Contrast-induced translocational hyponatremia and hyperkalemia in advanced kidney disease.

BACKGROUND: In patients with advanced kidney disease, administration of effective osmolar agents may lead to hyponatremia, hyperkalemia, metabolic acidosis, and intravascular expansion. To our knowledge, osmolar effects of contrast agents in patients with advanced kidney disease have not been previously elucidated. METHODS: This retrospective case series includes 5 patients with advanced kidney disease who underwent diagnostic and/or therapeutic cardiac catheterization and developed hyponatremia. Blood chemistry tests were performed before and after the procedure. Hyponatremia is defined as a plasma sodium concentration less than 135 mEq/L (mmol/L). RESULTS: Mean precontrast and postcontrast sodium levels were 138.6 mEq/L (mmol/L) and 122.6 mEq/L (mmol/L), respectively. Plasma potassium levels increased after contrast exposure. There was no difference in degree of hyperkalemia between patients with and without diabetes. Plasma bicarbonate levels were noted to decrease after contrast exposure in 4 of 5 patients, with the exception of a patient undergoing continuous ambulatory peritoneal dialysis. There was a strong correlation between dose of contrast administered and change in sodium level, with a correlation coefficient of 0.91. CONCLUSION: These data suggest that large volumes of contrast may result in hypertonic hyponatremia through a dual effect of exogenous fluid dilution and translocation. The fluid translocated from intracellular to extracellular spaces may lead to a decrease in sodium, chloride, and bicarbonate levels. All patients developed hyperkalemia, which may be caused by solvent drag and/or passive diffusion, in addition to impaired excretory capacity. Patients with advanced kidney disease exposed to large volumes of contrast should be monitored for osmolar-induced chemical changes so that timely postcontrast dialytic therapy can be instituted.

Decreased erythropoietin requirements in maintenance hemodialysis patients with statin therapy.

Inflammatory cytokines induce erythropoietin (EPO) resistance, anorexia, and suppression of hepatic albumin synthesis. Increased levels of C-reactive protein (CRP) have been associated with relative EPO resistance in dialysis patients. More recently, studies have shown that statin therapy decreases CRP. This study analyzed the effect of statin therapy on EPO requirements in dialysis patients. This retrospective, single center study stratified stable hemodialysis patients into two groups: Group 1, statin therapy (n = 19), and Group 2, nonstatin therapy (n = 19). Group 1 was subclassified into Group 1a (prestatin therapy) and Group 1b (poststatin therapy). Baseline demographics, biochemical parameters [serum lipid panel, hemoglobin (Hgb), transferrin saturation (TSAT), ferritin, parathyroid hormone (PTH), aluminum, albumin, KT/V, urea reduction ratio (URR), and protein catabolic rate (nPCR)] and EPO requirements (u/kg per treatment) were obtained. Poststatin labs were obtained at a mean of 4.7 months. Statistically significant changes were noted in Group 1 after initiation of statin therapy for cholesterol (174.68 +/- 53.8 to 142 +/- 32.7, p < 0.05), Hgb (10.61 +/- 1.2 to 12.48 +/- 0.79, p < 0.0005), ferritin (618 +/- 334.1 to 334 +/- 265, p < 0.05), and albumin (3.58 +/- 0.4 to 3.77 +/- 0.4, p < 0.005). EPO requirements decreased by 25%. Mean values for lipid panel showed reductions in cholesterol (18%), triglyceride (37.8%), and low density lipoprotein (LDL) (26%), as well as elevation in high density lipoprotein (HDL) (11%). These data suggest that statin therapy may decrease EPO requirements in dialysis patients. The improvement in EPO responsiveness may be caused by the effect of statins on CRP.

Slow-flow venous pressure for detection of arteriovenous graft malfunction.

BACKGROUND: Early detection with elective intervention of malfunctioning arteriovenous (AV) grafts improves access viability. Herein, we evaluated outlet venous pressure (OP), normalized by mean arterial blood pressure (MABP), at varying blood flow (Qb) rates in the detection of venous outlet stenosis. METHODS: This single-center, observational study included stable dialysis patients with polytetrafluoroethylene (PTFE) AV grafts. Phase I involved the determination of the optimal Qb (0, 50, 250, or 400 mL/min) and threshold OP/MABP. Sixty-one patients were followed up for 6 months. The primary end point was graft thrombosis. Phase II assessed serial slow-flow pressure (SFpr = OP/MABP at Qb of 50 mL/min) in a larger sample size (N = 152). The primary end point was graft thrombosis. Phase III implemented the use of SFpr monitoring in the detection and correction of outlet lesion(s). RESULTS: In phase I, 21 patients developed graft thrombosis. The most significant difference in pressure between the functioning and thrombosed grafts was at Qb of 0 mL/min and SFpr. The threshold of OP/MABP at Qb 0 (>0.53) and SFpr (>0.6) were predictive of graft thrombosis. In phase II, 37 of 42 patients with graft thrombosis had SFpr>0.6 (sensitivity 88.1%; specificity 97.2%; positive and negative predictive values were 90.2% and 95.5%, respectively). In phase III, 13 patients with SFpr>0.6 had outlet lesions on angiography. CONCLUSION: Serial SFpr used in conjunction with angiography and angioplasty provides a strategy for reducing the incidence of thrombosis. This technique has comparable sensitivity and specificity to other existing methods. This technique is both time-efficient and cost-effective.