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Biomedical subjects

A C Seguro

Publications and source records attributed to A C Seguro.

At least 37 records · Page 2Linked to original sources
PubMed1994

Effect of amphotericin B on water and urea transport in the inner medullary collecting duct.

The clinical usefulness of amphotericin B (AMP-B) is limited by its nephrotoxicity, as characterized by decreased RPF, decreased GFR, impaired urinary acidification, and potassium excretion defects. Defects of renal concentrating ability have been noted, but the mechanisms responsible for them have not been investigated. The chief objective of this research was to analyze directly the effect of AMP-B on arginine-vasopressin (AVP)- or dibutyrl cAMP (DcAMP)-stimulated water and urea transport of the inner medullary collecting duct (IMCD) obtained from rats by the in vitro microperfusion technique. AMP-B (10(-5) M) added to the bath fluid in the absence of AVP did not impair the hydraulic conductivity (Lp) and the urea permeability (Pu) of rat IMCD. AMP-B (10(-5) M) added to the bath fluid decreased the AVP-stimulated Lp (x 10(-6) cm/s.atm) of rat IMCD from 19.41 +/- 2.19 to 10.00 +/- 1.39 (P < 0.001), and the reversibility of its action was observed during a third period when Lp increased to 19.80 +/- 2.19 (P < 0.001) after the initial conditions were restored. In addition, AMP-B reduced DcAMP-stimulated Lp from 20.95 +/- 1.75 to 10.52 +/- 0.71 (P < 0.01) in a reversible manner when the drug was withdrawn from the bath. AMP-B also decreased AVP-stimulated Pu (x 10(-5) cm/s) when added to the bath fluid from 36.60 +/- 2.05 to 29.88 +/- 1.36 (P < 0.001), and this effect was reversible after AMP-B was withdrawn from the bath (37.40 +/- 1.36; P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Amphotericin B↗
PubMed1993

Evaluation of human kidney viability during cold storage.

Na-K-ATPase activity and "in vitro" PAH uptake were used to determine the possible presence of ischemic injuries in cadaver kidneys after different periods of cold storage, and the data were compared with those obtained for an experimental rabbit group. In rabbit kidneys, Na-K-ATPase activity remained stable up to 168 h of cold storage in the outer medulla and superficial cortex, and PAH uptake decreased significantly after 72 h. In human kidneys, Na-K-ATPase activity in the outer medulla was low during the first phase of the study (cold storage less than 20 h), suggesting early injury to the thick ascending limb of Henle's loop. In the superficial cortex, no apparent progression of injury was observed between PAH uptake and Na-K-ATPase activity. In conclusion, our results suggest the presence of early signs of injury in the thick ascending limb of Henle's loop and preservation of proximal tubule function in cadaver kidneys for up to 70 h of cold storage.

Animals↗
PubMed1992

Effects of acyclovir on renal function.

The renal effects of acyclovir (100 mg/kg body weight i.p. for 7 days) were studied in rats. All animals became polyuric and presented an increase in blood urea nitrogen and fractional excretion of sodium and potassium. During hypotonic saline infusion, the acyclovir-treated rats showed higher distal fractional delivery compared to normal rats (27.8 +/- 4.7 vs. 11.3 +/- 0.9%, p less than 0.01) and a lower ratio of free-water clearance to distal sodium delivery (33.5 +/- 7.8 vs. 57.2 +/- 3.9%, p less than 0.02). Following hypertonic saline infusion, the ratio of osmolar to inulin clearance was higher in acyclovir rats (47.8 +/- 7.4%) than in normal rats (27.0 +/- 4.8%), whereas the ratio of free-water reabsorption to osmolar clearance was lower in the acyclovir rats (13.6 +/- 4.6 vs. 38.2 +/- 3.2%, p less than 0.01). These findings suggest an effect of acyclovir on the proximal tubule, thick ascending limb and/or inner medullary collecting duct (IMCD). In vitro measurements of 3H2O permeability of perfused IMCD of normal rats showed that vasopressin (50 microU/ml) added to the bath increased the diffusional water permeability (43.4 +/- 4.8 vs. 105.6 +/- 9.1 x 10(-5) cm/s), while in acyclovir rats, the control value (58.8 +/- 9.1 x 10(-5) cm/s) did not increase significantly in the presence of vasopressin (71.3 +/- 13.6 x 10(-5) cm/s). These results suggest that high doses of acyclovir produce azotemia and an abnormal function of the proximal tubule and thick ascending limb associated with resistance to vasopressin of the IMCD.

Acyclovir↗
PubMed1992

Renal involvement in leptospirosis: a pathophysiologic study.

The kidney involvement in leptospirosis appears to be a special form of acute renal failure due to a higher frequency of polyuric forms and the presence of hypokalemia with an elevated urinary fractional excretion of potassium. Using a clearance technique, we detected higher fractional urinary potassium excretion in leptospirotic guinea pigs (26.5 +/- 4.7%) than in normal animals (14.1 +/- 2.8%, p < 0.05). After blocking distal NaCl reabsorption with furosemide, it was observed that in leptospirotic animals both fractional sodium excretion (40.0 +/- 7.4%) and fractional potassium excretion (136.3 +/- 32.7%) were higher than in normal animals (20.4 +/- 3.8%, p < 0.05, and 43.6 +/- 9.0%, p < 0.05, respectively). Microperfusion studies showed that the normal and leptospirotic medullary thick ascending limb had both identical transepithelial potential difference (+3.7 +/- 0.4 vs. 3.9 +/- 0.2 mV) and relative sodium-to-chloride permeability. The same technique showed that the osmotic water permeability (Posm; 0.9 +/- 0.4 x 10(-5) cm/s.atm) and diffusional permeability (34.7 +/- 6.6 x 10(-5) cm/s) observed in the leptospirotic inner medullary collecting duct (IMCD) in the presence of vasopressin were unchanged, as was also the case for urea permeability (3.74 +/- 0.7 x 10(-5) cm/s). These data show that acute renal failure in leptospirosis is characterized by tubular changes leading to potassium secretion probably due to a decrease in proximal sodium reabsorption. Furthermore, the inability to concentrate urine evidenced by the low P(o)sm present in leptospirotic animals is due, at least in part, to IMCD resistance to vasopressin.

Animals↗
PubMed1992

Acute renal failure following hemorrhagic shock: protective and aggravating factors.

Acute renal failure following hemorrhagic shock was studied in awake rats. The animals were bled to maintain the mean arterial blood pressure between 40 and 60 mm Hg during 180 min. After this period, the blood was reinfused and the rats were studied 24 h later. Hemorrhagic shock caused a less intensive renal injury than 60-min bilateral renal artery clamping. Renal function in the latter model was worse (p less than 0.05) as shown by serum creatinine (SCr) (0.75 +/- 0.10 vs 1.2 +/- 0.2 mg/dL), blood urea nitrogen (BUN) (26.0 +/- 2.8 vs 53.0 +/- 8.5 mg/dL), fractional excretion of sodium (FENa, %) (0.3 +/- 0.1 vs 1.8 +/- 1.0) and potassium (FEK, %) (41.4 +/- 5.7 vs 76.3 +/- 14.2) and urine/plasma creatine (U/PCr (86.4 +/- 15.7 vs 38.8 +/- 15.5). The rats which received verapamil (10 micrograms/kg/min) prior and during the HS did not show increase in SCr (0.5 +/- 0.06 vs 0.75 +/- 0.1 mg/dL, p less than 0.05). This effect was also observed in the rats which received intravenous allopurinol (40 mg/kg) before HS, SCr did not increase (0.5 +/- 0.04 vs 0.75 +/- 0.1 mg/dL, p = 0.05), suggesting a protective effect of those substances in HS.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1991

Renal concentrating defect in protein malnutrition: the role of the thick ascending limb of Henle and inner medullary collecting duct.

The present study was carried out to examine the effect of chronic dietary protein restriction on renal water handling in the rat. During hypotonic saline infusion, the malnourished rats showed a lower free-water clearance, corrected by inulin clearance (7.2 +/- 0.4%), than normal rats (13.6 +/- 2.5%, p less than 0.051), although the fractional distal delivery of sodium did not differ from normal. Throughout hypertonic saline diuresis the free-water reabsorption (TcCH20) corrected by inulin clearance was lower in malnourished rats (6.62 +/- 0.64%) than in control animals (9.25 +/- 0.62, p less than 0.05). Moreover, when TcH20 was referred to the osmolar clearance, malnourished animals showed lower values than normal. These results suggest a defect in NaCl transport in the thick ascending limb of Henle. In vitro measurements of diffusional water permeability (PDW) in the inner medullary collecting duct (IMCD) obtained from malnourished rats showed an increase from 40.0 +/- 5.4 x 10(5) cm/s to 71.3 +/- 5.4 x 10(5) cm/s by adding maximum effective concentration (50 microU/ml) of arginine vasopressin (VP) to the bath. These values were not different from the PDW observed in the IMCD of normal rats. In another series of microperfusion experiments, the hydraulic conductivity in IMCD of malnourished rats measured also in the presence of maximum effective concentration of VP was 29.7 +/- 3.4 x 10(-6) cm/atm/s, a mean value not significantly different from that observed in the IMCD of normal rats (35.2 +/- 4.3 x 10(-6) cm/atm/s).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Cellular immune response analysis of patients with leptospirosis.

Peripheral blood mononuclear cells (PBMC) from acute leptospirosis patients with and without acute renal failure were studied in order to investigate the status of cellular immunity in this disease. We analyzed the lymphocyte subsets of leptospirosis patients by immunofluorescence and their responsiveness to the mitogens phytohemagglutinin (PHA) and pokeweed mitogen (PWM). Additionally, we investigated the effect of the patients' sera on normal PBMC proliferative response. We observed a decrease in the CD3+ and CD4+ cell subsets in patients with and without acute renal failure, or in percentage values alone in those who had recovered from renal failure. An increase in the number of B lymphocytes was observed in all patients, compared with controls. This increase in B lymphocytes was seen even in patients who had recovered from renal failure, when the number of CD3+ and CD4+ lymphocytes had already returned to normal levels. The low PHA response observed only with lymphocytes from patients with acute renal failure suggests a suppressive effect. The proliferative response to PWM was comparable to controls, even in the patients with acute renal failure. This latter result and the expansion of the B cell number could be related to leptospiral-derived factor(s). We also showed that sera from patients with and without acute renal failure exerted some inhibitory activity on normal PBMC responses to PHA and PWM. Although the redistribution of lymphocyte subsets and the serum suppressor activity were related to acute renal failure and leptospiral factor(s), we suggest that the cellular immune system was not irreversibly affected, which is compatible with the good prognosis seen in the patients studied.

Adolescent↗
PubMed1990

Acute renal failure of leptospirosis: nonoliguric and hypokalemic forms.

Acute renal failure induced by leptospirosis was studied in 56 patients. A higher frequency of nonoliguric renal failure was observed with lower morbidity and mortality rates than in oliguric forms. In addition, 45% of the patients in this series were hypokalemic, and no hyperkalemic patients were seen. A prospective study in 11 patients showed an initially elevated urinary fractional potassium excretion that fell simultaneously with the high urinary fractional sodium excretion and the urinary K/Na ratio, suggesting an increased distal potassium secretion due to an increased distal sodium delivery consequent to functional impairment of the proximal reabsorption of sodium.

Acute Kidney Injury↗
PubMed1990

The effect of protein restriction on the severity and recovery from ischemic renal failure.

The effects of chronic dietary protein restriction on ischemic renal failure were evaluated in rats subjected to 90 min of bilateral renal clamping. The rats were kept on either 20% casein (regular) diet or casein-free (protein-free) diet 10 days before and 21 days after renal injury. Rats on regular protein diet showed higher levels of BUN and serum creatinine and had a lower inulin clearance (microliter/min/100 g BW) than animals on protein-free diet (289 +/- 34 vs 582 +/- 103, p less than 0.05) 2 days after ischemia. However, the inulin clearance measured 21 days following ischemia was significantly higher in rats on regular diet (1468 +/- 181) than those maintained on protein-free diet after ischemia (560 +/- 167). When unilateral 90 min ischemia was performed in rats on regular diet, the postischemic kidneys showed an incomplete recovery of the inulin clearance (226 +/- 35) compared to the contralateral kidney (900 +/- 116), 21 days after ischemia; whereas in rats on a protein-free diet the inulin clearance averaged 106 +/- 17 in the postischemic kidney and 345 +/- 41 in the right kidney. When left renal ischemia and contralateral nephrectomy were performed, the inulin clearance was 1149 +/- 74 in rats on regular diet and 534 +/- 60 in rats on protein-free diet, 21 days following renal insult. These results suggest that protein restriction can play a protective role against renal ischemia in an initial phase, but it limits the late recovery from ischemia. The presence of a normal contralateral kidney inhibits the functional recovery of the postischemic kidney and a contralateral nephrectomy produces a compensatory functional hypertrophy of the postischemic kidney, even in rats on a protein-free diet.

Analysis of Variance↗
PubMed1989

Renal concentration defect induced by cisplatin. The role of thick ascending limb and papillary collecting duct.

The effects of cisplatin (5 mg/kg BW given intraperitoneally) on renal concentration mechanism were evaluated initially by clearance studies in rats 5-7 days after cisplatin administration and compared to normal rats. During hypotonic saline infusion, cisplatin rats showed a lower inulin clearance (0.56 +/- 0.07 vs. 1.12 +/- 0.09 ml/min/100 g BW, p less than 0.01), a higher fractional distal delivery (CNa + CH2O/Cin) (36.3 +/- 4.4 vs. 22.8 +/- 4.5%, p less than 0.05), and lower CH2O/CNa + CH2O (33.6 +/- 5.8 vs. 56.5 +/- 5.0%, p less than 0.01). During hypertonic saline infusion the TcH2O/Cosm was lower in cisplatin (18.3 +/- 1.1%) than in normal rats (33.4 +/- 3.5%, p less than 0.01). These results suggest a defect in NaCl transport in the thick ascending limb of Henle and proximal tubule. In order to characterize these tubular defects, we measured Na-K-ATPase activity (microM Pi/mg protein/h). In the renal cortex of cisplatin rats the ATPase activity was lower (18.1 +/- 3.2) than in normal rats (33.4 +/- 6.4, p less than 0.05), also in the inner strip of the outer medulla of cisplatin rats Na-K-ATPase was reduced (26.0 +/- 5.7) when compared with normal rats (67.3 +/- 9.2, p less than 0.01), presumably representing a decrease in enzyme activity in the thick ascending limb.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of potassium depletion on ischemic renal failure.

The present study was carried out to examine the effect of potassium depletion in rat kidneys subjected to a temporary ischemic event produced by clamping of left renal artery. The postischemic kidneys of rats on a normal diet with adequate potassium intake showed an increase in H2O, Na and K excretion, with no change in inulin clearance whereas significant differences were found in potassium-deprived rats. Potassium depletion was brought about by dietary K deprivation for 10 days. K-depleted rats (serum K = 2.5 +/- 0.1 mEq/l) had a decrease in inulin clearance of the postischemic kidney from 1.01 +/- 0.10 to 0.43 +/- 0.05 ml/min (p less than 0.01), and a greater increase in fractional excretion of H2O, Na and K when compared to normal rats. The postischemic kidney from both normal and hypokalemic rats showed a decrease in Na-K-ATPase of the inner stripe of the outer medulla. These data indicate that short-term ischemia produces polyuria, increases natriuresis and kaliuresis, associated, at least in part, with a decrease in Na-K-ATPase in the inner stripe of the outer medulla (probably the thick ascending limb of Henle) and that K depletion potentiates ischemic renal failure.

Acute Kidney Injury↗
PubMedDate not supplied

Comparisons of models of cortical necrosis with segmental infarction.

Sodium and water excretion were studied by standard clearance techniques in three experimental models where renal mass was reduced by superficial cortical necrosis (CN) or ischemic segmental infarction (SI). During hydropenia either CN or SI were able to conserve and regulate sodium to a very similar degree. After expansion of extracellular volume, CN reabsorbed less sodium and water than SI. In free-water clearance (CH2O) experiments, the 'apparent distal' sodium delivery was higher in CN than in SI, suggesting a decreased sodium and water reabsorption in the proximal tubules of juxtamedullary nephrons (JM). Both kidneys had similar CH2O when factored for inulin clearance but when CH2O was corrected for 'apparent distal' sodium delivery it was lower in CN than in SI, demonstrating an incapacity of JM to dilute urine. CN also showed less capacity to reabsorb free water than SI. Thus, the use of CN and SI within the same animal was useful to study functional differences between superficial and juxtamedullary nephrons. The present study also suggests that the kidney with superficial CN was unable to perform maximal urine dilution and concentration.

Absorption↗
PubMedDate not supplied

Effect of low and high potassium diets on H(+)-K(+)-ATPase and Na(+)-K(+)-ATPase activities in the rat inner medullary collecting duct cells.

This study was designed to measure H-K-ATPase and Na-K-ATPase activities in rat inner medullary collecting duct (IMCD) cells during potassium depletion and loading. Both enzyme activities were similarly distributed from the proximal to the distal portion of this nephron segment. One week K depletion did not stimulate H-K-ATPase activity but reduced Na-K-ATPase activity. Within 2 weeks after the onset of potassium depletion, the rats developed metabolic alkalosis, and H-K-ATPase activity was suppressed while Na-K-ATPase activity had returned to control values. H-K-ATPase activity was suppressed following potassium loading whereas Na-K-ATPase activity was unchanged. The results are consistent with the presence of H-K-ATPase in IMCD and indicate that H-K-ATPase and Na-K-ATPase activities are modulated by potassium intake.

Animals↗