gene (CYP11B2) -344C/T polymorphism has been reported to be associated with serum aldosterone level, urinary aldosterone excretion, blood pressure, and left ventricular size and mass. The aim of this study was to evaluate the relation between CYP11B2 polymorphism and end-stage renal disease (ESRD) in the Korean population and the association with CYP11B2 polymorphism and cardiovascular morbidity in ESRD patients on hemodialysis. Genotyping was performed in 134 control subjects and 271 ESRD patients for CYP11B2 polymorphism using polymerase chain reaction through subsequent cleavage with restriction enzyme. Also current blood pressure, demographic, anthropometric and biochemical variables were investigated. The genotype distribution did not differ between ESRD patients and controls and there were no significant differences in blood pressure, use of antihypertensive medication, left ventricular hypertrophy and cardiovascular disease among the three genotypes in ESRD patients on hemodialysis. Our findings do not support the hypothesis that CYP11B2 polymorphism may be associated with prevalence of ESRD and suggest that CYP11B2 polymorphism may not be a genetic marker for cardiovascular morbidity in Korean ESRD patients.
Aldosterone ; Aldosterone Synthase ; Blood Pressure ; Cardiovascular Diseases ; Genetic Markers ; Genotype ; Humans ; Hypertrophy, Left Ventricular ; Kidney Failure, Chronic ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Prevalence ; Renal Dialysis

4

Cite

Share

Altered Regulation of Renal Sodium Transporters in Salt-Sensitive Hypertensive Rats Induced by Uninephrectomy.

Ji Yong JUNG ; Jay Wook LEE ; Sejoong KIM ; Eun Sook JUNG ; Hye Ryoun JANG ; Jin Suk HAN ; Kwon Wook JOO

Electrolytes & Blood Pressure.2009;7(2):58-66. doi:10.5049/EBP.2009.7.2.58

Uninephrectomy (uNx) in young rats causes salt-sensitive hypertension (SSH). Alterations of sodium handling in residual nephrons may play a role in the pathogenesis. Therefore, we evaluated the adaptive alterations of renal sodium transporters according to salt intake in uNx-SSH rats. uNx or sham operations were performed in male Sprague-Dawley rats, and normal-salt diet was fed for 4 weeks. Four experimental groups were used: sham-operated rats raised on a high-salt diet for 2 weeks (CHH) or on a low-salt diet for 1 week after 1 week's high-salt diet (CHL) and uNx rats fed on the same diet (NHH, NHL) as the sham-operated rats were fed. Expression of major renal sodium transporters were determined by semiquantitative immunoblotting. Systolic blood pressure was increased in NHH and NHL groups, compared with CHH and CHL, respectively. Protein abundances of Na+/K+/2Cl- cotransporter (NKCC2) and Na+/Cl- cotransporter (NCC) in the CHH group were lower than the CHL group. Expression of epithelial sodium channel (ENaC)-gamma increased in the CHH group. In contrast, expressions of NKCC2 and NCC in the NHH group didn't show any significant alterations, compared to the NHL group. Expressions of ENaC-alpha and ENaC-beta in the NHH group were higher than the CHH group. Adaptive alterations of NKCC2 and NCC to changes of salt intake were different in the uNx group, and changes in ENaC-alpha and ENaC-beta were also different. These altered regulations of sodium transporters may be involved in the pathogenesis of SSH in the uNx rat model.
Animals ; Blood Pressure ; Diet ; Diet, Sodium-Restricted ; Epithelial Sodium Channels ; Handling (Psychology) ; Humans ; Hypertension ; Immunoblotting ; Male ; Nephrectomy ; Nephrons ; Rats ; Rats, Sprague-Dawley ; Salicylamides ; Social Control, Formal ; Sodium ; Sodium Chloride Symporters ; Sodium-Potassium-Chloride Symporters

5

Cite

Share

Hyponatremia in Patients with Neurologic Disorders.

Dong Ki KIM ; Kwon Wook JOO

Electrolytes & Blood Pressure.2009;7(2):51-57. doi:10.5049/EBP.2009.7.2.51

The kidney and the brain play a major role in maintaining normal homeostasis of the extracellular fluid by neuroendocrine regulation of sodium and water balance. Therefore, disturbances of sodium balance are common in patients with central nervous system (CNS) disorders and clinicians should focus not only on the CNS lesion, but also on the potentially deleterious complications. Hyponatremia is the most common and important electrolyte disorder affecting patients with critical neurologic diseases. In these patients, the maladaptation to hyponatremia by impaired osmoregulation in pathologic lesions of brain may cause more aggressive cerebral edema and increased intracranial pressure due to hypoosmolality induced by hyponatremia. Furthermore, hyponatremia accompanied by CNS disorders has shown to increase delayed cerebral ischemia and mortality rates. Two main pathophysiologies of hyponatremia, excluding iatrogenic causes, are inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting (CSW) syndrome. Differential diagnosis between these two entities can be difficult due to considerable overlap in the laboratory findings and clinical situations. SIADH is in a volume expanded status due to inappropriately secreted arginine vasopressin (AVP) and requires water restriction. However, CSW syndrome is characterized by renal sodium wasting mainly due to increased natriuretic peptides resulting in volume depletion and follows appropriate secretion of AVP. Therefore, maintenance of volume status and sodium replacement is the mainstay of treatment in CSW syndrome. In this review, we aimed to describe the regulation of sodium and water balance, and pathophysiology, diagnosis and treatment of hyponatremia in neurologic patients, especially focusing on SIADH and CSW syndrome.
Arginine Vasopressin ; Brain ; Brain Edema ; Brain Ischemia ; Central Nervous System ; Diagnosis, Differential ; Extracellular Fluid ; Homeostasis ; Humans ; Hyponatremia ; Inappropriate ADH Syndrome ; Intracranial Pressure ; Kidney ; Natriuretic Peptides ; Nervous System Diseases ; Sodium ; Water-Electrolyte Balance

6

Cite

Share

Renal Dysfunction in Patients with Chronic Liver Disease.

Jay Wook LEE

Electrolytes & Blood Pressure.2009;7(2):42-50. doi:10.5049/EBP.2009.7.2.42

Renal dysfunction in patients with chronic liver disease encompasses a clinical spectrum of hyponatremia, ascites, and hepatorenal syndrome. Clinical observation has suggested that patients with cirrhosis have hyperdynamic circulation, and recent studies strongly suggest that peripheral arterial vasodilatation and subsequent development of hyperdynamic circulation are responsible for disturbances in renal function. Arterial vasodilatation predominantly occurs in the splanchnic vascular bed, and seems to precede an increase in blood flow in the splanchnic circulation. Nitric oxide plays a central role in progressive vasodilatation, as evidenced by in vivo and in vitro studies. Renal dysfunction negatively affects the prognosis of patients with cirrhosis, as hyponatremia, ascites, and azotemia are associated with increased rate of complications and mortality. Recent advances in understanding the pathophysiology of renal dysfunction have enabled clinicians to develop new diagnostic criteria and therapeutic recommendations. Hepatorenal syndrome is regarded as a potentially reversible disorder, as systemic vasoconstrictors with concomitant albumin administration are emerging as a promising management option, especially in terms of providing bridging therapy for patients awaiting liver transplantation.
Ascites ; Azotemia ; Fibrosis ; Hepatorenal Syndrome ; Humans ; Hyponatremia ; Liver ; Liver Cirrhosis ; Liver Diseases ; Liver Transplantation ; Nitric Oxide ; Prognosis ; Splanchnic Circulation ; Vasoconstrictor Agents ; Vasodilation

7

Cite

Share

Water and Sodium Regulation in Heart Failure.

Eun Hui BAE ; Seong Kwon MA

Electrolytes & Blood Pressure.2009;7(2):38-41. doi:10.5049/EBP.2009.7.2.38

Heart failure is the pathophysiological state characterized by ventricular dysfunction and associated clinical symptoms. Decreased cardiac output or peripheral vascular resistance lead to arterial underfilling. That is an important signal which triggers multiple neurohormonal systems to maintain adequate arterial pressure and peripheral perfusion of the vital organs. The kidney is the principal organ affected when cardiac output declines. Alterations of hemodynamics and neurohormonal systems in heart failure result in renal sodium and water retention. Activation of sympathetic nervous system, renin-angiotensin-aldosterone system and non-osmotic vasopressin release stimulate the renal tubular reabsorption of sodium and water. Dysregulation of aquaporin-2 and sodium transporters also play an important role in the pathogenesis of renal sodium and water retention.
Aquaporin 2 ; Aquaporins ; Arterial Pressure ; Cardiac Output ; Epithelial Sodium Channels ; Heart ; Heart Failure ; Hemodynamics ; Kidney ; Perfusion ; Renin-Angiotensin System ; Retention (Psychology) ; Sodium ; Sodium Chloride Symporters ; Sodium-Potassium-Chloride Symporters ; Sympathetic Nervous System ; Vascular Resistance ; Vasopressins ; Ventricular Dysfunction ; Water-Electrolyte Imbalance

8

Cite

Share

Dialysis Unphysiology and Sodium Balance.

Gheun Ho KIM

Electrolytes & Blood Pressure.2009;7(2):31-37. doi:10.5049/EBP.2009.7.2.31

Dialysis unphysiology was first discussed by Carl Kjellstrand in 1975 for the possible negative effects of the unphysiology of intermittent dialysis treatment. Current hemodialysis practices are still unphysiologic because they cannot keep blood chemistries within normal limits, both before and after dialysis. In addition, the discontinuous nature of hemodialysis causes saw-tooth volume fluctuations, and the extracellular fluid volume expansion during the interdialytic period may lead to hypertension and adverse cardiovascular consequences. Sodium, which is accumulated over the interdialytic period, may be divided into two fractions. The one is the fraction of osmotically active sodium which is mainly confined to the extracellular space, and the other is that of water-free (osmotically inactive) sodium which diffuses into the intracellular space. Both contribute to the pathogenesis of hypertension because the former may act to expand extracellular fluid volume and the latter may cause vasoconstriction in the long run by increasing cytosolic concentration of calcium in the vascular smooth muscle cells. Even in intensive hemodialysis, it may take several weeks to months for water-free sodium storage in the vascular smooth muscle cells to be relieved. This may be an explanation for the lag phenomenon, i.e., the delay of blood pressure decrease after normalization of extracellular fluid volume shown in the Tassin experience. Modest restriction of dietary sodium intake, the dialytic session length long enough to maintain a high ultrafiltration volume, and the reasonably low dialysate sodium concentration are required to avoid unphysiology of positive sodium balance in current hemodialysis practice.
Blood Pressure ; Calcium ; Cytosol ; Dialysis ; Extracellular Fluid ; Extracellular Space ; Hypertension ; Intracellular Space ; Muscle, Smooth, Vascular ; Renal Dialysis ; Sodium ; Sodium, Dietary ; Ultrafiltration ; Vasoconstriction

9

Cite

Share

Hypercalcemia Associated with Acute Kidney Injury and Metabolic Alkalosis.

Jong Hyeok JEONG ; Eun Hui BAE

Electrolytes & Blood Pressure.2010;8(2):92-94. doi:10.5049/EBP.2010.8.2.92

Most cases of hypercalcaemia are secondary to malignancy or primary hyperparathyroidism. We report a patient presenting with a triad of hypercalcemia, metabolic alkalosis, and renal failure secondary to treatment of iatrogenic hypoparathyroidism and osteoporosis. Persistent ingestion of calcium carbonate and vitamin D caused milk-alkali syndrome. The patient was managed with intravenous fluids and withdrawal of calcium carbonate and vitamin D. She responded well to the treatment and the calcium concentration, renal function and metabolic alkalosis were normalized. Milk-alkali syndrome may be important as a reemerging cause of hypercalcemia.
Acute Kidney Injury ; Alkalosis ; Calcium ; Calcium Carbonate ; Eating ; Humans ; Hypercalcemia ; Hyperparathyroidism, Primary ; Hypoparathyroidism ; Osteoporosis ; Renal Insufficiency ; Vitamin D

10

Cite

Share

Atherosclerotic Renovascular Hypertension : Lessons from Recent Clinical Studies.

Wookyung CHUNG ; Sejoong KIM

Electrolytes & Blood Pressure.2010;8(2):87-91. doi:10.5049/EBP.2010.8.2.87

Atherosclerotic renovascular hypertension is a form of secondary hypertension due to renal artery stenosis. After the introduction of medical therapy such as with statins and angiotensin blocking agents, it has been considered a very slowly progressive disease. In the 1990s, surgical methods were compared to radiological intervention and showed no additional benefits. Recent clinical data also demonstrate that in cases of relatively stable atherosclerotic renovascular disease, medical therapy is as effective as other interventions with regard to patient outcomes. In this paper the recent clinical outcomes are reviewed.
Angiotensins ; Atherosclerosis ; Humans ; Hypertension ; Hypertension, Renovascular ; Renal Artery Obstruction

DISPLAY OPTIONS

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share

Cite

Share