Effects of Sulindac and Ibuprofen in Patients with Chronic Glomerular Disease

Ciabattoni, Giovanni; Cinotti, Giulio A.; Pierucci, Alessandro; Simonetti, Bianca M.; Manzi, Massimo; Pugliese, Francesco; Barsotti, Paola; Pecci, G; Taggi, Franco; Patrono, Carlo

doi:10.1056/nejm198402023100502

Cited by 314 publications

(86 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ciabattoni et al (1980) have first reported that sulindac may be unique because it does not inhibit renal PG synthesis in normal volunteers and in a patient with Bartter's syndrome as measured by urinary PG excretion. These observations were later confirmed by several studies in normal subjects and in patients with chronic glomerular disease or hypertension (Bunning and Barth 1982;Salvetti et al 1982; Ciabattoni et al 1984; Sedor et al 1984; Puddey et al 1985; Vriesendorp et al 1986a). Recently, however, there are controversial results indicating that sulindac reduces urinary excretion of PGE2 and is not specifically renalsparing both in experimental animals and in healthy subjects or in patients with renal, liver of cardiac diseases (Berg and Talseth 1985;Brater et al 1985; Olanoff et al 1985; Roberts et al 1985;Laf et al 1986).…”

supporting

confidence: 67%

“…Such a dissociation between urinary excretion of PGE2 and changes in creatinine and para-amino hippurate clearance after treatment with an NSAID has been already reported by Ciabattoni et al (1984), in which they found the inverse relation between the reduction of these clearances after ibuprofen and basal excretion of 6-keto-PGE1 but not that of PGE2 in patients with chronic glomerular disease. Since human glomeruli mainly produce PGI2 (Hassid and Dunn 1980), these results indicate that changes in glomerular filtration rate is more linked with vascular or glomerular PGI2 synthesis than medullary PGE2 synthesis which is mostly reflected as urinary excretion of PGE2 (Frolich et al 1975).…”

Section: Discussionmentioning

confidence: 63%

See 1 more Smart Citation

Effect of Sulindac on Prostaglandin Synthesis in Human and in Cultured Rat Renal and Vascular Smooth Muscle Cells.

Sato¹,

Abe

Takeuchi³

et al. 1992

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

To examine the hypothesis that Sulindac does not inhibit renal prostaglandin (PG) synthesis, we investigated the effects of Sulindac and other nonsteroidal anti-inflammatory drugs on PG synthesis in human and in cultured rat renal and vascular smooth muscle (VSM) cells. In 7 patients with chronic glomerular disease, creatinine clearance and proteinuria were not changed by Sulindac but were significantly reduced by diclofenac sodium. However, urinary excretion of PGE2 was decreased by both drugs. In cultured glomerular mesangial (GM), renal papillary collecting tubule (RPCT) and VSM cells from mesenteric artery, indomethacin, tiaprofenic acid, aspirin and ibuprofen inhibited both basal and arachidonic acid (AA)-stimulated PG synthesis dose-dependently. Although Sulindac sulfoxide, at the same concentrations, inhibited both basal and AAstimulated PGE2 synthesis in RPCT cells, it was less potent to inhibit PGI2 synthesis in VSM cells or PGE2 synthesis in GM cells. Active form sulindac sulfide inhibited PG synthesis in all types of cells but its inactive form sulfone did not. We conclude that sulindac inhibits renal PG synthesis but has little effect on renal function. This may be explained by its relatively weak potency on glomerular or vascular PG synthesis inhibition possibly due to the different biotransformation of the sulfoxide to the active sulfide in these cells.sulindac ; prostaglandin synthesis ; renal-sparing effect ; renal cells ; nonsteroidal antiinflammatory drug Nonsteroidal anti-inflammatory drugs (NSAIDs) are the agents which are most frequently used in a variety of disease. As the number of patients taking NSAIDs increases, there are numerous reports on renal and electrolyte disturbances and attenuation of the hypotensive effect of antihypertensive drugs such as

show abstract

supporting

confidence: 67%

Section: Discussionmentioning

confidence: 63%

Effect of Sulindac on Prostaglandin Synthesis in Human and in Cultured Rat Renal and Vascular Smooth Muscle Cells.

Sato¹,

Abe

Takeuchi³

et al. 1992

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

show abstract

“…[15][16][17] Aspirin, 7 acetaminophen, 5,6 and NSAIDS 18 have each been shown to reduce formation of vasodilator prostaglandins from arachadonic acid. In the setting of volume depletion, PGI 2 and PGE 2 enhance glomerular filtration 15,19 and reduce fractional sodium reabsorption. 20,21 These actions help counterbalance the effects of constriction of the renal vasculature caused by angiotensin II and catecholamines 22 under conditions such as chronic kidney failure.…”

Section: Discussionmentioning

confidence: 99%

“…20,21 These actions help counterbalance the effects of constriction of the renal vasculature caused by angiotensin II and catecholamines 22 under conditions such as chronic kidney failure. 19 In addition, ibuprofen and indomethacin have been shown to preferentially inhibit extrarenal prostaglandin synthesis and to elevate blood pressure 16,17 in part, perhaps, by increasing endothelin-1 production. 23 Two cross-sectional studies in elderly populations suggest a link between NSAID use and hypertension.…”

Section: Discussionmentioning

confidence: 99%

Nonnarcotic Analgesic Use and the Risk of Hypertension in US Women

et al. 2002

View full text Add to dashboard Cite

Abstract-Acetaminophen, aspirin, and other nonsteroidal anti-inflammatory drugs (NSAIDs) are widely consumed. Each is theoretically capable of elevating blood pressure by altering prostaglandin homeostasis; however, there is little prospective information on the relation between these agents and physician-diagnosed hypertension. We examined the association between the use of aspirin, acetaminophen, or NSAIDs and incident hypertension in a prospective cohort study of 51 630 women 44 to 69 years of age in 1990 who had no history of hypertension or chronic renal insufficiency. Analgesic use was assessed in 1990 by a mailed questionnaire, and the women were followed for 8 years. Key Words: hypertension, essential Ⅲ drug therapy Ⅲ blood pressure Ⅲ risk factors A spirin, acetaminophen, and ibuprofen are the three most commonly used medications among adults 18 years of age and older, according to a national survey of US households conducted between 1998 and 1999. 1 Seventeen percent of respondents reported using aspirin in the preceding week, 23% reported acetaminophen use, and 17% ibuprofen use. Prevalence of use was greater among women than men for acetaminophen and ibuprofen.Short-term prospective studies suggest nonsteroidal antiinflammatory drugs (NSAIDs) can cause acute elevations in blood pressure, 2,3 but a diagnosis of hypertension was used as the primary outcome in only one case-control study. 4 Although aspirin and acetaminophen also influence prostaglandin homeostasis, 5-7 prospective data on their potential hypertensive effects have been sparse and inconclusive. 8,9 A recent study of these effects in a large cohort of younger US women demonstrated an increased incidence of hypertension in users of NSAIDs and acetaminophen but not aspirin (OR 1.86 and 2.00, respectively, for the highest use category, PϽ0.001). 10 Twenty-four percent of US adults and 50% to 70% of those Ͼ60 years of age have hypertension. 11 Even small elevations in blood pressure caused by nonnarcotic analgesic use could affect cardiovascular morbidity and mortality. 12 To examine this issue, we studied the association between the use of aspirin, acetaminophen, and NSAIDs and incident hypertension in a large cohort of US women. Methods The Nurses' Health StudyThe Nurses' Health Study cohort was assembled in 1976 when 121 700 female registered nurses, 30 to 55 years of age, completed and returned a mailed questionnaire. 13 Follow-up questionnaires have been mailed every 2 years to update information on healthrelated behaviors and medical events. In 1990, questions were included regarding frequency of use of acetaminophen, aspirin, and other NSAIDs. Study PopulationThe 1990 questionnaire was answered by 85 625 women. Women who reported a history of hypertension (nϭ27 344) or chronic kidney failure (nϭ10) on or before the 1990 questionnaire were excluded from the study, as were women who did not answer any of the questions on analgesic use (nϭ336). We also excluded subjects who did not report having had a physical examination between 1988

show abstract

“…Very few studies were devoted to relationships between kidney alterations and the urinary excretion of prostaglandins. 6KPGFj, but not PGE2 was reported to be decreased in patients with renal insufficiency by Ciabattoni et al (1984) and Mistry et al (1986), while Patrono et al (1983) found that the urinary TxB2 was not affected in similar conditions.…”

Section: Discussionmentioning

confidence: 98%

Influence of renal insufficiency on the pharmacokinetics of cicletanine and its effects on the urinary excretion of electrolytes and prostanoids.

Ferry¹,

Geoffroy²,

Pozet³

et al. 1988

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 The kinetics of a single oral dose (300 mg) of cicletanine a new antihypertensive drug with diuretic properties, and its effects on the urinary excretion of electrolytes and of the major stable metabolites of prostacyclin and thromboxane A2 were studied in patients with normal renal function (n = 6), mild (n = 9) and severe (n = 10) renal insufficiency. 2 In normotensive subjects with normal renal function, cicletanine was rapidly and regularly absorbed, its apparent elimination half-life established around 7 h, and both its renal clearance (0.4 ml min-') and its cumulative renal excretion (0.85% of the administered dose), were low. Mild renal insufficiency did not significantly alter these parameters, while severe renal impairment reduced the renal clearance and the cumulative urinary excretion of cicletanine and increased its apparent elimination half-life (31 h). However the area under the plasma curve was not changed due to reduced plasma concentrations in these patients. 3 Cicletanine induced a rapid and marked (four fold as a mean) increase in the urinary excretion of water, sodium and potassium which lasted for 6 to 10 h, in subjects with normal renal function. Renal insufficiency did not alter the slope of the calculated plasma concentration-effects curves but reduced the maximum effect observed for water, sodium and potassium. 4 A single oral dose of cicletanine did not change the urinary excretion of 6-ketoprostaglandin Fla and thromboxane B2 in the three groups of patients studied, the basal values of which being found to be closely related to the creatinine clearance. 5 It was concluded that i) from a pharmacokinetic view point, the dosage of cicletanine should only be slightly reduced in patients with a glomerular filtration rate below 30 ml min-', ii) as with most of the diuretic agents, its natriuretic properties were markedly decreased in these patients and iii) an alteration in the renal synthesis of prostacyclin or thromboxane seems unlikely to participate in the pharmacological effects of cicletanine.

show abstract

Effects of Sulindac and Ibuprofen in Patients with Chronic Glomerular Disease

Cited by 314 publications

References 16 publications

Effect of Sulindac on Prostaglandin Synthesis in Human and in Cultured Rat Renal and Vascular Smooth Muscle Cells.

Effect of Sulindac on Prostaglandin Synthesis in Human and in Cultured Rat Renal and Vascular Smooth Muscle Cells.

Nonnarcotic Analgesic Use and the Risk of Hypertension in US Women

Influence of renal insufficiency on the pharmacokinetics of cicletanine and its effects on the urinary excretion of electrolytes and prostanoids.

Contact Info

Product

Resources

About