Direct Effects of Salicylate on Renal Function in the Dog

Quintanilla, A.; Kessler, Richard H.

doi:10.1172/jci107514

Cited by 31 publications

(14 citation statements)

References 25 publications

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“…In 2 others and in 1 normal volunteer the changes were slight or moderate. Such changes were conceivably due to a diuretic effect of salicylates (22) or perhaps to a drug interaction. However aspirin probably had a direct effect on the kidneys of these patients.…”

Section: Discussionmentioning

confidence: 99%

Effect of aspirin on liver tests in patients with ra or sle and in normal volunteers

Seaman

Plötz

1976

Arthritis & Rheumatism

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Aspirin was given to 20 patients with RA, 16 patients with SLE, and 3 normal volunteers. Four of the RA patients, 7 of the SLE patients, and 1 normal volunteer developed abnormal liver tests during the study. The abnormalities (elevated transaminases) were most frequent and of rapid onset in patients with clinically active SLE. Increases in BUN and creatinine related to aspirin were observed in several subjects. In a retrospective survey of 80 patients with SLE, aspirin appeared responsible for two-thirds of episodes of liver test abnormalities in 19 patients.

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Section: Discussionmentioning

confidence: 99%

Effect of aspirin on liver tests in patients with ra or sle and in normal volunteers

Seaman

Plötz

1976

Arthritis & Rheumatism

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“…The interplay between these two opposing acid-base pertur bations will depend in part on the dose of salicylate, the age of the patient and the duration of exposure. The plasma concentration of potassium in salicylate intoxi cation has been reported as increased [95], decreased [96] or unchanged [97,98], Salicylate administration to anes thetized dogs [99] results in elevation of plasma potassium and phosphorus levels. In the dog, the renal clearance of potassium is increased following the systemic or renal artery injection of salicylate [99].…”

Section: Rarer Forms Of Organic Acidemiasmentioning

confidence: 99%

Serum Potassium Concentration in Acidemic States

Pérez¹,

Oster²,

Vaamonde³

1981

Nephron

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It has been generally accepted that acidosis results in hyperkalemia because of shifts of potassium from the intracellular to the extracellular compartment. There is ample clinical and experimental evidence, however, to support the conclusion that uncomplicated organic acidemias do not produce hyperkalemia. In acidosis associated with mineral acids (respiratory acidosis, end-stage uremic acidosis, NH₄CI- or CaCl₂-induced acidosis), acidemia per se, results in predictable increases in serum potassium concentration. In acidosis associated with nonmineral organic acids (diabetic and alcoholic acidosis, lactic acidosis, methanol and the less common forms of organic acidemias secondary to methylmalonic and isovaleric acids, and ethylene glycol, paraldehyde and salicylate intoxications), serum potassium concentration usually remains within the normal range in uncomplicated cases. A number of factors, however, may be responsible for hyperkalemia in some of these patients other than the acidemia per se. These include dehydration and renal hypoperfusion, preexisting renal disease, hypercatabolism, diabetes mellitus, hypoaldosteronism, the status of potassium balance, and therapy. The mechanism(s) of this differing effect of mineral and organic acidemias on transmembrane movement of potassium remains undefined. The prevalent hypothesis, however, favors the free penetrance of the organic anion into cells without creating a gradient for the hydrogen ions and, thus, obviating the efflux of intracellular potassium. The importance of the presence of hyperkalemia in clinical states of organic acidemias is obvious. A search for the complicating factors reviewed above should be undertaken since organic acidemias per se, should not be expected to be accompanied by elevations of serum potassium concentration. Moreover, the classical teaching that the absence of hyperkalemia during severe acidosis is indicative of severe potassium deficiency, may not be universally valid in patients with uncomplicated organic acidemias.

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“…Previous workers have differed in their conclusions as to whether salt retention follows ASA administration (9)(10)(11)30). The absence of a clearcut biological response in the presence of binding suggests that the drug-receptor complexes formed are either suboptimally active or inactive (19,26,31).…”

Section: In Vitro Mineralocorticoid Binding Studies Nsaidmentioning

confidence: 99%

Intrinsic mineralocorticoid agonist activity of some nonsteroidal anti-inflammatory drugs. A postulated mechanism for sodium retention.

Feldman¹,

Couropmitree²

1976

J. Clin. Invest.

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A B S T R A C T Because some nonsteroidal anti-inflammatory drugs (NSAID) induce salt and water retention and exhibit other steroid-like actions, studies were performed to ascertain whether these drugs possess intrinsic mineralocorticoid agonist activity. In vitro competitive binding assays utilizing tissue from adrenalectomized rats demonstrated that some NSAID can displace [3H]-aldosterone from renal cytoplasmic mineralocorticoid receptors. Displacement potency for these sites was in the sequence: aldosterone > spironolactone > phenylbutazone (PBZ) > aspirin (ASA) > indomethacin (IDM). Concentration ratios required to obtain significant displacement of ['H]aldosterone were high but clearly within the therapeutic range for PBZ and ASA but not IDM. The analogues oxyphenbutazone (OBZ) and sodium salicylate (SS) were similar in binding activity to PBZ and ASA, respectively. Lineweaver-Burk analysis revealed that the inhibition of [8H]aldosterone binding was competitive in nature. In addition, PBZ was shown to prevent the nuclear binding of ['H]aldosterone.In vivo injection of PBZ and ASA resulted in competition for [8H]aldosterone renal binding comparable to the in vitro studies. Administration of PBZ and OBZ to adrenalectomized rats resulted in significant salt retention whereas ASA and SS did not differ significantly from controls. Salt retention elicited by PBZ and OBZ was inhibited by spironolactone, a competitive mineralocorticoid antagonist. These data suggest that, despite nonsteroidal structures, PBZ and OBZ induce salt retention via a receptor-mediated mineralocorticoid pathway analogous to aldosterone action.

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Direct Effects of Salicylate on Renal Function in the Dog

Cited by 31 publications

References 25 publications

Effect of aspirin on liver tests in patients with ra or sle and in normal volunteers

Effect of aspirin on liver tests in patients with ra or sle and in normal volunteers

Serum Potassium Concentration in Acidemic States

Intrinsic mineralocorticoid agonist activity of some nonsteroidal anti-inflammatory drugs. A postulated mechanism for sodium retention.

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