A Systematic Approach To Promoting Home Hemodialysis during End Stage Kidney Disease.

Home dialysis has garnered much attention since the advent of the Advancing American Kidney Health initiative. For many patients and nephrologists, home dialysis and peritoneal dialysis are synonymous. However, home hemodialysis (HHD) should not be forgotten. Since 2004, HHD has grown more rapidly than other dialytic modalities. The cardinal feature of HHD is customizability of treatment intensity, which can be titrated to address the vexing problems of volume and pressure loading during interdialytic gaps and ultrafiltration intensity during each hemodialysis session. Growing HHD utilization requires commitment to introducing patients to the modality throughout the course of ESKD. In this article, we describe a set of strategies for introducing HHD concepts and equipment. First, patients initiating dialysis may attend a transitional care unit, which offers an educational program about all dialytic modalities during 3-5 weeks of in-facility hemodialysis, possibly using HHD equipment. Second, prevalent patients on hemodialysis may participate in "trial-run" programs, which allow patients to experience increased treatment frequency and HHD equipment for several weeks, but without the overt commitment of initiating HHD training. In both models, perceived barriers to HHD-including fear of equipment, anxiety about self-cannulation, catheter dependence, and the absence of a care partner-can be addressed in a supportive setting. Third, patients on peritoneal dialysis who are nearing a transition to hemodialysis may be encouraged to consider a home-to-home transition (i.e., from peritoneal dialysis to HHD). Taken together, these strategies represent a systematic approach to growing HHD utilization in multiple phenotypes of patients on dialysis. With the feature of facilitating intensive hemodialysis, HHD can be a key not only to satiating demand for home dialysis, but also to improving the health of patients on dialysis.

Brain natriuretic peptide and impedance cardiography to assess volume status in peritoneal dialysis patients.

Assessment of volume status in patients with end-stage renal disease has long been a problem. Objective tools for estimating dry weight are necessary. The present study was designed to determine if better assessment of volume status could be achieved by measuring brain natriuretic peptide (BNP) and thoracic fluid content (TFC) by bioimpedance. We prospectively surveyed 51 medically stable peritoneal dialysis (PD) patients during their routine visits to our PD facility. There were no exclusion criteria. Clinical volume status was assessed by the attending nephrologist as hypovolemic, euvolemic, or hypervolemic. Once the clinical assessment was complete, plasma BNP concentration was measured. The TFC was determined by bioimpedance cardiography measured in the supine position. Of 51 patients, 19 (37.3%) were considered hypervolemic, 30 (58.8%) euvolemic, and 3 (5.9%) hypovolemic by clinical assessment. As defined by systolic blood pressure > or = 130 mmHg or diastolic pressure > or = 80 mmHg (or both), 57% were hypertensive. The hypovolemic group was excluded from the statistical analysis because of the small sample size. Logistic regression analysis did not show a significant correlation between clinical assessment of volume and BNP (p = 0.76) or TFC (p = 0.39). Our data demonstrate the limitations of BNP and thoracic impedance in helping with the clinical evaluation of volume status in a cohort of chronic PD patients.

Recurrent high anion gap metabolic acidosis secondary to 5-oxoproline (pyroglutamic acid).

High anion gap metabolic acidosis in adults is a severe metabolic disorder for which the primary organic acid usually is apparent by clinical history and standard laboratory testing. We report a case of recurrent high anion gap metabolic acidosis in a 48-year-old man who initially presented with anorexia and malaise. Physical examination was unrevealing. Arterial pH was 6.98, P co 2 was 5 mm Hg, and chemistry tests showed a bicarbonate level of 3 mEq/L (3 mmol/L), anion gap of 32 mEq/L (32 mmol/L), and a negative toxicology screen result, except for an acetaminophen (paracetamol) level of 7.5 mug/mL. Metabolic acidosis resolved with administration of intravenous fluids. Subsequently, he experienced 5 more episodes of high anion gap metabolic acidosis during an 8-month span. Methanol, ethylene glycol, acetone, ethanol, d -lactate, and hippuric acid screens were negative. Lactate levels were modestly elevated, and acetaminophen levels were elevated for 5 of 6 admissions. These episodes defied explanation until 3 urinary organic acid screens, obtained on separate admissions, showed striking elevations of 5-oxoproline levels. Inborn errors of metabolism in the gamma-glutamyl cycle causing recurrent 5-oxoprolinuria and high anion gap metabolic acidosis are rare, but well described in children. Recently, there have been several reports of apparent acquired 5-oxoprolinuria and high anion gap metabolic acidosis in adults in association with acetaminophen use. Acetaminophen may, in susceptible individuals, disrupt regulation of the gamma-glutamyl cycle and result in excessive 5-oxoproline production. Suspicion for 5-oxoproline-associated high anion gap metabolic acidosis should be entertained when the cause of high anion gap metabolic acidosis remains poorly defined, the anion gap cannot be explained reasonably by measured organic acids, and there is concomitant acetaminophen use.