Potassium is abundant in the ICF compartment in the body and its excretion primarily depends on renal (about 90%), and to a lesser extent (about 10%) on colonic excretion. Total body potassium approximated to 50mmol/kg body weight and 2% of total body potassium is in the ECF compartment and 98% of it in the intracellular compartment.Dyskalemia is a frequent electrolyte imbalance observed among the maintenance hemodialysis patients. In case of hyperkalemia, it is frequently “a silent and a potential life threatening electrolyte imbalance” among patients with ESRD under maintenance hemodialysis. The prevalence of hyperkalemia in maintenance HD patients was reported to be about 8.7-10%. Mortality related to the hyperkalemia has been shown to be about 3.1/1,000 patient-years and about 24% of patients with HD required emergency hemodialysis due to severe hyperkalemia. In contrast to the hyperkalemia, much less attention has been paid to the hypokalemia in hemodialysis patients because of the low prevalence under maintenance hemodialysis patients. Severe hypokalemia in the hemodialysis patients usually was resulted from low potassium intake (malnutrition), chronic diarrhea, mineralocorticoid use, and imprudent use of K-exchange resins. Recently, the numbers of the new patients with advanced chronic kidney disease undergoing maintenance hemodialysis are tremendously increasing worldwide. However, the life expectancy of these patients is still much lower than that of the general population. The causes of excess mortality in these patients seem to various, but dyskalemia is a common cause among the patients with ESRD undergoing hemodialysis.

• Potassium
• Balance
• Hemodialysis

Cardio-renal syndromes are disorders of the heart and kidney wherein acute or long-term dysfunction in one organ may induce acute or long-term dysfunction of the other. Because of this complex organ interaction, management of cardiorenal syndrome must be tailored to the underlying pathophysiology. Clinical guidelines exist for the treatment of heart failure or renal failure as separate conditions. Thus far, however, there has been no consensus about managing patients with cardio-renal and reno-cardiac syndromes. Pharmacologic treatment remains a controversial subject. Standard cardiac drugs such as diuretics and inotropes may have limited effect because resistance often develops after long- term use. Recent studies of patients with acute cardio-renal syndromes have focused on newer therapies, including phosphodiesterase inhibitors, vasopressin antagonists, adenosine A1 receptor antagonists, and renal protective dopamine. Initial clinical trials of these agents have shown encouraging results in some patients with heart failure, but have failed to demonstrate a clear superiority over more conventional treatments. Similarly, the benefits of diuretics, aspirin, erythropoietin agents, and iron supplements for management of chronic cardiorenal syndromes are unknown.

• Cardio-renal syndrome
• Management
• Drug

Catecholamine secretory traits were significantly heritable, as were stress-induced blood pressure changes. Tyrosine hydroxylase (TH) is the rate-limiting enzyme in catecholamine biosynthesis. In the tyrosine hyroxylase promoter, significant associations were found for urinary catecholamine excretion and for blood pressure response to stress. TH promoter haplotype 2 (TGGG) showed pleiotropy, increasing both norepinephrine excretion and blood pressure during stress. In hypertension, 2 independent case-control studies (1,266 subjects with 53% women and 927 subjects with 24% women) replicated the effect of C-824T in the determination of blood pressure. Chromogranin A (CHGA) plays a fundamental role in the biogenesis of catecholamine secretory granules. Changes in the storage and release of CHGA in clinical and experimental hypertension prompted us to study whether genetic variation at the CHGA locus might contribute to alterations in autonomic function, and hence hypertension and its target organ consequences such as hypertensive kidney disease (nephrosclerosis). Systematic polymorphism discovery across the human CHGA locus revealed such regulatory regions as the proximal promoter and 3`-UTR. In chromaffin cell-transfected CHGA 3`-UTR and promoter/luciferase reporter plasmids, the functional consequences of the regulatory/non-coding allelic variants were documented. Variants in both the proximal promoter and the 3`-UTR displayed statistical associations with hypertension and hypertensive end stage renal disease. Therefore, I would like to review the common genetic variation in TH and CHGA as a cause of inter-individual variation in sympathetic activity, and ultimately blood pressure and hypertensive kidney disease.

• Blood pressure
• Chromogranin A
• Tyrosine hydroxylase
• Hypertensive renal disease
• Genomics

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 ≥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.

• Hypernatremia
• Uremia
• Hemodialysis
• Paranoid