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Biomedical subjects

J B Copley

Publications and source records attributed to J B Copley.

At least 19 recordsLinked to original sources
PubMed1999

The risks of exercise.

Patients with end-stage renal disease (ESRD) can benefit from exercise. At a minimum, progressive deconditioning will be prevented and cardiovascular and musculoskeletal status quo maintained, but it is also possible that physical functioning will be improved and mortality reduced. The risks of exercise must be assessed along with potential benefits. The most serious inherent risk of exercise in this population is a cardiac event, but the most common injuries sustained are to the musculoskeletal system. The exercise prescription must include measures to minimize both cardiovascular and musculoskeletal risk. These include provision of a prolonged warm-up and exercise adaptation period and time allowance for adequate cool-down. If these guidelines are followed and the exercise is begun at a low to moderate intensity, the associated risk to the ESRD patients should be minimal. For most ESRD patients, the risk benefit ratio will fall in favor of exercise, with the majority of patients exposed to greater risk by not exercising. Increased physical activity should be fostered in ways so that it becomes a routine part of the medical therapy and the mindset of the patient who then strives for self-improvement.

Cardiovascular Diseases↗
PubMed1997

Xanthogranulomatous pyelonephritis in a renal allograft recipient.

Xanthogranulomatous pyelonephritis rarely occurs in renal allografts. This is the fifth reported case. Diagnosis was made by renal biopsy, which is usually performed to evaluate an elevated serum creatinine. Associated patient symptomology is nonspecific, and graft imaging with ultrasonography and computed tomography was not helpful as it would be with native kidney xanthogranulomatous pyelonephritis. Successful treatment with antibiotics may depend on the serum creatinine at presentation. Prognosis, therefore, is guarded, with a common outcome of irreversible renal dysfunction.

Adult↗
PubMed1997

Effect of calcium channel or beta-blockade on the progression of diabetic nephropathy in African Americans.

beta-Blockers are known to slow the progression of diabetic nephropathy by lowering arterial pressure. Moreover, in individuals with diabetic nephropathy, antihypertensive agents that provide sustained reductions in proteinuria slow the rate of decline in renal function compared with agents without this antiproteinuric effect. To examine whether differential effects on proteinuria affect the progression of diabetic nephropathy, we conducted a randomized study that compared the effects of a heart rate-lowering calcium channel blocker, sustained-release verapamil, with those of a beta-blocker, atenolol, on the progression of diabetic renal disease. The primary end point of the study was a change in creatinine clearance slope. Thirty-four African Americans with the following inclusion criteria were randomized to one of the two groups: serum creatinine greater than 1.4 mg/dL, proteinuria greater than 1500 mg/d, longer than a 5-year history of both non-insulin-dependent diabetes mellitus and hypertension, and exclusion of other renal diseases. Goal blood pressure was less than 140/90 mm Hg. All subjects received loop diuretics as second line agents to help achieve the blood pressure goal. Twenty-four-hour urinary protein and sodium excretions as well as creatinine clearance were measured at 6-month intervals. Blood pressure was measured every 3 months. After a mean follow-up of 54+/-6 months, the calcium channel blocker group demonstrated both a slower rate of decline in creatinine clearance (-1.7+/-0.9 versus -3.7+/-1.4 mL/min per year per 1.73 m2, P<.01) and a greater reduction in proteinuria compared with the atenolol group. Additionally, a greater proportion of the atenolol group had a 50% or more increase in serum creatinine compared with the verapamil group (32+/-9% versus 16+/-7%, P<.05). These between-group differences could not be explained by differences in blood pressure control. These data support the concept that antihypertensive agents that persistently maintain reductions in both arterial pressure and proteinuria slow the progression of diabetic renal disease in African Americans to a greater extent than those agents without these effects.

Adrenergic beta-Antagonists↗
PubMed1996

Calcium channel blockers versus other antihypertensive therapies on progression of NIDDM associated nephropathy.

Treatment of hypertension with ACE inhibitors in diabetic patients reduces proteinuria and slows progression of nephropathy compared with agents that do not maintain declines in proteinuria. Calcium channel blockers (CCBs) have variable effects on proteinuria; their long-term effects on progression of diabetic nephropathy are not known. The current study examines the hypothesis that CCBs that maintain reductions in proteinuria slow progression of nephropathy associated with non-insulin dependent diabetes mellitus (NIDDM) by a degree comparable to ACE inhibitors, given similar levels of blood pressure control. To test this hypothesis we randomized 52 patients with NIDDM associated nephropathy and hypertension, mean age of 63 +/- 8 years, to either the ACE inhibitor, lisinopril (N = 18), nondihydropyridine CCBs (NDCCBs), verapamil SR (N = 8) or diltiazem SR (N = 10), or the beta blocker, atenolol (N = 16). Goal blood pressure was < or = 140/90 mm Hg. Patients were followed for a mean period of 63 +/- 7 months. The primary end point was change in creatinine clearance (CCr) slope in each group. There was no significant difference in mean arterial pressure reduction among the groups over the study period (P = 0.14). The mean rate of decline in CCr was greatest in the atenolol group (-3.48 ml/min/year/1.73 m2; P < 0.0001). There was no difference in the CCr slopes between lisinopril and NDCCBs groups (P = 0.36). Proteinuria was reduced to a similar extent in the lisinopril and NDCCBs groups (P > 0.99). Therefore, in persons with renal insufficiency secondary to NIDDM, similar levels of blood pressure control with either lisinopril or NDCCBs slowed progression of renal disease to a greater extent than atenolol. Moreover, this enhanced slowing of renal disease progression correlated with sustained and significant reductions in proteinuria, findings not observed in the atenolol group.

Aged↗
PubMed1996

Peritoneoscopic placement of Swan neck peritoneal dialysis catheters.

Peritoneoscopic placement of peritoneal dialysis catheters, although accomplished in only about 10% of dialysis centers, is a nonsurgical technique that fulfills requirements for safety and dependability. Over a 40-month period, 136 catheters were placed with the peritoneoscope, 135 of which were double-cuffed, Swan neck curled catheters, with a uniform radiopaque stripe. Patients were followed longitudinally for outcome. Catheters were placed in 44 diabetic patients, 1 human immunodeficiency virus (HIV)-positive patient, and 18 morbidly obese patients. No complications occurred as a direct result of placement. Catheters were used, on average, nine days after placement (many on days 1 to 4) usually with 1.5 to 2 L exchanges. With 1183 patient-months' experience, complications were few: 28 patients experienced catheter-related infections, and there were five leaks that resolved with supine, low-volume dialysis for several days. Leakage did not correlate with time of usage after placement. Of ten outflow/mechanical problems that required catheter removal, nine involved catheter migration, probably due to lack of attention during placement to orientation of the radiopaque stripe. One was due to a preperitoneal placement early in this institution's experience with the peritoneoscope. Five of the migrated catheters were removed and then successfully replaced with the peritoneoscope at the same sitting. Four patients requested surgical removal and replacement. Sixteen catheters were removed because of catheter-related infections: five refractory Staphylococcus aureus, six Pseudomonas aeruginosa, two fungal, two Serratia species, and one Mycobacterium chelonei. Actuarial life-table analysis showed that at the end of the 40-month follow-up, 62% of the catheters were expected to survive. Because more than 50% survived, median catheter survival could not be calculated. The adverse responses were removal because of infection or catheter migration. Peritoneal dialysis catheter implantation with the peritoneoscope represents a safe and dependable method for catheter placement. Literature review and comparison indicate that catheter-related complications are fewer and catheter longevity is better with peritoneoscopic placement than with surgical placement. Our experience with prompt postplacement utilization suggests the need for further evaluation of catheter break-in procedure with the peritoneoscope.

Bacterial Infections↗
PubMed1993

Longitudinal study of bone mass in end-stage renal disease patients: effects of parathyroidectomy for renal osteodystrophy.

The effectiveness of parathyroidectomy (PTHX) for the control of secondary hyperparathyroidism was assessed in 46 adult end-stage renal disease (ESRD) patients whose bone mineral content at the midshaft and distal radius was measured using single-photon absorptiometry (SPA) every 6 months before and after the surgery. They were compared to 46 age-, race-, and sex-matched ESRD patient controls who had not undergone surgery but who had had at least five SPA studies at similar intervals. Presurgery midradius bone mass was significantly lower for PTHX patients compared to controls. Comparing changes in bone mass of PTHX patients across surgery to controls in comparable time periods showed that PTHX patients lost significantly less bone mass after surgery. Similar results were obtained when rates of change in bone mass were evaluated. When patient characteristics were examined, the effect of surgery was found to be diminished in elderly patients and in oophorectomized patients. It is concluded that PTHX can have a salutary effect on renal osteodystrophy in the appendicular skeleton, but factors other than bone mass also need to be considered in identifying those patients who will benefit from surgery.

Absorptiometry, Photon↗
PubMed1993

Calcium citrate without aluminum antacids does not cause aluminum retention in patients with functioning kidneys.

It has been suggested that calcium citrate might enhance aluminum absorption from food, posing a threat of aluminum toxicity even in patients with normal renal function. We therefore measured serum and urinary aluminum before and following calcium citrate therapy in patients with moderate renal failure and in normal subjects maintained on constant metabolic diets with known aluminum content (967-1034 mumol/day, or 26.1-27.9 mg/day, in patients and either 834 or 1579 mumol/day, or 22.5 and 42.6 mg/day, in normal subjects). Seven patients with moderate renal failure (endogenous creatinine clearance of 43 ml/min) took 50 mmol (2 g) calcium/day as effervescent calcium citrate with meals for 17 days. Eight normal women received 25 mmol (1 g) calcium/day as tricalcium dicitrate tablets with meals for 7 days. In patients with moderate renal failure, serum and urinary aluminum were normal before treatment at 489 +/- 293 SD nmol/l (13.2 +/- 7.9 micrograms/l) and 767 +/- 497 nmol/day (20.7 +/- 13.4 micrograms/day), respectively. They remained within normal limits and did not change significantly during calcium citrate treatment (400 +/- 148 nmol/l and 600 +/- 441 nmol/day, respectively). Similarly, no significant change in serum and urinary aluminum was detected in normal women during calcium citrate administration (271 +/- 59 vs 293 +/- 85 nmol/l and 515 +/- 138 vs 615 +/- 170 nmol/day, respectively). In addition, skeletal bone aluminum content did not change significantly in 14 osteoporotic patients (endogenous creatinine clearance of 68.5 ml/min) treated for 24 months with calcium citrate, 10 mmol calcium twice/day separately from meals (29.3 +/- 13.9 ng/mg ash bone to 27.9 +/0- 10.4, P = 0.727). In them, histomorphometric examination did not show any evidence of mineralization defect. Thus, calcium citrate given alone without aluminum-containing drugs does not pose a risk of aluminum toxicity in subjects with normal or functioning kidneys, when it is administered on an empty stomach at a recommended dose of 20 mmol calcium/day.

Absorption↗
PubMed1993

Effect of citrate on serum aluminum concentrations in hemodialysis patients: a prospective study.

Twenty hemodialysis patients were prospectively evaluated to determine if concomitant citrate and aluminum administration enhances the absorption of aluminum, thereby increasing the possibility of toxicity. The four-phase study consisted of phase I, a washout phase; phase II, an aluminum treatment phase; phase III, a treatment phase combining aluminum and soluble calcium citrate; and phase IV, a treatment phase with the patient's original prestudy phosphate binder. Results disclosed a progressive rise in serum aluminum levels (microgram/L) from 47 +/- 8 (phase I) to 62 +/- 12 (phase II) to 74 +/- 13 (phase III) and a drop to 58 +/- 12 (phase IV). The difference in levels between phases I and III was significant. Additionally, and despite the fact that serum calcium concentrations did not change, serum phosphate and immunoreactive parathyroid hormone concentrations were significantly lower when aluminum and citrate were used together. This suggests that citrate enhances the absorption of aluminum and therefore increases the possibility of toxicity in the patient with end-stage renal disease.

Adult↗
PubMed1992

Free and total 1,25-dihydroxyvitamin D levels in subjects with renal disease.

Patients with nephrotic syndrome and varying degrees of renal failure, including those on chronic hemo- and peritoneal dialysis, may have low serum concentrations of total 1,25-dihydroxyvitamin D [1,25(OH)2D]. However, it is unknown whether the true activity of 1,25(OH)2D is better reflected by the free 1,25(OH)2D fraction. We measured total 1,25(OH)2D, free 1,25(OH)2D, and vitamin-D-binding protein (DBP) in normal subjects (group A), subjects with moderate renal failure (group B), subjects on hemodialysis (group C), subjects on peritoneal dialysis (group D), and subjects with nephrotic syndrome (group E). The serum concentrations of total and free 1,25(OH)2D decreased with worsening renal function in groups A through C, with a high degree of correlation (r = 0.974, P less than 0.0001). Levels of DBP and the percent free 1,25(OH)2D remained constant in these groups. Patients on peritoneal dialysis and nephrotic patients had lower levels of DBP (203 +/- 14 micrograms/ml and 371 +/- 46 micrograms/ml, respectively) than normal subjects (436 +/- 33 micrograms/ml) and had significantly higher percent free 1,25(OH)2D (0.98 +/- 0.13% and 1.27 +/- 0.14%, respectively) compared to 0.63 +/- 0.03% (P less than 0.05). Thus, the loss of DBP in these patients correlated with a rise in the percent free 1,25(OH)2D. We conclude that levels of total 1,25(OH)2D are an accurate representation of 1,25(OH)2D status in normal subjects, subjects with renal insufficiency without nephrotic syndrome, and hemodialysis patients. In peritoneal dialysis and nephrotic patients, who lose DBP, measurements of free 1,25(OH)2D may be necessary in order to accurately assess 1,25(OH)2D status.

Aged↗
PubMed1990

Effect of hypertension and type II diabetes on renal function in an urban population.

End-stage renal disease is a devastating complication of essential hypertension and type II diabetes mellitus, conditions that commonly occur together. We and others have previously suggested that the outcome of both conditions may be influenced by more aggressive treatment. We examined a large general medicine outpatient population; 72% were black and 41% were diabetic (95% type II). Decreased renal function, defined as a serum creatinine greater than or equal to mg/dL, developed in 18.1%. A multivariable logistic regression analysis identified glucose control, systolic blood pressure level, and male gender as indicators of decreased renal function. These data suggested that both glucose and blood pressure control may decrease the frequency of impaired renal function. However, when these variables were controlled, blacks still had almost twice the risk for renal dysfunction of whites. The data draw attention to, and elucidate the exceptionally high incidence of renal dysfunction in hypertensive blacks with or without diabetes. Further, they may explain the inordinate numbers of blacks with hypertension requiring dialysis. Prospective trials to test the efficacy of blood pressure and glucose control on the course of renal disease in hypertensive and/or type II diabetic patients are warranted.

Adult↗
PubMed1990

Lysine vasopressin in the treatment of refractory hemodialysis-induced hypotension.

The etiology of hemodialysis-induced hypotension is multifactorial. We assessed the efficacy of intranasal lysine vasopressin (LV) in 6 patients with refractory hemodialysis-induced hypotension. Autonomic testing was abnormal in all. Intranasal LV and placebo were assessed in a double-blind crossover fashion. With LV, the mean number of hypotensive episodes was less (0.9 +/- 0.8 vs. 1.5 +/- 1; t = 3.95, p less than 0.05), as was the total volume of intravenous fluid administered because of hypotension (155 +/- 57 vs. 280 +/- 123 cm3; t = 2.98, p less than 0.05). Systolic, diastolic, and mean arterial blood pressures were significantly greater at 90 min of the dialysis session. Measured baseline epinephrine, norepinephrine, and antidiuretic hormone levels were elevated above normal levels and fell with hypotension despite the use of LV. The results from this study demonstrate the utility of LV in the treatment of refractory hemodialysis-induced hypotension.

Administration, Intranasal↗
PubMed1990

Soft tissue calcification in renal failure.

Disorders of phosphorus, calcium, and vitamin D are common in patients with renal failure. Medical management, including dietary phosphorus restriction, administration of phosphate binding agents, and calcium and vitamin D sterol supplementation, must be instituted to control serum concentrations of these substances because of the loss of normal homeostatic mechanisms. If these measures are not employed, soft tissue calcification and hyperparathyroidism may result. We report the case of a 22-year-old woman with endstage renal disease treated with continuous ambulatory peritoneal dialysis who developed secondary hyperparathyroidism and tumorous calcinosis as a result of noncompliance with dietary phosphorus restriction and phosphate-binding agent therapy. The etiology and treatment of soft tissue calcification in patients with renal disease are discussed. Compliance with dietary restrictions and phosphate binding agents is frequently problematic in this population. Pharmacists should play an active role in educating patients with renal disease on the consequences of noncompliance with dietary and drug therapy.

Adult↗