We describe a patient with severe hypernatremia and uremia caused by paranoid adipsia who was treated successfully with hydration and hemodialysis. A previously healthy 40-year-old woman developed the paranoid idea that her water was poisoned, so she refused to drink any water. On admission, her blood urea nitrogen was 208mg/dL, creatinine 4.90mg/dL, serum osmolality 452mOsm/L, serum sodium 172mEq/L, urine specific gravity > or =1.030, urine osmolality 698mOsm/L, and urine sodium/potassium/chloride 34/85.6/8mEq/L. We diagnosed her with uremic encephalopathy and started intravenous dextrose, but the sodium correction was incomplete. She underwent two sessions of hemodialysis to treat the uremic encephalopathy and hypernatremia, and recovered fully without neurological sequelae. Although the standard treatment for severe hypernatremia is hydration, hemodialysis can be an additional treatment in cases of combined uremic encephalopathy.
Blood Urea Nitrogen ; Creatinine ; Female ; Glucose ; Humans ; Hypernatremia ; Osmolar Concentration ; Renal Dialysis ; Sodium ; Specific Gravity ; Uremia ; Water

Osmotic demyelination syndrome is a demyelinating disorder associated with rapid correction of hyponatremia. But, it rarely occurs in acute hypernatremia, and it leads to permanent neurologic symptoms and is associated with high mortality. A 44-year-old woman treated with alternative medicine was admitted with a history of drowsy mental status. Severe hypernatremia (197mEq/L) with hyperosmolality (415mOsm/kgH2O) was evident initially and magnetic resonance imaging revealed a high signal intensity lesion in the pons, consistent with central pontine myelinolysis. She was treated with 0.45% saline and 5% dextrose water and intravenous corticosteroids. Serum sodium normalized and her clinical course gradually improved. Brain lesion of myelinolysis also improved in a follow-up imaging study. This is the first report of a successful treatment of hypernatremia caused by iatrogenic salt intake, and it confirms the importance of adequate fluid supplementation in severe hypernatremia.
Adrenal Cortex Hormones ; Adult ; Brain ; Complementary Therapies ; Demyelinating Diseases* ; Female ; Follow-Up Studies ; Glucose ; Humans ; Hypernatremia* ; Hyponatremia ; Magnetic Resonance Imaging ; Mortality ; Myelinolysis, Central Pontine ; Neurologic Manifestations ; Pons ; Sodium ; Water

BACKGROUND: The relationship between abdominal obesity (AO) and mortality in peritoneal dialysis (PD) patients is controversial. METHODS: The prevalence of AO in 84 PD patients was assessed in a cross-section manner and followed up for 9 years at a single center. AO was defined as a waist circumference (WC) of more than 90 cm in males or more than 80 cm in females. The patients were classified as either with AO(AO group) or without AO(nAO group). RESULTS: The AO group was older, contained more diabetics, more females, and had higher Charlson comorbidity index (aCCI) scores, BMI, and triglyceride and lower serum creatinine than the non-AO subjects. The follow-up duration was 53.2+/-34.4 months. At the end of the follow-up, eighteen patients (21.4%) were dead; 9 died of cardiovascular causes. The five year survival rate was 40.8%. Kaplan-Meier analysis revealed that both all-cause and cardiovascular-cause mortalities were similar in the AO and nAO groups. Multivariate analysis revealed the presence of AO not to be an independent risk factor of all-cause and cardiovascular-cause mortality. CONCLUSION: AO itself might not be a risk factor for mortality in PD patients. Nevertheless, further prospective studies with a large number of patients will be needed to prove this.
Comorbidity ; Creatinine ; Female ; Follow-Up Studies ; Humans ; Kaplan-Meier Estimate ; Kidney Failure, Chronic ; Male ; Mortality* ; Multivariate Analysis ; Obesity, Abdominal* ; Peritoneal Dialysis ; Peritoneal Dialysis, Continuous Ambulatory* ; Prevalence ; Risk Factors ; Survival Rate ; Triglycerides ; Waist Circumference

Diuretics are commonly used to control edema across various clinical fields. Diuretics inhibit sodium reabsorption in specific renal tubules, resulting in increased urinary sodium and water excretion. Loop diuretics are the most potent diuretics. In this article, we review five important aspects of loop diuretics, in particular furosemide, which must be considered when prescribing this medicine: (1) oral versus intravenous treatment, (2) dosage, (3) continuous versus bolus infusion, (4) application in chronic kidney disease patients, and (5) side effects. The bioavailability of furosemide differs between oral and intravenous therapy. Additionally, the threshold and ceiling doses of furosemide differ according to the particular clinical condition of the patient, for example in patients with severe edema or chronic kidney disease. To maximize the efficiency of furosemide, a clear understanding of how the mode of delivery will impact bioavailability and the required dosage is necessary.
Biological Availability ; Diuretics ; Edema ; Furosemide ; Humans ; Renal Insufficiency, Chronic ; Sodium ; Sodium Potassium Chloride Symporter Inhibitors*

Hypertension is a complex trait determined by both genetic and environmental factors and is a major public health problem due to its high prevalence and concomitant increase in the risk for cardiovascular disease. With the recent large increase of dietary salt intake in most developed countries, the prevalence of hypertension increases tremendously which is about 30% of the world population. There is substantial evidence that suggests some people can effectively excrete high dietary salt intake without an increase in arterial BP, and another people cannot excrete effectively without an increase in arterial BP. Salt sensitivity of BP refers to the BP responses for changes in dietary salt intake to produce meaningful BP increases or decreases. The underlying mechanisms that promote salt sensitivity are complex and range from genetic to environmental influences. The phenotype of salt sensitivity is therefore heterogeneous with multiple mechanisms that potentially link high salt intake to increases in blood pressure. Moreover, excess salt intake has functional and pathological effects on the vasculature that are independent of blood pressure. Epidemiologic data demonstrate the role of high dietary salt intake in mediating cardiovascular and renal morbidity and mortality. Almost five decades ago, Guyton and Coleman proposed that whenever arterial pressure is elevated, pressure natriuresis enhances the excretion of sodium and water until blood volume is reduced sufficiently to return arterial pressure to control values. According to this hypothesis, hypertension can develop only when something impairs the excretory ability of sodium in the kidney. However, recent studies suggest that nonosmotic salt accumulation in the skin interstitium and the endothelial dysfunction which might be caused by the deterioration of vascular endothelial glycocalyx layer (EGL) and the epithelial sodium channel on the endothelial luminal surface (EnNaC) also play an important role in nonosmotic storage of salt. These new concepts emphasize that sodium homeostasis and salt sensitivity seem to be related not only to the kidney malfunction but also to the endothelial dysfunction. Further investigations will be needed to assess the extent to which changes in the sodium buffering capacity of the skin interstitium and develop the treatment strategy for modulating the endothelial dysfunction.
Arterial Pressure ; Blood Pressure ; Blood Volume ; Cardiovascular Diseases ; Developed Countries ; Epithelial Sodium Channels ; Glycocalyx ; Homeostasis ; Hypertension* ; Kidney* ; Mortality ; Natriuresis ; Negotiating ; Phenobarbital ; Phenotype ; Prevalence ; Public Health ; Skin ; Sodium ; Water

The kidney collecting duct is an important renal tubular segment for the regulation of body water and salt homeostasis. Water reabsorption in the collecting duct cells is regulated by arginine vasopressin (AVP) via the vasopressin V2-receptor (V2R). AVP increases the osmotic water permeability of the collecting duct cells through aquaporin-2 (AQP2) and aquaporin-3 (AQP3). AVP induces the apical targeting of AQP2 and transcription of AQP2 gene in the kidney collecting duct principal cells. The signaling transduction pathways resulting in the AQP2 trafficking to the apical plasma membrane of the collecting duct principal cells, include AQP2 phosphorylation, RhoA phosphorylation, actin depolymerization and calcium mobilization, and the changes of AQP2 protein abundance in water balance disorders have been extensively studied. These studies elucidate the underlying cellular and molecular mechanisms of body water homeostasis and provide the basis for the treatment of body water balance disorders.
Actins ; Aquaporin 2* ; Aquaporins ; Arginine Vasopressin ; Body Water ; Calcium ; Cell Membrane ; Homeostasis ; Kidney Tubules, Collecting* ; Permeability ; Phosphorylation ; Vasopressins ; Water-Electrolyte Balance Body Water

Hypernatremia in adults is a common problem that has been associated with mortality rates ranging from 40% to 60%. Clinical characteristics of hospital-acquired hypernatremia have not been well defined. To evaluate the difference between hypernatremia on admission and hospital-acquired hypernatremia, we reviewed 50 patients with hypernatremia at Hanyang University Guri Hospital for 51-month period from 1 March 2001 to 31 May 2005. We defined hypernatremia as serum sodium concentration more than or equal to 150 mEq/L. Hospital-acquired hypernatremia was more frequently (62%) observed than hypernatremia on admission (38%). Patients with hypernatremia on admission (73.1+/-11.7 years) were older than those with hospital-acquired hypernatremia (59.3+/-13.7 years). Only 30% of patients was alert in mental status. Fifty six percent of all patients (n=50) had neurologic problem such as head injury, cerebral infarction or hemorrhage. Admission hypernatremia was caused by severe dehydration due to no access to water. Seventy seven percent of hospital-acquired hypernatremic patients were associated with diuretics and solute diuresis. Treatments of hospital-acquired hypernatremia were also delayed and inadequate. Rate of correction in 6, 12, 24 hours after peak sodium level was not different between hypernatremia on admission and hospital-acquired hypernatremia. More rapid correction during 6 hours in hypernatremia on admission was associated with higher mortality (survival 2.1+/-0.7 mEq/L, death 7.1+/-4.9 mEq/L, p<0.05). Higher mortality was observed in patients with more severe renal insufficiency. In conclusion, hospital-acquired hypernatremia is largely avoidable by clinical attention and appropriate therapy. Patients with cerebrovascular events or renal insufficiency, patients treated with diuretics or hypertonic solute need careful fluid management and the close monitoring of blood sodium level. Particularly, the rate of correction during the first 6 hours should be also managed very cautiously in hypernatermia on admission.
Adult ; Cerebral Infarction ; Craniocerebral Trauma ; Dehydration ; Diuresis ; Diuretics ; Hemorrhage ; Humans ; Hypernatremia* ; Mortality ; Renal Insufficiency ; Sodium

Chronic renal failure, which has an increased single nephron glomerular filtration rate in remnant kidney, is known to cause characteristic structural alterations in renal tubule epithelia in association with impaired urinary concentration and deranged urinary sodium excretion. This mini-review will deal with the changes in the renal expression of aquaporins (AQPs) and sodium transporters for elucidating the underlying cellular and molecular mechanisms for the urinary abnormalities of decreased urinary concentration and increased urinary sodium excretion.
Aquaporins* ; Glomerular Filtration Rate ; Kidney ; Kidney Failure, Chronic* ; Membrane Transport Proteins ; Nephrons ; Renal Insufficiency ; Sodium*

Although the obstruction is potentially reversible with treatment, marked and sometimes prolonged diuresis and natriuresis associated with an impaired ability to concentrate the urine may follow relief of the obstruction. Various factors contributing to the postobstructive diuresis and natriuresis have been suggested, including decreases of tubular sodium reabsorption, retention of urea and expansion of extracellular fluid volume. Tubular damage as a consequence of obstruction may occur one or more nephron segments and may result in decreased reabsorption of filtrate. The discovery of aquaporin (AQP) membrane water channels and sodium (co)transporters and channels provided insight, at the molecular level, into the fundamental physiology and pathophysiology of water and sodium balance. In addition, recent studies have shown that the kidney per se is also a site of production and release of atrial natriuretic peptide (ANP). The locally synthesized ANP may act in a paracrine manner to increase the urinary excretion of sodium and water. In this context, an altered regulation of ANP in the kidney may result in an altered urinary excretion. The combined interactions of multiple independent mechanisms are thought to be involved in the pathogenesis of postobstructive diuresis and natriuresis. We examined the changes of AQP water channels, sodium (co)transporters and natriuretic peptide system in obstructed kidneys. The expression of AQP water channels and sodium transporters was decreased in the obstructed kidneys, which may at least in part account for the urinary concentration defect associated with postobstructive diuresis and natriuresis. In addition, the postobstructive natriuresis was associated with an enhanced renal expression of ANP mRNA and an increased urinary excretion of ANP. The plasma dendroaspis natriuretic peptide (DNP) level was increased following an experimental ureteral obstruction. The urinary excretion of DNP was increased along with the postobstructive diuresis. An enhanced activity of DNP system may in part play a role in mediating the postobstructive diuresis
Animals ; Aquaporins* ; Atrial Natriuretic Factor ; Diuresis* ; Elapidae ; Extracellular Fluid ; Kidney* ; Membranes ; Natriuresis ; Natriuretic Peptides ; Negotiating ; Nephrons ; Physiology ; Plasma ; Rats* ; RNA, Messenger ; Sodium* ; Urea ; Ureteral Obstruction

All urate transport occurs across the renal epithelial cells of the proximal tubule. Most of the filtered urate is reabsorbed in the S1 segment of the early proximal tubule. This is followed by tubular secretion in the S2 segment of the proximal tubule and approximately 50% of the filtered urate flows back into the tubular lumen. Most of the secreted urate undergoes postsecretory reabsorption that occurs predominantly in the last S3 segment of the proximal tubule. Recently, four proteins that transport urate have been identified at the molecular level. These proteins are an electrogenic urate uniporter, urate transporter/channel (UAT), two members of the organic anion transporter (OAT) family, OAT1 and OAT3, and a protein with some homology to OAT4, designated URAT1.
Epithelial Cells ; Humans ; Ion Transport ; Uric Acid*