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Biomedical subjects

W B Duffy

Publications and source records attributed to W B Duffy.

7 recordsLinked to original sources
PubMed1985

Microinjection study of renal calcium absorption in the phosphate-depleted rat.

Tracer microinjection studies were performed in chronically phosphate-depleted (CPD) and phosphate-supplemented (PS) rats in order to determine the site of the defect in calcium absorption which developed in CPD. Calcium recovery in the final urine was significantly higher in CPD than in PS rats after microinjections into the early and the late proximal tubules. However, there was no significant difference in the urinary recovery between the two groups after injection into the early and late distal convoluted tubules. The difference in calcium recovery in late proximal studies persisted during PTH infusion. This indicates that there is a defect in calcium absorption in phosphate-depleted rats between late proximal and early distal tubules, which is not correctable with PTH infusion.

Animals↗
PubMed1984

IgA nephropathy in a patient with ankylosing spondylitis and a solitary kidney.

We describe a patient with ankylosing spondylitis and psoriasis who was found to have IgA nephropathy in a solitary kidney. Renal biopsy demonstrated mesangial proliferation and interstitial nephritis with mesangial deposition of IgA. Although the renal disease and the rheumatic disease could have been present together by chance association, evidence is presented to suggest a possible common pathogenesis.

Glomerulonephritis↗
PubMed1983

Modulation of the hydro-osmotic effect of vasopressin on the rabbit cortical collecting tubule by adrenergic agents.

The effects of catecholamines on antidiuretic hormone ([Arg(8)]-vasopressin [AVP])-induced water absorption were evaluated in cortical collecting tubules isolated from the rabbit kidney and perfused in vitro. In the presence of AVP (100 muU/ml), net fluid volume absorption (J(v), nanoliters per minute per millimeter) was 1.14+/-0.12 and osmotic water permeability coefficient (P(f), X 10(-4) centimeters per second) was 217.3+/-39.9. The addition of the alpha-adrenergic agonist, phenylephrine (PE), in a concentration of 10(-6) M resulted in a significant decrease in J(v) and P(f) to 0.83+/-0.13 (P < 0.001) and 148.8+/-41.8 (P < 0.02), respectively. Increasing the concentration of PE to 10(-5) M resulted in a further decrease in J(v) and P(f) to 0.53+/-0.05 (P < 0.05 vs. PE 10(-6) M) and 88.5+/-9.0 (P 0.05 vs. PE 10(-6) M), respectively. In a separate group of tubules, in the presence of AVP (100 muU/ml) and PE (10(-5) M), J(v) and P(f) were 0.35+/-0.07 and 66.0+/-17.3, respectively. The addition of the alpha-adrenergic antagonist, phentolamine (PH), in a concentration of 10(-6) M resulted in a significant increase in J(v) to 1.07+/-0.19 (P < 0.001) and P(f) to 193.3+/-35.9 (P < 0.005). PH (10(-5) M) alone did not significantly affect J(v) and P(f) in the presence of AVP (100 muU/ml) nor in the presence of 8-bromo adenosine 3',5' cyclic monophosphate (8-BrcAMP). J(v) and P(f) were 1.20+/-0.21 and 174.0+/-25.8, respectively, in the presence of 8-BrcAMP (10(-4) M). We next examined the effect of the beta-adrenergic agonist, isoproterenol (ISO), on J(v) and P(f) in the presence of AVP. J(v) and P(f) were 1.04+/-0.10 and 202.6+/-17.2, respectively, in the presence of AVP (100 muU/ml) and 1.06+/-0.18 and 193.4+/-27.7, respectively, in the presence of AVP (10muU/ml). However, in the presence of AVP in a concentration of 2.5 muU/ml, J(v) was 0.60+/-0.07 and P(f) was 100.7+/-24.7. ISO (10(-6) and 10(-5) M) did not have any significant effect in the presence of the above maximal and submaximal concentrations of AVP. In the absence of AVP, control J(v) was 0.01+/-0.12 and P(f) was 4.6+/-11.0. The addition of ISO at 25 or 37 degrees C did not result in any significant change in J(v) or P(f). These studies indicate that alpha-adrenergic agonists directly inhibit AVP-mediated water absorption at the level of the tubule, an effect that can be blocked by a specific alpha-adrenergic antagonist. This effect appears to be exerted at the level of activation of adenylate cyclase since it is absent in the presence of cAMP. The beta-adrenergic agonists do not directly inhibit or enhance AVP-mediated water absorption at the level of the renal tubule.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1982

Pseudomonas peritonitis and continuous ambulatory peritoneal dialysis.

In a population of 44 patients receiving continuous ambulatory peritoneal dialysis (CAPD) for a total of 591 patient months, there were 104 episodes of peritonitis. The organisms were gram-positive in 65.4%, gram-negative in 23.1%, and cultures of the dialysate were sterile in 11.5%. Pseudomonas aeruginosa was the most frequently encountered gram-negative organism, accounting for 38.5% of the gram-negative infections or 9.6% of all infections. In all cases of P aeruginosa peritonitis, aminoglycoside antibiotic therapy for up to four weeks failed to eradicate the infection, and all patients required removal of the Tenckhoff catheter because of the presence of a sinus tract infection. We conclude that P aeruginosa is the most frequent cause of gram-negative peritonitis in patients receiving CAPD. The presence of a sinus tract infection should be suspected in all patients in whom peritonitis secondary to this organism develops. Removal of the Tenckhoff catheter will be required to cure the peritoneal infection.

Adult↗
PubMed1981

Management of asymptomatic hyperuricemia.

Although the incidence of gout, renal stones, or both is increased in patients with hyperuricemia, there is no evidence that long-term therapy offers any substantial long-term benefits. Recent data also suggest that no clear relationship exists between hyperuricemia and the development of interstitial nephritis (so-called urate nephropathy). Finally, the relationship between elevations in the serum concentration of uric acid and the risk of developing cardiovascular disease remains undefined. It is recommended that, in a patient with asymptomatic hyperuricemia, a conservative approach be taken and hypouricemic therapy not be instituted as a matter of routine.

Acute Disease↗