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Biomedical subjects

W G Kirkpatrick

Publications and source records attributed to W G Kirkpatrick.

7 recordsLinked to original sources
PubMed1996

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.

Adolescent↗
PubMed1991

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)

Acetates↗
PubMed1991

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.

Aldehyde Reductase↗
PubMed1990

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.

Acute Kidney Injury↗
PubMed1990

Can the rate of progression of chronic renal failure be altered?

The cost of renal replacement therapy for end-stage renal disease in the United States exceeds three billion dollars per year. Nonimmunologic mechanisms may contribute to progressive renal injury in renal failure of diverse etiologies. Based on the potential adverse renal effects of these processes, a number of dietary and pharmacologic interventions have been proposed as being potentially beneficial in slowing the rate of progression of chronic renal failure to end-stage renal disease. This article reviews current evidence in animal models and humans supporting the efficacy of each of the proposed interventions.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1984

Albumin homeostasis in the nephrotic rat: nutritional considerations.

Albumin catabolism and the relationship between plasma albumin concentration and albuminuria were studied in male Sprague-Dawley rats with Heymann nephritis. The rats were placed on isocaloric diets of 8.5, 21, or 40% protein. Serum albumin concentration correlated negatively with urinary albumin excretion for each of these dietary groups, but the correlation was dependent on dietary protein intake. The magnitude of albuminuria reflected the increase in albumin synthesis rate plus the decrease in albumin catabolic rate. Maximal urinary albumin loss was dependent on dietary protein intake. Albumin catabolism was studied in the different groups of nephrotic animals. Albumin catabolism correlated inversely with the rate of albuminuria in the 21 and 40% protein-fed rats and contributed nearly half of the albumin that was lost in these groups of animals. Albumin catabolism was independent of albuminuria in the rats fed 8.5% protein. The rats were fed 18% of their normal caloric intake, and albumin catabolism was studied in nephrotic and control animals. Albumin catabolism increased with increased albuminuria, in contrast to the well-nourished group, and there was no relationship between serum albumin concentration and urinary albumin excretion. Increased catabolism of albumin plays little or no role in albumin homeostasis in the well-nourished nephrotic rat but may be significant in protein- and calorie-malnourished animals.

Albumins↗