Frequency of complications with prolonged femoral vein catheterization for hemodialysis access.

Analysis of 120 cases of femoral vein catheterization for > or = 2 days for hemodialysis in 89 hospitalized patients was performed to determine the frequency of catheter-related complications including infection and venous thrombosis. The rate of clinically significant complications was < 3.5% and compared favorably with published complication rates of central vein catheters. We conclude that prolonged femoral vein catheterization for hemodialysis is associated with an acceptably low rate of complications when appropriate techniques for placement and catheter care are followed and should be considered a reasonable option for vascular access in hospitalized patients.

Calcium acetate control of serum phosphorus in hemodialysis patients.

Calcium acetate has many characteristics of an ideal phosphorus binder. It is a readily soluble salt that avidly binds phosphorus in vitro at pH 5 and above. One-dose/one-meal balance studies show it to be more potent than calcium carbonate or calcium citrate. We studied chronic (3-month) phosphorus binding with calcium acetate in 91 hyperphosphatemic dialysis patients at four different centers. All phosphorus binders were stopped for 2 weeks. Calcium acetate at an initial dose of 8.11 mmol (325 mg Ca2+) per meal was then used as the only phosphorus binder. Dose was adjusted to attempt control of predialysis phosphorus level less than 1.78 mmol/L (5.5 mg/100 mL). Final calcium acetate dose was 14.6 mmol (586 mg) Ca2+ per meal. Sixteen patients developed mild transient hypercalcemia (mean, 2.84 mmol/L [11.4 mg/dL]. Initial phosphorus values in mmol/L (mg/dL) were 2.39 (7.4); at 1 month, 1.91 (5.9); and at 3 months, 1.68 (5.2). Initial calcium values in mmol/L (mg/dL) were 2.22 (8.9); at 1 month, 2.37 (9.5); and at 3 months, 2.42 (9.7). Initial aluminum values in mumol/L (micrograms/L) were 2.99 (80.7); and at 3 months were 2.54 (68.4). Initial C-terminal parathyroid hormone (C-PTH) values in ng/mL were 14.6; at 1 month, 11.9; and at 3 months, 13.2. Sixty-nine patients then entered a double-blind study. Phosphorus binders were stopped for 1 week. Calcium acetate (at a dose established in a prior study) or placebo was then administered for 2 weeks. Next, patients were crossed to the opposite regimen for 2 weeks. Initial phosphorus was 2.36 mmol/L (7.3 mg/100 mL) and calcium 2.22 mmol/L (8.9 mg/100 mL).(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetic nephropathy: new directions in management.

Approximately 6 million people in the United States are known to be diabetic, with an estimated 4 million individuals having undiagnosed diabetes mellitus. The metabolic derangements of both insulin-dependent diabetes mellitus (IDDM) and noninsulin-dependent diabetes mellitus (NIDDM) result in widespread end-organ damage, including progressive kidney failure. Since its initial description in 1936, the incidence of diabetic nephropathy has progressively increased, and it is now the most common cause of newly diagnosed end-stage renal disease (ESRD) requiring renal replacement therapy in the United States. While basic research efforts into pathogenesis continue, there is significant interest in clinical interventions that may slow the progression of diabetic renal disease. In addition, the options available for renal replacement therapy have increased and improved substantially in recent years.

Renal disease in noninsulin-dependent diabetes mellitus.

Diabetic nephropathy now accounts for approximately one-third of all patients who develop end-stage renal disease. The estimated cost to supply renal replacement therapy for this population now exceeds $750 million. The relatively recent realization that half of these individuals suffer from noninsulin-dependent diabetes mellitus has sparked increased interest in attempts to understand the pathologic processes involved and how they may be similar or different from those alterations seen in insulin-dependent diabetes mellitus. Basic and clinical investigation continues in an attempt to solve the puzzle of pathogenesis, as well as answer questions about the clinical usefulness of microalbuminuria and the appropriate management of hypertension in this population.

Acute renal failure. What to do until the nephrologist comes.

Careful medical management of acute renal failure is critically important to prevent serious complications. In some instances, it may obviate or delay the need for dialysis. History taking, physical examination, and laboratory assessment usually establish the cause from among the many possibilities--from prerenal (eg, hypotension) to postrenal (obstruction of the urinary tract). Derangement of urinary output, hyperkalemia, hyperphosphatemia, hypermagnesemia, metabolic acidosis, anemia, and bleeding are common and treatable disorders found in these patients. The patient's primary care physician can and should be involved with the delivery of appropriate care.