Comparison of loop diuretics in patients with chronic renal insufficiency

Voelker, James R.; Cartwright–Brown, Debbie; Anderson, Shirley; Leinfelder, Jeff; Sica, Domenic A.; Kokko, Juha P.; Brater, D. Craig

doi:10.1038/ki.1987.246

Cited by 107 publications

(61 citation statements)

References 32 publications

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“…However, like in decompensated cirrhotic patients 14,15 the urinary furosemide excretion rate, as well as the urinary recovery of furosemide were significantly decreased. The mechanisms behind the decreased renal excretion rate of furosemide during severe cirrhosis with ascites are not fully known, but an increased volume of distribution 26 and competitive inhibition of the secretion of furosemide in the proximal tubules 15 may be involved. Another mechanism involved in the resistance to furosmide could be hyperreabsorption of sodium in tubular segments distal to the TAL due to increased plasma levels of aldosterone.…”

Section: Pharmacokinetic Changes Of Furosemide In Decompensated Cirrhmentioning

confidence: 99%

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

et al. 2000

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The authors examined the natriuretic efficiency of furosemide in rats with cirrhosis induced by carbon tetrachloride (CCl 4 ). Rats were treated for 17 weeks with intraperitoneal injections of CCl 4 in groundnut oil twice a week throughout the study. Control rats were treated with vehicle (groundnut oil). Studies in metabolic cages showed that sodium retention was present from week 14. Renal clearance experiments were performed in chronically, instrumented conscious rats at the end of week 14 and at the termination of the study (end week 16) when ascites and hyponatremia were present. After 14 weeks, cirrhotic rats had sodium retention along with increased renal plasma flow, normal GFR, normal renal lithium handling, and a significantly increased diuretic (؉41% vs. control) and natriuretic (؉56% vs. control) response to a test dose furosemide (7.5 mg/kg b.w., intravenously). The natriuretic efficiency of furosemide, i.e., the natriuresis expressed relative to the furosemide excretion rate (⌬U Na V/U FUR V) was increased by 51% versus control. After 17 weeks, ascites and hyponatremia had developed, and significant decreases in renal plasma flow (؊33%), GFR (؊30%), and fractional lithium excretion (؊44%) were observed. At this stage urinary recovery of furosemide was significantly decreased and the diuretic (؊27% vs. Control) and natriuretic (؊38% vs. control) responses to furosemide were significantly impaired. However, the increased natriuretic efficiency of furosemide was still present (؉34% vs. control). Together these results suggest that increased sodium reabsoprtion in the thick ascending limb of Henle's loop is involved in the renal sodium retention in cirrhosis in rats that eventually results in decompensation with the

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Section: Pharmacokinetic Changes Of Furosemide In Decompensated Cirrhmentioning

confidence: 99%

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

et al. 2000

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“…We employed assays previously described by our laboratories to measure frusemide in urine by h.p.l.c. [17] and PRA, plasma ACE activity and PAC by radioimmunoassay [18,19].…”

Section: Experimental Protocolmentioning

confidence: 99%

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

Reed

Greene

Ryan

et al. 1995

Brit J Clinical Pharma

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1. To test the hypothesis that basal renin angiotensin aldosterone system (RAAS) activity impairs the acute natriuretic response to frusemide in patients with mild or moderate congestive heart failure (CHF), we studied eight adult volunteers with preserved renal function, stable New York Heart Association Class II or III CHF, and echocardiographic evidence of left ventricular dysfunction due to myocardial infarction, hypertension, or both causes. 2. All patients received three dosing regimens administered in random order: (a) intravenous frusemide: 40 mg bolus then 40 mg h‐1 for 3 h, (b) captopril: two 12.5 mg oral doses separated by 2 h, (c) combined dosing: the first captopril dose preceded the frusemide bolus by 30 min. Sodium balance on an 80 mmol day‐1 sodium diet was documented prior to each dosing regimen. Sodium excretion was quantitated in urine collected at intervals until 3.5 h after initiating drug administration. During this time, urine output was replaced intravenously with an equivalent volume of 0.45% saline. 3. Captopril significantly lowered plasma angiotensin converting enzyme (ACE) activity and plasma aldosterone concentration, and raised inulin clearance. The drug had essentially no effect on the time course of magnitude of frusemide's natriuretic effect. Maximal fractional sodium excretion during frusemide infused by itself and in combination with captopril was 24.7 +/‐ 1.9% vs 28.2 +/‐ 3.8%, respectively (difference 3.5%; 95% CI, ‐4.0 to 11.0%; P > 0.05). Cumulative sodium excretion ending at 3.5 h was 429 +/‐ 53 mmol when frusemide was given alone and 455 +/‐ 69 mmol when captopril was added (difference, 26 mmol; CI, ‐121 to 174 mmol; P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Halveringstiden er en time, og den øker bare i liten grad ved lav glomerulaer filtrasjonsrate. Dette forklarer at forholdet mellom ekvipotente doser furosemid og bumetanid endres fra 40 : 1 hos nyrefriske til 20 : 1 der det er alvorlig nyresvikt (9).…”

Section: Farmakokinetikkunclassified

“…Økt dose og dermed høyere serumnivå av diuretikum kan kompensere for dette. Ved GFR 15 ml/min/ 1,73 m 2 utløses maksimal respons med 160 -200 mg furosemid eller 4 -5 mg bumetanid intravenøst (9). Tiaziddosen må på samme måte økes for å oppnå effektiv konsentrasjon i urinen ved nedsatt glomerulaer filtrasjonsrate.…”

Section: Farmakokinetikkunclassified

Bruk av diuretika ved nyresykdom

Heramb¹,

Hallan²,

Aasarød³

2014

Tidsskriftet

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OversiktsartikkelBruk av diuretika ved nyresykdom 840 -4 Ototoksisitet og hudreaksjoner forekommer ved bruk av høye doser slyngediuretika BAKGRUNN Diuretika er en viktig del av behandlingen ved en rekke indremedisinske tilstander, som hjertesvikt, leversvikt, nyresvikt og hypertensjon. I denne artikkelen presenteres oppdatert kunnskap om bruk av diuretika ved nyresykdom. KUNNSKAPSGRUNNLAG Artikkelen bygger på litteratursøk i PubMed, kunnskap hentet fra laerebøker i nyrefysiologi og nyresykdommer samt forfatternes kliniske erfaring.RESULTATER Nyresykdom påvirker diuretikas farmakokinetikk og farmakodynamikk, noe som må tas hensyn til ved valg og dosering av medikament. Dette gjelder spesielt ved nefrotisk syndrom og alvorlig kronisk nyresykdom (GFR < 30 ml/min/1,73 m 2 ).

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Comparison of loop diuretics in patients with chronic renal insufficiency

Cited by 107 publications

References 32 publications

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

Increased natriuretic efficiency of furosemide in rats with carbon tetrachloride-induced cirrhosis

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

Bruk av diuretika ved nyresykdom

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