1.Diagnosis and treatment of sodium balance disorders.
Korean Journal of Medicine 2009;77(4):444-447
No abstract available.
Sodium
2.The Role of Nitric Oxide in the Expression of Renal Aquaporins in Ischemic Acute Renal Failure.
Korean Journal of Nephrology 2006;25(1):1-5
No abstract available.
Acute Kidney Injury*
;
Aquaporins*
;
Nitric Oxide*
3.Edematous Hyponatremia Treated with Tolvaptan in a Patient with Amyotrophic Lateral Sclerosis.
Electrolytes & Blood Pressure 2017;15(2):37-41
Amyotrophic lateral sclerosis (ALS) patients rarely present with either syndrome of inappropriate antidiuretic hormone secretion or generalized edema. Tolvaptan is a selective vasopressin V2 receptor antagonist that produces effective aquaresis, and its use in ALS patients has not been previously reported. A 50-year-old male ALS patient was admitted because of both generalized edema and dilutional hyponatremia. These manifestations were refractory to conventional diuretics and fluid therapy, but a very brisk diuresis was induced by tolvaptan administration. Edema and hyponatremia were also improved, and the patient was able to be discharged without tolvaptan. In this case report, we postulate how edema and dilutional hyponatremia developed in the patient, and discuss the mechanism of tolvaptan in treating hypervolemic hyponatremia. Further experience is necessary to evaluate the usefulness of tolvaptan in patients with neurological disorders.
Amyotrophic Lateral Sclerosis*
;
Diuresis
;
Diuretics
;
Edema
;
Fluid Therapy
;
Humans
;
Hyponatremia*
;
Male
;
Middle Aged
;
Nervous System Diseases
;
Receptors, Vasopressin
4.Corrigendum to "Hwang KS, Kim GH: Thiazide-induced Hyponatremia. Electrolyte Blood Press 8:51-57, 2010".
Electrolytes & Blood Pressure 2012;10(1):35-36
In several sections of our review paper, cited in the title, we have found some errors in quotation of sentences from the Dr. Aaron Spital's review article entitled "Diuretic-induced hyponatremia" published in American Journal of Nephrology 19:447-452, 1999. Quotation marks were missed, and we should have specifically acknowledged the source of our statements.
5.Treatment of Urinary Tract Infection.
Korean Journal of Medicine 2005;68(3):342-345
No abstract available.
Urinary Tract Infections*
;
Urinary Tract*
6.Dialysis Unphysiology and Sodium Balance.
Electrolytes & Blood Pressure 2009;7(2):31-37
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
7.Gaps between Global Guidelines and Local Practices in CKD-MBD.
Electrolytes & Blood Pressure 2014;12(2):35-40
The term 'chronic kidney disease-mineral bone disorder' (CKD-MBD) is a new term that, in contrast to the old term 'renal osteodystrophy', implies a systemic syndrome associated with cardiovascular morbidity and mortality. This new terminology is in line with previous studies that show elevated serum calcium, phosphorus, and parathyroid hormone (PTH) levels associated with increased cardiovascular and all-cause mortality. In order to improve outcomes in patients with CKD-MBD, many countries have developed clinical practice guidelines. Globally, the Kidney Disease Outcome Quality Initiative (KDOQI) and Kidney Disease: Improving Global Outcomes (KDIGO) guidelines are the most commonly used. However, whether these global guidelines can be successfully implemented on a local level needs to be studied. Differences in medical care and social factors between countries may limit the generalizability of global guidelines. Reports from the Korean registry and the Dialysis Outcomes and Practice Patterns Study (DOPPS) suggest that many dialysis patients are not within the target ranges recommended by the KDOQI and KDIGO guidelines for serum calcium, phosphorus, and PTH, suggesting gaps between global guidelines and local practices. Clinical studies with Korean CKD-MBD patients are necessary to compare Korean practices and outcomes to those suggested by global guidelines and to determine the target serum mineral levels associated with the best local outcomes.
Calcium
;
Dialysis
;
Humans
;
Kidney
;
Kidney Diseases
;
Mortality
;
Parathyroid Hormone
;
Phosphorus
;
Renal Dialysis
8.Treatment of renal anemia: Erythropoiesis stimulating agents and beyond.
Kidney Research and Clinical Practice 2017;36(3):209-223
Anemia, complicating the course of chronic kidney disease, is a significant parameter, whether interpreted as subjective impairment or an objective prognostic marker. Renal anemia is predominantly due to relative erythropoietin (EPO) deficiency. EPO inhibits apoptosis of erythrocyte precursors. Studies using EPO substitution have shown that increasing hemoglobin (Hb) levels up to 10–11 g/dL is associated with clinical improvement. However, it has not been unequivocally proven that further intensification of erythropoiesis stimulating agent (ESA) therapy actually leads to a comprehensive benefit for the patient, especially as ESAs are potentially associated with increased cerebro-cardiovascular events. Recently, new developments offer interesting options not only via stimulating erythropoeisis but also by employing additional mechanisms. The inhibition of activin, a member of the transforming growth factor superfamily, has the potential to correct anemia by stimulating liberation of mature erythrocyte forms and also to mitigate disturbed mineral and bone metabolism as well. Hypoxia-inducible factor prolyl hydroxylase inhibitors also show pleiotropic effects, which are at the focus of present research and have the potential of reducing mortality. However, conventional ESAs offer an extensive body of safety evidence, against which the newer substances should be measured. Carbamylated EPO is devoid of Hb augmenting effects whilst exerting promising tissue protective properties. Additionally, the role of hepcidin antagonists is discussed. An innovative new hemodialysis blood tube system, reducing blood contact with air, conveys a totally different and innocuous option to improve renal anemia by reducing mechanical hemolysis.
Activins
;
Anemia*
;
Apoptosis
;
Erythrocytes
;
Erythropoiesis*
;
Erythropoietin
;
Hematinics*
;
Hemolysis
;
Hepcidins
;
Humans
;
Metabolism
;
Miners
;
Mortality
;
Prolyl-Hydroxylase Inhibitors
;
Renal Dialysis
;
Renal Insufficiency, Chronic
;
Transforming Growth Factors
9.Hepcidin as a Biomarker of Cardiorenal Syndrome
Journal of Korean Medical Science 2020;35(1):20-
No abstract available.
Cardio-Renal Syndrome
;
Hepcidins