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Biomedical subjects

J B Puschett

Publications and source records attributed to J B Puschett.

At least 55 records · Page 3Linked to original sources
PubMed1986

Evaluation of cardiovascular risk for renal transplantation in diabetic patients.

Cardiovascular disease contributes in a major way to morbidity and mortality in diabetic patients with end-stage renal disease. Sixty patients with type I diabetes were evaluated prior to renal transplantation to determine the risk of cardiovascular complications. On the basis of results of thallium stress testing and/or cardiac catheterization, each patient was assigned to one of five categories. There were no cardiovascular events in the seven patients who had negative results on stress testing. Of the remaining 53 patients, all of whom underwent cardiac catheterization, 30 had normal coronary arteries. None of these 30 patients had any cardiac morbidity, and the two deaths that occurred in this group were not attributable to cardiac causes. Significant coronary artery disease was present in 38 percent of the patients. The overall mortality rate was 5.4 percent in those patients without coronary artery disease and 43.5 percent in those with the disease. In addition, the mortality rate in patients with coronary disease classified as severe was 62 percent, whereas it was 20 percent in those categorized as having moderate disease. The data indicate that patients with diabetes and end-stage renal disease who are at highest risk for cardiovascular events can be identified, and these patients probably should not undergo renal transplantation.

Adult↗
PubMed1986

Spontaneous hypercalcemia in patients undergoing dialysis. Etiologic and therapeutic considerations.

Ten dialysis-treated patients with hypercalcemia (11.5 +/- 0.3 mg/dl, mean +/- SE) due to renal osteodystrophy were compared with 30 control dialysis-treated patients who were not hypercalcemic (9.5 +/- 0.1 mg/dl). The hypercalcemic patients were more disabled than the control patients. Fifty percent of the hypercalcemic patients and 37 percent of the control patients had a mineralization defect (p greater than 0.6). In the control group, intact parathyroid hormone level was significantly higher in patients with osteitis fibrosa than in those with osteomalacia (247 +/- 39 pg/ml versus 60 +/- 20 pg/ml, respectively, p less than 0.005) whereas in the hypercalcemic patients, parathyroid hormone measurements did not discriminate between these two types of bone disease. Osteomalacia was more severe and bone aluminum staining was stronger in the hypercalcemic patients than in the control patients (2.02 +/- 0.47 versus 0.35 +/- 0.11 mm/mm2 tissue area, p less than 0.001). The mean serum calcium level fell from 11.2 +/- 0.2 mg/dl to 10.5 +/- 0.3 mg/dl (p less than 0.01) in eight hypercalcemic patients treated with 24,25-dihydroxyvitamin D. It is concluded that hypercalcemia in patients undergoing dialysis is associated with an increase in bone aluminum level, and with more severe osteomalacia. Intact parathyroid hormone levels are useful for predicting bone histomorphometric parameters but only when hypercalcemia is not present. The drug, 24,25-dihydroxyvitamin D, was effective in lowering the serum calcium level.

Adolescent↗
PubMed1986

Serum electrolyte patterns in end-stage renal disease.

The charts of 70 successive patients presenting for dialysis therapy for end-stage renal disease (ESRD) were evaluated for their serum electrolyte values. The "classical" pattern of low total CO2 (tCO2), elevated anion gap ("delta"), and normal chloride was found in a minority of patients (14 of 70, or 20%). Hyperchloremia was noted in 46%; in 21 patients (30%), this was associated with a normal delta and in 11 (16%), hyperchloremia was accompanied by an elevated delta. Fourteen patients (20%), most with diabetic nephropathy, had normal serum electrolytes. Patients with chronic glomerulonephritis had a hyperchloremic pattern as often as not, and two of four patients with interstitial nephritis demonstrated hyperchloremia without an elevated delta. We conclude that the previously held thesis that hyperchloremia is a rare or absent finding by the time renal failure progresses to ESRD is no longer tenable. Furthermore, a significant minority of ESRD patients may require the initiation of dialysis at a time when their serum electrolytes are still normal.

Acid-Base Equilibrium↗
PubMed1986

Renal osteodystrophy in patients on hemodialysis for more than 10 years.

We performed bone biopsies on 13 patients who had been on dialysis from 11.1 to 17.6 years (mean 14.5 +/- 2.1 years) to evaluate renal osteodystrophy in long-term dialysis patients. Seven patients had osteitis fibrosa and 6 had a mineralization defect. Stainable bone aluminum was present in 9 of the patients. Serum phosphorus and parathyroid hormone levels were higher and bone aluminum lower in patients with osteitis fibrosa compared to those with a mineralization defect. Those seriously disabled with decreased mobility due to bone pain (7 of 13) had more bone aluminum than those patients with minimal or no disability (1.55 +/- 1.0 mm/mm2 vs. 0.11 +/- 0.18, respectively, p less than 0.01). A history of fractures during the years on dialysis was also associated with elevated stainable bone aluminum (p = 0.04). We conclude that in long-term dialysis patients aluminum-related osteodystrophy results in greater morbidity than osteitis fibrosa. We recommend that aluminum-containing phosphate binders be used sparingly in patients who are to remain indefinitely on dialysis.

Adult↗
PubMed1985

Diuretic effects on renal brush border membrane transport and metabolism.

Previous studies have indicated that the thiazide diuretics exert effects on proximal electrolyte transport. To determine whether the locus of these effects is at the brush border membrane (BBM) and if renal metabolism is affected, adult female Sprague-Dawley rats were acutely treated with either 1 mg/kg metolazone, 20 mg/kg chlorothiazide followed by a 20 mg/kg/hr maintenance infusion, 10 mg/kg acetazolamide followed by a 10 mg/kg/hr maintenance infusion, or the vehicles only. Administration of these agents resulted in an approximately tenfold increase in sodium excretion. Neither urinary phosphate nor inulin excretion changed significantly in any group. Sodium dependent BBM vesicle phosphate transport was examined at 0.15, 0.5, and 1 and 120 minute incubation periods in the diuretic treated groups and their respective control groups. Decreased uptake was seen in all pre-equilibrium time points in rats treated with metolazone: 0.15 minutes: 221 +/- 24 pmoles/mg protein (pmol/mg prot) in control rats versus (vs) 185 +/- 23 pmoles/mg prot in metolazone-treated animals (P less than .05) ; 0.5 minutes: 463 +/- 54 vs 369 +/- 49 pmol/mg prot (P less than .005); 1 minute: 549 +/- 74 vs 460 +/- 61 pmol/mg prot (P less than .05); no significant difference in phosphate transport was noted at the two hour equilibrium time point. No significant differences in sodium dependent phosphate transport existed between chlorothiazide or acetazolamide treated rats and control animals. Substrate-stimulated renal gluconeogenesis did not differ between metolazone treated and control animals. We therefore conclude that metolazone inhibits phosphate transport through an effect on the BBM and does not affect renal gluconeogenesis in the rat.

Acetazolamide↗
PubMed1985

Effects of end-stage renal disease and aluminum hydroxide on temazepam kinetics.

The kinetics of temazepam, 30 mg, were evaluated in 11 patients with end-stage renal disease. Age ranged from 18 to 65 years. On two occasions separated by 1 week, single oral 30 mg doses of temazepam were given once with water (TM) and once with 3600 mg aluminum hydroxide gel (TM + AHG). There were no significant differences in the maximum plasma concentration, the time to reach maximum concentration, or elimination rates between TM and TM + AHG dosing. In approximately half the subjects there were secondary temazepam peak concentrations. In the remaining subjects, temazepam elimination was biphasic, with the terminal t1/2 ranging from 11 to 77 hours. There was a lag time before absorption in all subjects. The percent free temazepam in plasma from dialysis subjects ranged from 4.4% to 8.8% (mean = 5.9%). Compared with literature reports of subjects with normal renal function, the maximum plasma concentration was lower and the percent free temazepam was higher in dialysis subjects. When sedation score was plotted against plasma temazepam concentration, there was clockwise hysteresis consistent with tolerance or adaptation to effects of the drug. Thus aluminum hydroxide gel does not affect temazepam absorption. The clinical significance of the low plasma concentrations and high free temazepam fraction in dialysis subjects is uncertain.

Absorption↗
PubMed1985

Effects of end stage renal disease and aluminium hydroxide on triazolam pharmacokinetics.

Triazolam 0.5 mg was administered to 11 dialysis patients and 11 age, weight and sex matched controls. Peak plasma concentrations (Cmax) were higher in control subjects, but there were no other differences between the groups. When dialysis patients took triazolam with 3600 mg aluminum hydroxide suspension, Cmax and AUC were increased into the range observed in control subjects. It appears that triazolam can be used at normal doses in patients with renal dysfunction, without regard to interaction with aluminum hydroxide gel, or to alterations in elimination.

Adolescent↗
PubMed1985

Renal hemodynamic and tubular transport effects of nitrendipine.

Nitrendipine, a 1,4-dihydropyridine derivative, is a new calcium entry blocker with marked antihypertensive effects. Because relatively few data are available regarding its renal effects, we studied the drug's action on renal hemodynamics and electrolyte excretion in normal male volunteers. During sustained water diuresis, 5 to 10 mg nitrendipine given orally caused an increase in urine flow rate and a modest but consistent increase in sodium excretion (from 1.0% to 2.2% of filtered load, P less than 0.01). Furthermore, both solute-free water clearance and percentage of free water excreted rose (from 10.1 +/- 0.6 ml/min to 12.0 +/- 0.8 ml/min and from 8.7% +/- 0.5% to 10.5% +/- 1.1%, respectively, P less than 0.05 in each case). In addition, during the peak effect of the drug on sodium and free water excretion, there was no consistent change in either glomerular filtration rate or effective renal plasma flow. Nitrendipine was also phosphaturic and calciuric but did not alter acid excretion. When administered to subjects with hydropenia receiving hypertonic saline infusion, the drug had no effect on solute-free water reabsorption. We interpret these results to indicate that nitrendipine has direct tubular effects on renal electrolyte transport and that the locus of these effects is probably the proximal tubule. Thus, nitrendipine appears to differ from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive.

Administration, Oral↗
PubMed1985

Effects of 1,25-dihydroxyvitamin D3 on membrane transport and intermediary metabolism.

To investigate the mechanism of the renal tubular transport effects of 1,25-dihydroxyvitamin D3 (1,25-D3), brush border membrane vesicle inorganic phosphate (Pi) uptake and gluconeogenesis were measured in renal cortex obtained from vitamin D deficient thyroparathyroidectomized rats which had been infused with 6 pmol/h of 1,25-D3 and 0.2 U/h of parathyroid hormone (PTH), a nonphosphaturic ('permissive') dose, for 6 h. When compared to vitamin D deficient animals receiving the vehicles alone, there was a significant increase in Pi transport by those vesicles obtained from the 1,25-D3-treated animals. Substrate-stimulated gluconeogenesis in thyroparathyroidectomized vitamin D deficient animals was decreased in animals which received the 1,25-D3 plus PTH combination. In all groups receiving 1,25-D3 plus PTH, there was a significant decline in urinary Pi excretion. We, therefore, conclude that 1,25-D3 promotes proximal tubular Pi reabsorption through an effect that occurs at the brush border membrane. Furthermore, the administration of 1,25-D3 causes a reduction in renal cortical gluconeogenesis. The administration of a permissive dose of PTH is necessary for these effects to occur.

Animals↗
PubMed1984

Use of procainamide in chronic ambulatory peritoneal dialysis: report of a case.

A patient on chronic ambulatory peritoneal dialysis (CAPD) was treated with procainamide for control of ventricular arrhythmias. A procainamide half-life of 11.5 hours was observed, with a dialysis clearance of 6.5 mL/min. The N-acetylprocainamide (NAPA) dialysis clearance was 5.3 mL/min. The CAPD clearance of procainamide and its active metabolite, NAPA, is much lower than that reported for hemodialysis. Procainamide therapy should be initiated with reduced dosages in patients with renal failure.

Acecainide↗
PubMed1984

Prostaglandin E2 and parathyroid hormone: comparisons of their actions on the rabbit proximal tubule.

Recent studies demonstrated that prostaglandin E2 (PGE2) participates in the regulation of glomerular and distal tubular function. A functional role for PGE2 on the proximal tubule has only recently been explored. Thus, we reported that PGE2 antagonizes the phosphaturic effect of PTH in the dog, which suggests that PGE2 may influence the transport functions of the mammalian proximal tubule. The present studies were designed to examine the direct effect of parathyroid hormone (PTH) and PGE2 on the fluxes of fluid (Jv) and phosphate (Jl-b PO4) in the rabbit proximal convoluted and straight tubules (PCT and PST). The activation of adenylate cyclase by the two agents was also examined. Finally, the combined effects of PTH and PGE2 on Jv and Jl-b PO4 were also studied in the PST. In the PCT, PTH (1 microgram/ml) inhibited Jv by 31% (P less than 0.05) but did not alter Jl-b PO4. PGE2 (10(-5) M) failed to act on either Jv or Jl-b PO4. In this segment, PTH stimulated adenylate cyclase but PGE2 did not. In the PST, PTH (1 microgram/ml) inhibited Jv and Jl-b PO4 by 34 and 20%, respectively (P less than 0.01). PGE2 (10(-5) M) also inhibited Jv and Jl-b PO4, by 33 and 12%, respectively (P less than 0.02). In contrast, PGF2 alpha, a related prostanoid, failed to influence these transport parameters. In the PST, PTH activated adenylate cyclase but PGE2 failed to do so. When both PTH (1 microgram/ml) and PGE2 (10(-7) M) were present simultaneously, Jv and Jl-b PO4 were comparable to that seen during control collections.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1984

Peritoneal eosinophils during intermittent peritoneal dialysis.

Peritoneal eosinophil counts were investigated in 61 intermittent dialysis patients over the course of 1 year. The peritoneal eosinophil percentage fell from 18 +/- 2% (mean +/- SEM) in the first 2 months of dialysis to 3 +/- 0.4% after 6 months of dialysis. Absolute eosinophils per cubic millimeter fell from 586 +/- 126 to 61 +/- 18 (p less than 0.01 for both percentage and absolute values). There was a wide range in the mean eosinophil percentages per patient in the first 6 months of dialysis (0-84%) that narrowed to 0-9% after 6 months. The majority of the high initial eosinophil counts resolved after 2 months. Peripheral eosinophilia was seen in 8 of the 10 patients with the highest mean peritoneal eosinophil percentages during the first 2 months of dialysis. Patients who developed peritonitis had a significantly lower percentage of eosinophils in the first 1.5 months of dialysis than patients who did not develop peritonitis. At the time of diagnosis of peritonitis, the peritoneal eosinophil count was near zero. 4 cases of peritoneal eosinophilia which developed after antibiotic therapy are described.

Adult↗
PubMed1984

Prostaglandin E2 antagonizes the renal effects of parathyroid hormone but not those mediated by a cyclic AMP analog.

An infusion of PGE2 resulted in the development of refractoriness to the phosphaturic effects of PTH in the chronically TPTX dog. The antagonism of PGE2 to the actions of PTH was not observed when the phosphaturia was stimulated by the cAMP analog, 8-bromo cAMP. We propose that the development of antagonism to the actions of PTH by PGE2 is localized to cellular events proximal to the generation of tubular cAMP. This antagonism by PGE2 could be an effective regulatory mechanism of hormonal action at the local level.

8-Bromo Cyclic Adenosine Monophosphate↗