The role of daily dialysis in the control of hyperphosphatemia

The role of daily dialysis in the control of hyperphosphatemia.In patients with end-stage renal disease (ESRD), hyperphosphatemia occurs in the vast majority of patients. The numerous clinical sequelae of hyperphosphatemia include secondary hyperparathyroidism and increased risk of cardiovascular death. Chronic hemodialysis as it is currently practiced in the United States does not remove sufficient phosphate to control serum levels within accepted guidelines. The inadequacy of conventional hemodialysis in removing phosphate mandates the use of phosphate binders in virtually all hemodialysis patients. Despite their proven efficacy, these medications fail to control phosphorous in 70% of hemodialysis patients. Additionally, these medications may have untoward side effects that must be considered since they are typically intended for lifetime use. Quotidian hemodialysis has in previous uncontrolled studies shown promise in reducing serum phosphorus while at the same time reducing or eliminating the need for phosphate binders. Recent results from our group demonstrate for the first time in a controlled fashion the efficacy of short daily dialysis in controlling serum phosphorus

The Role of Daily Dialysis in the Control of Hyperphosphatemia Artículo de Actualización

Abstract In patients with end-stage renal disease (ESRD), hyperphosphatemia occurs in the vast majority of patients. The numerous clinical sequelae of hyperphosphatemia include secondary hyperparathyroidism and increased risk of cardiovascular death. Chronic hemodialysis as it is currently practiced in the United States does not remove sufficient phosphate to control serum levels within accepted guidelines. The inadequacy of conventional hemodialysis in removing phosphate mandates the use of phosphate binders in virtually all hemodialysis patients. Despite their proven efficacy, these medications fail to control phosphorous in seventy percent of hemodialysis patients. Additionally, these medications may have untoward side effects that must be considered since they are typically intended for lifetime use. Quotidian hemodialysis has in previous uncontrolled studies shown promise in reducing serum phosphorus while at the same time reducing or eliminating the need for phosphate binders. Recent results from our group demonstrate for the first time in a controlled fashion the efficacy of short daily dialysis in controlling serum phosphorus. Key Words: Phosphorus, phosphorus control, daily hemodialysis, short daily hemodialysis, quotidian hemodialysis, secondary hyperparathyroidism Cardiovascular disease is present in ESRD patients at rates 10-20 times higher than in the general population and accounts for 50% of deaths among ESRD patients. 1,2 Hyperphosphatemia is an emerging risk factor for cardiovascular mortality in the ESRD population.2 The pathogenesis of cardiac disease in the ESRD population is complex but involves the interplay of traditional risk factors along with risk factors that are specific to the dialysis population. The novel risk factors among dialysis patients include hyperphosphatemia, elevated calcium x phosphorus (Ca x P) product, lipoprotein (a), hyperhomocysteinemia, chronic inflammation and left ventricular hypertrophy. 2-9 Recently, in a rodent model, hyperphosphatemia has been shown to induce myocardial hypertrophy, independent of effects on hyperparathyroidism or cardiovascular calcification.10 Thus hyperphosphatemia must be viewed in the broad context of a cardiovascular risk factor in addition to its role in initiating secondary hyperparathyroidism. Conventional hemodialysis does not remove sufficient phosphate to maintain phosphorus balance in the vast majority of hemodialysis patients. 2,11 A four hour hemodialysis session will clear 34 mmol of phosphate (1054 mg of phosphorus), 12,13 which is not sufficient to keep up with the typical phosphorus intake of 800-2000 mg per day (equivalent to 25.8-64.5 mmol of phosphate) in the Western diet. Attempts to enhance phosphate removal through alterations in dialysate composition and dialysis membranes have been largely unsuccessful. 14,15 The inability of hemodialysis to adequately remove phosphorus is mainly due to the inaccessibility of phosphate during the treatment. Phosphate exists mainly in the intracellular compartment. During a hemodialysis session with either a high flux or low flux dialyzer, serum phosphorus decreases rapidly, reaching a hypophosphatemic nadir at about 120 minutes. 13 Phosphate efflux then falls off, but remains at roughly half the initial value at the end of the treatment despite a stable serum phosphorus levels

Desmopressin acetate (DDAVP)-associated hyponatremia and brain damage: a case series.

BackgroundDesmopressin (DDAVP) is typically prescribed for central diabetes insipidus, von Willebrands disease and for enuresis. DDAVP-associated hyponatremia is a known complication of DDAVP therapy. The currently recommended treatment for this condition calls for discontinuing DDAVP as part of the initial therapy. This recommendation could lead to a water diuresis and potentially over-correction of the serum sodium.MethodsThe 15 patients in this case series developed symptomatic DDAVP-associated hyponatremia and were admitted to acute care hospitals. Thirty-eight percent presented with symptomatic hyponatremia and 62% developed symptomatic hyponatremia due to concomitant DDAVP and hypotonic intravenous fluid administration during a hospital stay. Group 1 patients (n = 13) were treated by withholding DDAVP and providing intravenous saline. Group 2 patients (n = 2) were treated by continuing DDAVP and providing DDAVP and intravenous hypertonic saline.ResultsAmong Group 1 patients, in whom DDAVP was withheld as initial management of DDAVP-associated hyponatremia (n = 13), the mean change in serum sodium in the first 2 days of treatment was 37.1 ± 8.1 mEq/L. The ultimate outcome in this group was death in 23%, severe brain damage in 69% and moderate brain damage in 8%. In Group 2 patients, in whom DDAVP was continued (n = 2) as part of the initial management strategy, the mean change in serum sodium was 11.0 ± 0 mEq/L in the first 2 days. The ultimate outcome was survival without neurological sequelae in both cases.ConclusionsDiscontinuing DDAVP in a patient with symptomatic DDAVP-associated hyponatremia can lead to rapid correction of the serum sodium and resultant severe neurological injury. In contrast, continuing the medication while correcting DDAVP-associated hyponatremia may lead to better outcomes by avoiding over-correction of the serum sodium. Thus, an alternative approach that we propose is to continue DDAVP as part of the initial management of this disorder

Desmopressin acetate (DDAVP)-associated hyponatremia and brain damage: a case series.

BackgroundDesmopressin (DDAVP) is typically prescribed for central diabetes insipidus, von Willebrands disease and for enuresis. DDAVP-associated hyponatremia is a known complication of DDAVP therapy. The currently recommended treatment for this condition calls for discontinuing DDAVP as part of the initial therapy. This recommendation could lead to a water diuresis and potentially over-correction of the serum sodium.MethodsThe 15 patients in this case series developed symptomatic DDAVP-associated hyponatremia and were admitted to acute care hospitals. Thirty-eight percent presented with symptomatic hyponatremia and 62% developed symptomatic hyponatremia due to concomitant DDAVP and hypotonic intravenous fluid administration during a hospital stay. Group 1 patients (n = 13) were treated by withholding DDAVP and providing intravenous saline. Group 2 patients (n = 2) were treated by continuing DDAVP and providing DDAVP and intravenous hypertonic saline.ResultsAmong Group 1 patients, in whom DDAVP was withheld as initial management of DDAVP-associated hyponatremia (n = 13), the mean change in serum sodium in the first 2 days of treatment was 37.1 ± 8.1 mEq/L. The ultimate outcome in this group was death in 23%, severe brain damage in 69% and moderate brain damage in 8%. In Group 2 patients, in whom DDAVP was continued (n = 2) as part of the initial management strategy, the mean change in serum sodium was 11.0 ± 0 mEq/L in the first 2 days. The ultimate outcome was survival without neurological sequelae in both cases.ConclusionsDiscontinuing DDAVP in a patient with symptomatic DDAVP-associated hyponatremia can lead to rapid correction of the serum sodium and resultant severe neurological injury. In contrast, continuing the medication while correcting DDAVP-associated hyponatremia may lead to better outcomes by avoiding over-correction of the serum sodium. Thus, an alternative approach that we propose is to continue DDAVP as part of the initial management of this disorder

Effects of erythropoietin on left ventricular hypertrophy in adults with severe chronic renal failure and hemoglobin <10 g/dL

Effects of erythropoietin on left ventricular hypertrophy in adults with severe chronic renal failure and hemoglobin <10 g/dL.BackgroundLeft ventricular hypertrophy (LVH) frequently complicates chronic renal insufficiency. Anemia is also common in these patients and may contribute to LVH.MethodsWe conducted an open-label interventional trial to evaluate the effect of recombinant erythropoietin (rhEPO) on left ventricular mass index (LVMI) in anemic patients with renal insufficiency. Adults with creatinine clearance 10 to 30mL /min (nondiabetics) or 20 to 40mL /min (diabetics) were recruited, and rhEPO was given to those with anemia (hemoglobin level <10 g/dL). Baseline and 6-month LVMI and LVH (LVMI >130 g/m2 in men and >100 g/m2 in women), hemoglobin levels, creatinine clearance, blood pressure, medications, and medical history were obtained. Forty anemic and 61 nonanemic control subjects were enrolled.ResultsOverall, the prevalence of LVH was 68.3% (95% CI 58.3-77.2), and entry hemoglobin level was the only significant predictor of baseline LVH (adjusted OR 0.69 per g/dL increase in hemoglobin, 95% CI 0.50-0.94). After 6 months, LVMI decreased in anemic patients receiving rhEPO (142 ± 56 vs. 157 ± 56 g/m2) (P = 0.007), with an increase in hemoglobin (11.3 ± 1.9 vs. 9.1 ± 0.7 g/dL) (P = 0.001). There were no changes in LVMI or hemoglobin level among controls. After adjusting for confounders and change in hemoglobin, receipt of rhEPO was associated with a significant reduction in LVMI (P = 0.01).ConclusionTreatment with rhEPO was not independently associated with significant changes in blood pressure or renal function. LVH is a common finding in chronic renal insufficiency and is associated with lower hemoglobin levels. Treatment with rhEPO may decrease LVH in patients with severe renal insufficiency and anemia