Indomethacin-induced renal dysfunction in patients with well-compensated cirrhosis

Wong, Florence; Massie, Denise; Hsu, Paul; Dudley, F. J.

doi:10.1016/0016-5085(93)91024-c

Cited by 51 publications

(23 citation statements)

References 16 publications

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“…9,29 This was not termined NO x and cGMP in plasma and urine reflecting for-the case in our patients. The possible mediators of aa-induced mation of NO as a possible mediator of altered renal hemody-glomerular hyperfiltration are still under discussion.…”

Section: Discussionmentioning

confidence: 49%

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Renal functional reserve and nitric oxide in patients with compensated liver cirrhosis

et al. 1997

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To investigate the role of nitric oxide (NO) with respect to In this context, some authors have postulated that patients with compensated liver cirrhosis already show hyperfiltration kidney function and liver cirrhosis, we evaluated renal function, as well as cyclic guanosine monophosphate (cGMP) and in an unstimulated state, which suggests a preponderate NOformation in the kidney. 9 However, the role of NO with NO x (nitrite/nitrate [NO 3 -/NO 2 -]) as indirect markers of NO formation in plasma and urine at rest and during amino acid respect to renal dysfunction has been ill-defined. Thus, the aim of the present study was two-fold: first, to find out if (aa)-induced glomerular hyperfiltration in patients with Child A liver cirrhosis and portal hypertension (n Å 12), and in renal function is altered in patients with compensated liver cirrhosis (Child A) with respect to glomerular filtration rate healthy controls (n Å 10). Baseline filtration rate (GFR) and effective renal plasma flow (ERPF) were significantly lower (GFR), effective renal plasma flow (ERPF), renal vascular resistance (RVR), and filtration fraction (FF) both before in patients with cirrhosis than in controls (GFR: mean 88 { SD 16 mL/min vs. 106 { 15 mL/min, P Å .01, ERPF: 477 { and during testing renal functional reserve (RFR Å difference between stimulated GFR and baseline GFR) by an amino 93 vs. 561{ 72 mL/min, P Å .002). In both groups amino acid (aa) infusion increased GFR, ERPF, as well as cGMP acid (aa) infusion compared with healthy controls. 5,6,[10][11][12] Second, to evaluate whether changes in renal function correand urinary NO x . Changes in GFR were similar in cirrhotic patients and controls (28.3% { 14% in cirrhotics and 26% { spond to alterations in plasma NO x (nitrite/nitrate [NO 3 -/ NO 2 -]) and cyclic guanosine monophosphate (cGMP) levels 11% in controls), but the degree of aa-induced changes in ERPF was more marked in patients with liver cirrhosis (31.8% as well as renal NO excretion as determined by urinary nitrite/nitrate and cGMP. NO x and cGMP are indirect markers { 17% vs. 18.6% { 12%, P Å .02). Plasma levels of NO x and cGMP were similar in either group at baseline and during aa of NO release, which itself, because of its short half-life, is difficult to determine in humans. infusion, whereas NO x and cGMP excretion in cirrhotics was constantly 14% to 24% lower than in the control group. We tors and vasodilators such as NO. It is also believed that NO served as controls. Throughout the study period all subjects neither is a mediator of renal hyperfiltration following aa infusion. [5][6][7][8] smoked nor took any medication. There were no vegetarians in either group and the participants continued their regular western diet that contained 0.9 { 0.15 g/kg body weight protein, as calculated from the 24-hour urine collection. 13 The 24-hour urinary soAbbreviations: NO, nitric oxide; GFR, glomerular filtration rate; ERPF, effective dium output on the day before the study was 126 { 18 mmol in renal plasma flow; RVR, renal vascu...

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Section: Discussionmentioning

confidence: 49%

“…20 One might patients, ranging between 100 and 150 mL/m 2 /1.73. 9,[27][28][29] speculate that their patients had a higher degree of renal This discrepancy in our results may be caused of different dysfunction leading to a passive accumulation of NO x . Unpatient populations or a different study design.…”

Section: Discussionmentioning

confidence: 77%

Renal functional reserve and nitric oxide in patients with compensated liver cirrhosis

et al. 1997

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“…24,25 Of the patients with a hospitalization for CHF in our population, we found a total of 6 patients with a history of liver disease, of whom 2 had a hospitalization for cirrhosis (alcoholic in 1 and nonalcoholic in 1). No evidence was found for a higher risk of CHF after use of an NSAID in patients with a history of cirrhosis.…”

Section: Commentmentioning

confidence: 99%

NSAIDs Associated With Increased Risk of Congestive Heart Failure in Elderly Patients Taking Diuretics

Heerdink¹,

Leufkens²,

Herings³

et al. 1998

Arch Intern Med

261

120

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“…In humans and experimental animals whose renal functions are normal, administration of indomethacin or aspirin causes no change in the GFR and a slight decrease in the RBF, resulting in little effect on renal function [16]. However, NSAIDs are known to cause renal insufficiency in patients with impaired renal or cardiac function [17, 18, 19, 20]. In these disorders, PG are thought to become operative in the maintenance of the RBF.…”

Section: Introductionmentioning

confidence: 99%

Subtotal Nephrectomy Stimulates Cyclooxygenase 2 Expression and Prostacyclin Synthesis in the Rat Remnant Kidney

Horiba¹,

Kumano²,

Watanabe³

et al. 2002

Nephron

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Background: Recently, two isoforms of cyclooxygenase (COX) have been identified, a constitutive form (COX-1) and a mitogen-inducible form (COX-2). Several studies have suggested that COX is activated in renal insufficiency, but little is known about the relationship between progression of renal insufficiency and the COX isoforms. Methods: Five-sixths-nephrectomized (NX) rats were used. 4, 8, and 12 weeks after nephrectomy, the renal cortical prostaglandin contents and the expression levels of the two isoforms of COX were determined by enzyme immunoassay and Western-blotting, respectively. The localization of COX was examined by immunohistochemistry. Results: Renal cortical prostacyclin (PGI₂) and COX-2 were significantly upregulated 8 and 12 weeks after NX, while COX-1 remained at the basal level. There was a high correlation between COX-2 and creatinine clearance (r = –0.845). There was also a high correlation between COX-2 and PGI₂ (r = 0.816). Immunohistochemistry revealed the expression of COX-2 to be enhanced in the macula densa in NX rats. Conclusions: Renal cortical COX-2 and prostacyclin were upregulated corresponding to the progression of renal insufficiency in NX rats. These results suggest enhancement of COX-2 expression in the macula densa, perhaps stimulated by a decrease in renal blood flow which upregulates PGI₂ synthesis to protect the kidney from ischemia in renal insufficiency.

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Indomethacin-induced renal dysfunction in patients with well-compensated cirrhosis

Cited by 51 publications

References 16 publications

Renal functional reserve and nitric oxide in patients with compensated liver cirrhosis

Renal functional reserve and nitric oxide in patients with compensated liver cirrhosis

NSAIDs Associated With Increased Risk of Congestive Heart Failure in Elderly Patients Taking Diuretics

Subtotal Nephrectomy Stimulates Cyclooxygenase 2 Expression and Prostacyclin Synthesis in the Rat Remnant Kidney

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