Renal prostaglandins in cirrhosis of the liver

1986 ◽  
Vol 70 (5) ◽  
pp. 477-484 ◽  
Author(s):  
C. Guarner ◽  
I. Colina ◽  
F. Guarner ◽  
J. Corzo ◽  
J. Prieto ◽  
...  
Keyword(s):  
Renal Failure ◽  
Urinary Excretion ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Bed Rest ◽  
Control Group ◽  
Fractional Excretion Of Sodium ◽  
Cirrhotic Patients ◽  
The Relationship

1. Urinary prostaglandin excretion was studied in 42 patients with liver cirrhosis and in nine control subjects on restricted sodium intake and on bed rest. Creatinine clearance (CCr), sodium excretion (UNaV), plasma renin activity (PRA) and plasma aldosterone were also evaluated. 2. Patients without ascites and ascitic patients without renal failure showed increased urinary excretion of immunoreactive 6-ketoprostaglandin F1α (i6-keto-PGF1α), prostaglandin E2 (iPGE2) and thromboxane B2 (iTXB2) when compared with controls, while immunoreactive PGF2α (iPGF2α) levels did not differ from those in the control group. Patients with functional renal failure (FRF) presented a significant reduction of vasodilator prostaglandins but urinary excretion of iTXB2 was higher than in controls. 3. On the whole, cirrhotic patients with higher urinary excretion of prostaglandins had normal or nearly normal PRA and aldosterone levels. i6-keto-PGF1α and iPGE2 inversely correlated with PRA and aldosterone. 4. The relationship between i6-ketoPGF1α and CCr was found to be highly significant in cirrhotic patients but not in the control group. On the other hand, iPGE2 significantly correlated with UNaV and with the fractional excretion of sodium (FENa). 5. We concluded that: (a) enhanced renal prostaglandin synthesis in cirrhosis, inversely related to PRA and aldosterone, may be dependent on volume status; and (b) preserved renal function in these patients is associated with the ability to synthesize prostacyclin and PGE2.

Atrial natriuretic factor and changes in dietary sodium intake in patients with chronic renal failure

1990 ◽  
Vol 78 (3) ◽  
pp. 327-334 ◽  
Author(s):  
J. C. Dussaule ◽  
C. Michel ◽  
J. P. Wolf ◽  
S. Czekalski ◽  
F. Mignon ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Plasma Renin Activity ◽  
Atrial Natriuretic Factor ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Renin Activity ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

1. In order to examine the potential role of atrial natriuretic factor in modulating the increased sodium excretion per nephron in chronic renal failure, we studied 12 uraemic patients on the last day of two successive 7 day periods during which their sodium intake was 100 and 20 mmol of sodium/day, respectively. 2. There was a parallel decrease from 6.31 ± 0.75 to 2.17 ± 0.32% in the fractional excretion of filtered sodium and from 234.4 ± 74.9 to 80.6 ± 20.3 pg/ml (supine position) or 140.1 ± 43.6 to 60.7 ± 14.6 pg/ml (upright position) in plasma atrial natriuretic factor. Both parameters were significantly correlated during the two periods of different sodium intake (P <0.05). The ratio of plasma guanosine 3′:5′-cyclic monophosphate to plasma creatinine changed proportionally to plasma atrial natriuretic factor. Plasma aldosterone and plasma renin activity increased during the sodium-depleted period but only plasma renin activity was significantly correlated with fractional excretion of filtered sodium. 3. The predominant role of atrial natriuretic factor compared with that of aldosterone in the renal response to varying sodium intake is suggested both by regression analysis and by the effect of 5 day's treatment with a converting enzyme inhibitor (enalapril) in six other uraemic patients on a normal (100 mmol/day) sodium intake. Such treatment, although resulting in a significant increase in plasma renin activity and a significant decrease in plasma aldosterone, at least in the supine position, did not modify the fractional excretion of sodium and plasma atrial natriuretic factor. 4. Taken together, these results suggest a role for plasma atrial natriuretic factor in promoting the adaptation of sodium excretion on chronic changes of sodium intake in patients with chronic renal failure.

Effect of Proportional Reduction of Sodium Intake on the Adaptive Increase in Glomerular Filtration Rate/Nephron and Potassium and Phosphate Excretion in Chronic Renal Failure in the Rat

1975 ◽  
Vol 49 (3) ◽  
pp. 193-200 ◽  
Author(s):  
C. H. Espinel
Keyword(s):  
Renal Failure ◽  
Glomerular Filtration Rate ◽  
Chronic Renal Failure ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Control Group ◽  
Phosphate Excretion

1. The influence of dietary sodium intake on the glomerular filtration rate (GFR/nephron) and potassium and phosphate excretion was examined at three stages of progressive chronic renal failure produced in rats by sequential partial nephrectomies. 2. The adaptive increased sodium excretion per nephron in the control group receiving a constant sodium intake did not occur in the experimental group that had a gradual reduction of dietary sodium in direct proportion to the fall in GFR. 3. Despite the difference in sodium excretion, the increase in GFR/nephron, the daily variation in the amount of potassium and phosphate excreted, the increase in potassium and phosphate excretion per unit nephron, and the plasma potassium and phosphate concentrations were the same in the two groups. 4. The concept of ‘autonomous adaptation’ in chronic renal failure is presented.

Effect of intrarenal renin inhibition on renal hemodynamics and excretory function

1990 ◽  
Vol 259 (1) ◽  
pp. R7-R14 ◽  
Author(s):  
K. M. Verburg ◽  
J. R. Kadam ◽  
G. A. Young ◽  
S. H. Rosenberg ◽  
H. D. Kleinert
Keyword(s):  
Recovery Period ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Urine Flow ◽  
Electrolyte Excretion ◽  
Angiotensin System ◽  
Excretory Function ◽  
Fractional Excretion Of Sodium ◽  
Renin Inhibition

This study was designed to investigate in sodium-depleted monkeys the renal hemodynamic and excretory effects resulting from blockade of the renin-angiotensin system induced by intrarenal infusion of the primate-selective renin inhibitor A-65317. Intrarenal infusion of A-65317 (n = 6) at a dose of 0.01 micrograms.kg-1.min-1 elicited an increase (P less than 0.05) in renal blood flow (RBF) from 43.5 +/- 2.7 to 49.4 +/- 4.4 ml/min and glomerular filtration rate (GFR) from 6.3 +/- 0.3 to 6.9 +/- 0.4 ml/min, with no significant changes in mean arterial pressure (MAP) or plasma renin activity (PRA). Increases (P less than 0.05) in the urine flow rate (0.18 +/- 0.04 to 0.28 +/- 0.04 ml/min) and the fractional excretion of sodium (0.18 +/- 0.06 to 0.35 +/- 0.13%) were also observed. After a recovery period, the intrarenal infusion dose of A-65317 was increased to 0.1 microgram.kg-1.min-1 and RBF increased (P less than 0.05) from 42.9 +/- 3.9 to 53.0 +/- 3.7 ml/min in conjunction with a significant 85 +/- 4% inhibition of PRA and a 14 +/- 4 mmHg reduction in MAP. GFR and electrolyte excretion remained at control levels. Intrarenal infusion of vehicle (n = 6) had no significant effect on any of the variables studied. In a separate group of monkeys, intravenous (iv) infusion of A-65317 at 0.01 microgram.kg-1.min-1 (n = 5) did not result in significant changes from control.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of neutral endopeptidase stimulates renal sodium excretion in patients with chronic renal failure

1993 ◽  
Vol 84 (1) ◽  
pp. 31-39 ◽  
Author(s):  
J. C. Dussaule ◽  
C. Michel ◽  
M. N. Peraldi ◽  
J. M. Lecomte ◽  
C. Gros ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cyclic Gmp ◽  
Atrial Natriuretic Factor ◽  
Fractional Excretion ◽  
Neutral Endopeptidase ◽  
Factor Level ◽  
Natriuretic Factor ◽  
Fractional Excretion Of Sodium ◽  
Atrial Natriuretic

1. The acute effects of a single oral dose of sinorphan (100 mg), an inhibitor of neutral endopeptidase, on the plasma atrial natriuretic factor level and the fractional excretion of sodium were examined in 12 patients with severe chronic renal failure who were not on maintenance haemodialysis and who ingested a normal sodium diet. The drug was administered against placebo by a double-blind cross-over protocol. 2. Basal plasma atrial natriuretic factor level and fractional excretion of sodium were high (23.2 ± 3.7 pmol/l and 2.64 ± 0.38%, respectively). Sinorphan inhibited plasma neutral endopeptidase activity by 68–75% 30 min after ingestion. This effect persisted for at least 4 h. There were simultaneously increases in plasma atrial natriuretic factor and cyclic GMP levels to 1.9 and 1.4 times the basal values, respectively. Fractional excretion of sodium increased during the second and third hour periods after ingestion of the drug with a peak of 1.9 times the basal value in the second period. Changes in fractional excretion of sodium were significantly correlated with those in plasma atrial natriuretic factor and cyclic GMP levels. Plasma aldosterone level, creatinine clearance and mean blood pressure were unchanged, whereas plasma renin activity increased slightly. An increase in urinary cyclic GMP excretion was observed in parallel with the increase in plasma cyclic GMP level. 3. The results of the present study indicate that (i) high basal values of plasma atrial natriuretic factor level and fractional excretion of sodium, as observed in patients with chronic renal failure, are associated with marked effects of neutral endopeptidase inhibition; (ii) fractional sodium excretion increases after protection of endogenous atrial natriuretic factor from degradation independently of any initial change in extracellular fluid volume or sodium intake, which suggests that this hormone may play a role in the control of sodium excretion in chronic renal failure.

Use of fractional lithium clearance in clinical and epidemiological investigation: A methodological assessment

1988 ◽  
Vol 74 (6) ◽  
pp. 651-657 ◽  
Author(s):  
P. Strazzullo ◽  
L. Iacoviello ◽  
R. Iacone ◽  
N. Giorgione
Keyword(s):  
Sodium Intake ◽  
Fractional Excretion ◽  
Lithium Carbonate ◽  
Individual Variability ◽  
Dietary Sodium ◽  
Epidemiological Investigation ◽  
Experimental Conditions ◽  
Renal Handling ◽  
Water Handling ◽  
Fractional Excretion Of Sodium

1. The fractional clearance of lithium (FCLi) has been validated in the rat under controlled experimental conditions as a reliable indicator of sodium and water handling in the proximal tubule. The purpose of the present study was to evaluate some key methodological aspects related to the use of the FCLi in clinical and epidemiological investigation. 2. FCLi was determined in healthy normotensive, or in some cases, in borderline/mild essential hypertensive subjects, by a morning urine collection obtained between 09.00 and 13.00 hours after a 300 mg oral lithium carbonate load (= 8.1 mmol of elemental lithium). 3. The ratio of intra-individual to inter-individual variance of FCLi, measured in free-living subjects on unrestricted diet, was shown to be low enough (0.33) to allow adequate characterization of individuals in a population with a single measurement, or at most with two (compared with at least four measurements needed to characterize the fractional excretion of sodium). 4. The remarkable influence of dietary sodium intake on FCLi, demonstrated under metabolic ward conditions, might explain a major portion of the observed intra-individual variability. 5. At the dosage employed in the present study, oral lithium administration did not affect the renal handling of sodium, potassium or calcium. Likewise, it did not induce any change in a series of 17 metabolic parameters and indicators of renal and liver function. 6. It is concluded that the FCLi may be a safe and useful tool for the clinical and epidemiological investigation of renal sodium and water handling. The possibility of a confounding effect of dietary sodium intake, however, should be kept in mind.

scholarly journals Early effects of contrast media on renal hemodynamics and tubular function in chronic renal failure.

1995 ◽  
Vol 6 (5) ◽  
pp. 1451-1458
Author(s):  
D Russo ◽  
R Minutolo ◽  
B Cianciaruso ◽  
B Memoli ◽  
G Conte ◽  
...  
Keyword(s):  
Renal Failure ◽  
Single Dose ◽  
Chronic Renal Failure ◽  
Contrast Media ◽  
Fractional Excretion ◽  
Sodium Concentration ◽  
Renal Hemodynamics ◽  
Fractional Excretion Of Sodium ◽  
Urinary Levels ◽  
Renal Hypoperfusion

The pathophysiology and prevention of contrast media (CM)-induced nephropathy in chronic renal failure (CRF) are still ill defined. GFR, RPF, endothelin-1 (ET-1) levels, urinary sodium concentration, and fractional excretion of sodium were measured in CRF patients undergoing water diuresis in basal conditions and 20 to 120 min after an iv bolus of either the high-osmolar CM diatrizoate (D) or the low-osmolar CM iopamidol (I). The two CM induced an immediate and progressive decline of both GFR and RPF in the absence of hypovolemia, more pronounced in D (-36% at 120 min) than after I (-19% at 120 min; P < 0.05 versus D). Both CM determined a marked and steady increase of the fractional excretion of sodium. The natriuresis could not be totally ascribed to a CM-induced osmotic diuresis as because the urinary sodium concentration markedly increased. In two further groups of patients receiving D, we studied the effects of pretreatment with a single dose of either captopril or nifedipine. Both drugs, although not preventing the increase of natriuresis, partially antagonized D-induced renal hypoperfusion: GFR and RPF were equally reduced by 20% in D/captopril and D/nifedipine (P < 0.05 versus D). In unpretreated patients receiving either D or I, plasma ET-1 did not change but urinary levels increased; these changes were, however, dissociated from those observed in renal hemodynamics. Both plasma and urinary levels of ET-1 did not vary in pretreated groups. The 72-h follow-up evidenced a significant reduction of renal function only in the unpretreated D group. Therefore, the main findings after CM administration in CRF patients are: (1) an immediate GFR decline proportional to the osmolarity of CM and secondary to the renal hypoperfusion that is neither caused by hypovolemia nor mediated by ET-1, (2) an early tubular dysfunction at the level of the proximal nephron, and (3) a protective effect of single-dose pretreatment with either captopril or nifedipine on D-induced acute and short-term GFR changes.

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