Treatment Guidelines for Hyponatremia: Stay the Course.

International guidelines designed to minimize the risk of complications that can occur when correcting severe hyponatremia have been widely accepted for a decade. On the basis of the results of a recent large retrospective study of patients hospitalized with hyponatremia, it has been suggested that hyponatremia guidelines have gone too far in limiting the rate of rise of the serum sodium concentration; the need for therapeutic caution and frequent monitoring of the serum sodium concentration has been questioned. These assertions are reminiscent of a controversy that began many years ago.

Urea for hyponatremia?

Once the standard of care for cerebral edema, urea can also be used to treat hyponatremia. The 2014 European Clinical Practice Guidelines recommend urea for the treatment of the syndrome of inappropriate antidiuretic hormone, while discouraging use of vasopressin antagonists. Although there is evidence that urea can diminish hypertonic injury to brain cells caused by rapid correction of hyponatremia, clinical trials are needed that include patients at high risk to develop complications from overcorrection.

Safe and effective use of chronic transdermal estradiol for life-threatening uremic bleeding in a patient with coronary artery disease.

Uremic platelet dysfunction rarely causes significant bleeding in adequately dialyzed patients. When encountered, the management is complicated by a lack of well-supported treatment modalities. Estrogen use in uremic platelet dysfunction has been described, but enthusiasm for the treatment has been dampened by the risk of thrombotic events in vasculopathic dialysis patients.

Managing combined critical hypothermia, diabetic ketoacidosis and cocaine intoxication noninvasively.

Severe hypothermia with a core temperature below 28°C is critical especially in patients with diabetic ketoacidosis (DKA) and carries a high risk of mortality. Our case of a 52-year-old woman presenting with DKA, pH of 6.9, potassium of 7.

Management of hyponatremia in the ICU.

Hyponatremia is common in critical care units. Avoidance of neurologic injury requires a clear understanding of why the serum sodium (Na) concentration falls and why it rises, how the brain responds to a changing serum Na concentration, and what the goals of therapy should be. A 4 to 6 mEq/L increase in serum Na concentration is sufficient to treat life-threatening cerebral edema caused by acute hyponatremia.

Hypertonic saline and desmopressin: a simple strategy for safe correction of severe hyponatremia.

Background: Prompt correction of severe hyponatremia is important, but correction also must be limited to avoid iatrogenic osmotic demyelination. Expert opinion recommends that serum sodium level not be increased by more than 10-12 mEq/L in any 24-hour period and/or 18 mEq/L in any 48-hour period. However, inadvertent overcorrection is common, usually caused by the unexpected emergence of a water diuresis.

Diuretic-associated hyponatremia.

Soon after their introduction in 1957, thiazide diuretics became a recognized cause of hyponatremia. Thiazides may be the sole cause and they may exacerbate hyponatremia in patients with disorders that cause the syndrome of inappropriate antidiuretic hormone secretion. Although thiazides do not inhibit the ability to concentrate the urine, they impair diluting ability in several ways: inhibition of sodium and chloride transport at cortical diluting sites; stimulation of vasopressin release; reduction of glomerular filtration and enhanced proximal water reabsorption, which reduce delivery to the distal diluting sites; and, possibly, a direct effect on water flow in the collecting duct.

Treating profound hyponatremia: a strategy for controlled correction.

An alcoholic patient presented with profound hyponatremia (serum sodium concentration, 96 mEq/L) caused by the combined effects of a thiazide diuretic, serotonin reuptake inhibitor, beer potomania, and hypovolemia. A computed tomographic scan of the brain was indistinguishable from one obtained 3 weeks earlier when he was normonatremic. Concurrent administration of 3% saline solution and desmopressin controlled the rate of correction to an average of 6 mEq/L daily and resulted in full neurologic recovery without evidence of osmotic demyelination.

Treatment of hyponatremia.

Purpose Of Review: We review literature from the past 18 months on the treatment of hyponatremia. Therapy must address both the consequences of the untreated electrolyte disturbance (including fatal cerebral edema due to acute water intoxication) and the complications of excessive therapy (the osmotic demyelination syndrome).

Recent Findings: Correction of hyponatremia by 4-6 mEq/l within 6 h, with bolus infusions of 3% saline if necessary, is sufficient to manage the most severe manifestations of hyponatremia.

Atrial natriuretic peptide for preventing and treating acute kidney injury.

Background: Acute kidney injury (AKI) is common in hospitalised patients and is associated with significant morbidity and mortality. Despite recent advances, outcomes have not substantially changed in the last four decades. Atrial natriuretic peptide (ANP) has shown promise in animal studies, however randomised controlled trials (RCTs) have shown inconsistent clinical benefits.

Overcorrection of hyponatremia is a medical emergency.

Overcorrection of hyponatremia is a medical emergency. Excessive correction usually results from the unexpected emergence of a water diuresis after resolution of the cause of water retention. The concurrent administration of desmopressin and 5% dextrose in water can be given to cautiously re-lower the serum sodium concentration when therapeutic limits have been exceeded.

The treatment of hyponatremia.

Virtually all investigators now agree that self-induced water intoxication, symptomatic hospital-acquired hyponatremia, and hyponatremia associated with intracranial pathology are true emergencies that demand prompt and definitive intervention with hypertonic saline. A 4- to 6-mmol/L increase in serum sodium concentration is adequate in the most seriously ill patients and this is best achieved with bolus infusions of 3% saline. Virtually all investigators now agree that overcorrection of hyponatremia (which we define as 10 mmol/L in 24 hours, 18 mmol/L in 48 hours, and 20 mmol/L in 72 hours) risks iatrogenic brain damage.

Off-pump coronary artery bypass surgery and acute kidney injury: a meta-analysis of randomized and observational studies.

Background: Acute kidney injury (AKI) after coronary artery bypass grafting (CABG) is associated with significant morbidity and mortality. Controversy exists regarding whether an off-pump technique can reduce post-CABG renal injury.

Study Design: Systematic review and meta-analysis.

The role of natriuretic peptide administration in cardiovascular surgery-associated renal dysfunction: a systematic review and meta-analysis of randomized controlled trials.

Objective: Randomized controlled trials involving natriuretic peptide administration in the perioperative cardiovascular setting have shown inconsistent effects for renal and other clinical endpoints. The authors aimed to systematically review these trials to ascertain the role of natriuretic peptide administration in the management of cardiovascular surgery-associated renal dysfunction.

Design: A systematic review and meta-analysis.

Atrial natriuretic peptide for management of acute kidney injury: a systematic review and meta-analysis.

Background And Objectives: Randomized controlled trials (RCTs) with atrial natriuretic peptide (ANP) have shown inconsistent effects for renal end-points. The authors aimed to systematically review these trials to ascertain the benefit of ANP in prevention and treatment of acute kidney injury (AKI).

Design, Setting, Participants, & Measurements: The authors searched MEDLINE, EMBASE, and Cochrane Renal Health Library that investigated ANP in adult patients considered with or at risk for AKI.

Calciphylaxis from nonuremic causes: a systematic review.

Background And Objectives: Calciphylaxis, or calcific uremic arteriolopathy, is a well-described entity in end-stage kidney disease and renal transplant patients; however, little systematic information is available on calciphylaxis from nonuremic causes. This systematic review was designed to characterize etiologies, clinical features, laboratory abnormalities, and prognosis of nonuremic calciphylaxis.

Design, Setting, Participants, & Measurements: A systematic review of literature for case reports and case series of nonuremic calciphylaxis was performed.

Effect of off-pump coronary artery bypass graft surgery on postoperative acute kidney injury and mortality.

Objective: Risk of mortality after cardiac surgery is associated with severity of acute kidney injury. The aim of this study is to examine the effect of off-pump coronary artery bypass surgery on the risk of postoperative acute kidney injury and its association with mortality.

Design: Observational cohort study.

Association of impaired diurnal blood pressure variation with a subsequent decline in glomerular filtration rate.

Background: Most healthy people exhibit a decrease in systolic blood pressure (SBP) at night. A drop of less than 10% from mean daytime values (nondipping) is associated with chronic kidney disease, insulin resistance, and cardiovascular events. Whether nondipping precedes a decline in renal function remains unclear.

Pathophysiology, clinical consequences, and treatment of tumor lysis syndrome.

Tumor lysis syndrome is an oncologic emergency that is characterized by severe electrolyte abnormalities and, frequently, by acute renal failure. The syndrome typically occurs in patients with lymphoproliferative malignancies, most often after initiation of treatment. The pathophysiology involves massive tumor cell lysis resulting in the release of large amounts of potassium, phosphate, and uric acid.