Biomedical subjects

A C Seguro

Publications and source records attributed to A C Seguro.

At least 19 recordsLinked to original sources

PubMed2006

Urinary NO3 excretion and renal failure in indinavir-treated patients.

Treatment with indinavir (IDV), a protease inhibitor, is frequently associated with renal abnormalities. We determined the incidence of renal failure (creatinine clearance <80 mL min-1 1.73 (m(2))-1) in HIV patients treated with highly active antiretroviral therapy, including IDV, and investigated the possible mechanisms and risk factors of IDV nephrotoxicity. Thirty-six patients receiving IDV were followed for 3 years. All were assessed for age, body weight, duration of infection, duration of IDV treatment, sulfur-derivative use, total cholesterol, triglycerides, magnesium, sodium, potassium, creatinine, and urinalysis. We also determined renal function in terms of creatinine clearance, urine osmolality and fractional excretion of sodium, potassium, and water. Urinary nitrate (NO3) excretion was measured in 18 IDV-treated patients and compared with that of 8 patients treated with efavirenz, a drug without renal side effects. Sterile leukocyturia occurred in 80.5% of the IDV-treated patients. Creatinine clearance <80 mL min-1 1.73 (m(2))-1 was observed in 22 patients (61%) and was associated with low body weight and the use of sulfur-derivatives. These patients also had lower osmolality, lower urine volume and a higher fractional excretion of water compared to the normal renal function group. Urinary NO3 excretion was significantly lower in IDV-treated patients (809 +/- 181 microM NO3-/mg creatinine) than in efavirenz-treated patients (2247 +/- 648 microM NO3-/mg creatinine, P < 0.01). The lower NO3 excretion suggests that IDV decreases nitric oxide production.

Adult↗

PubMed2004

Effect of cyclooxygenase inhibitors on gentamicin-induced nephrotoxicity in rats.

The frequent use of nonsteroidal anti-inflammatory drugs (NSAID) in combination with gentamicin poses the additional risk of nephrotoxic renal failure. Cyclooxygenase-1 (COX-1) is the main enzyme responsible for the synthesis of renal vasodilator prostaglandins, while COX-2 participates predominantly in the inflammatory process. Both are inhibited by non-selective NSAID such as indomethacin. Selective COX-2 inhibitors such as rofecoxib seem to have fewer renal side effects than non-selective inhibitors. The objective of the present study was to determine whether the combined use of rofecoxib and gentamicin can prevent the increased renal injury caused by gentamicin and indomethacin. Male Wistar rats (250-300 g) were treated with gentamicin (100 mg/kg body weight, ip, N = 7), indomethacin (5 mg/kg, orally, N = 7), rofecoxib (1.4 mg/kg, orally, N = 7), gentamicin + rofecoxib (100 and 1.4 mg/kg, respectively) or gentamicin + indomethacin (100 and 5 mg/kg, respectively, N = 8) for 5 days. Creatinine clearance and alpha-glutathione-S-transferase concentrations were used as markers of renal injury. Animals were anesthetized with ether and sacrificed for blood collection. The use of gentamicin plus indomethacin led to worsened renal function (0.199 +/- 0.019 ml/min), as opposed to the absence of a nephrotoxic effect of rofecoxib when gentamicin plus rofexicob was used (0.242 +/- 0.011 ml/min). These results indicate that COX-2-selective inhibitors can be used as an alternative treatment to conventional NSAID, especially in situations in which risk factors for nephrotoxicity are present.

Animals↗

PubMed2003

Effects of hypokalemia and hypomagnesemia on zidovudine (AZT) and didanosine (ddI) nephrotoxicity in rats.

BACKGROUND: Zidovudine (AZT) and didanosine (ddI) are antiretroviral drugs widely used in AIDS patients. Hypokalemia and hypomagnesemia are frequently encountered in AIDS patients using AZT and/or ddI. OBJECTIVE: To verify the effects of AZT and ddI on rat renal function submitted to normal diet, low potassium diet and magnesium-free diet. METHODS: Glomerular filtration rate and renal hemodynamic were measured in Wistar rats submitted to a normal or a potassium-depleted diet. The animals were given AZT, ddI for 15 days. Six groups of rats were studied: normal diet, normal diet + AZT, normal diet + ddI, low K diet, low K diet + AZT and low K diet + ddI. Three additional groups of rats submitted to magnesium depletion for 15 days were also studied: magnesium-free diet, magnesium-free diet + AZT and magnesium-free diet + ddI. RESULTS: AZT and didanosine did not modify renal function of rats on a normal diet. However, in hypokalemic rats, both drugs produced a decrease in glomerular filtration rate and in renal blood flow consequent to renal vasoconstriction and associated with alterations in tubular function (characterized by an increased fractional excretion of sodium). Hypomagnesemia induced a decrease in glomerular filtration rate and in renal blood flow only in AZT-treated rats. CONCLUSION: Our data suggest that hypokalemia predisposes to AZT and ddI nephrotoxicity, while hypomagnesemia predisposes only to AZT nephrotoxicity. Thus, chronic AZT and ddI administration may produce acute renal failure in AIDS patients with hypokalemia and/or hypomagnesemia. Serum K and Mg levels should be carefully monitored in these patients.

Acute Kidney Injury↗

PubMed2001

Effects of sodium artesunate, a new antimalarial drug, on renal function.

BACKGROUND: Sodium artesunate is currently used in malaria treatment. Adverse effects of this drug have not been described, probably because they cannot be differentiated from malaria-related effects. METHODS: The effects on renal function of an acute infusion of sodium artesunate (12 mg/kg body weight) were studied in the rat with clearance techniques. We also evaluate the effect of sodium artesunate on chloride lumen-bath flux (Cl Jlb) in the isolated thick ascending limb of the loop of Henle (TALH) microperfused in vitro. RESULTS: Acute infusion of artesunate to the rat decreased inulin clearance, despite an increase in renal blood flow. These effects were associated with an increase in urinary excretion of sodium, chloride, potassium, and nitric oxide metabolites (NO(2)/NO(3)). In water-loaded animals, artesunate increased sodium and water distal delivery and decreased free water clearance (C(H(2)O)) factored for sodium and water delivery. Following hypertonic NaCl infusion, artesunate decreased free water excretion (Tc(H(2)O)) corrected by clearance of osmolarity (C(Osm)). In vitro, artesunate 10(-6) and 10(-3) mol/L added to bath solution decreased chloride lumen-bath flux in isolated rabbit TALH in a dose-dependent manner, with the threshold effect at 10(-4) mol/L. This effect was completely blocked by N(G)-nitroL-arginine-metilester (L-NAME) 5 mmol/L. Artesunate 10(-4) mol/L added to the perfusion solution did not change Cl Jlb. CONCLUSION: These findings suggest that artesunate decreases glomerular filtration rate and increases renal blood flow and urinary excretion of Na, Cl, and K. These effects were due, at least in part, to the inhibition of Cl transport across cortical and medullary TALH, and were mediated by local production of nitric oxide, since it is associated with an increase in NO(2)/NO(3) urinary excretion and it is blocked by L-NAME in vitro.

Animals↗

PubMed2000

[Meningoencephalitis in the acute phase of measles. Report of 6 cases].

We present the clinical and laboratory manifestations of encephalitis following measles in six patients which were diagnosed during the epidemics that occurred in the city of São Paulo, Brazil, in 1997. We performed retrospective case analysis of the six patients diagnosed as having encephalitis due to measles. Encephalitis was diagnosed based on clinical grounds and on the cerebrospinal fluid (CSF) alterations. All the cases were serologically confirmed. Of 467 patients with measles who presented themselves for medical care at the Instituto de Infectologia Emílio Ribas six were diagnosed with encephalitis. Patient's age was 2 months to 28 years old. The most frequent symptoms were drowsiness and nuchal rigidity. CSF showed an increased of white cell count in all cases. Four patients were admitted to the intensive care unit. Two of them required mechanical ventilation. In only two patients did the computerized tomography show abnormalities. All showed good recovery without sequelae.

Acute Disease↗

PubMed2000

The role of potassium in the regulation of adenosine production by ATP-diphosphohydrolase on the endothelial cell membrane.

Endothelial cells have ectonucleotidases that catabolize extracellular nucleotides and are sensitive to the presence of cations. Our aim was to determine whether the metabolism of extracellular nucleotides is influenced by exposure of endothelial cells to high potassium relevant to human pathophysiology. Human umbilical vein endothelial cells were incubated with 25 mM potassium and without potassium. The metabolism of radioactive substrates was measured and activities were 7.0+/-1.3 and 12.2+/-1.4 microM P/h/mg of protein with and without potassium. Also incubation with membrane pellet from endothelial cells was used, this assay showed 15.5+/-1.9 and 20.9+/-0.7 microM P/ h/mg of protein with and without potassium, respectively. HPLC analysis of supernatant showed that AMP production was lower in the presence of 25 mM potassium. Analysis of different potassium levels showed that a progressive reduction occurred above 10 mM potassium. We conclude those potassium levels above 10 mM, which can be found in ischemia, inhibit the catabolism of extracellular adenine nucleotides by the ectonucleotidases of endothelial cells and may thus modify the pathophysiology of ischemia-reperfusion injury.

Adenosine↗

PubMed2000

Skeletal muscle pathology in 2 siblings infected with Toxoplasma gondii.

Skeletal muscle can be the site of inflammatory diseases that lead to muscle weakness, pain, and increased myogenic serum enzymes. Most of these inflammatory myopathies are idiopathic. In some cases inflammatory myopathies are due to infectious agents. We describe the pathological aspects of muscle biopsies of 2 Brazilian siblings who acquired toxoplasmosis at the same time and in similar conditions. One developed a tetraplegia that was confirmed to be due to inflammatory myositis due to toxoplasma. The other developed myocarditis, with heart failure, without skeletal muscle weakness. In both cases many toxoplasma organisms were observed in the muscle biopsies, but in case 1 only was there an inflammatory myopathy with myofiber necrosis; the inflammatory cells were predominantly macrophages with some CD4+ cells and rare CD20+ cells. In case 1, expression of CD54 was observed in many inflammatory cells as well in endothelial cells, but only in endothelial cells in case 2. After treatment with clindamycin and corticosteroids both cases had only partial improvement, case 1 with a residual muscle weakness and case 2 with residual cardiac insufficiency (requiring digoxin). These cases show that the presence of the parasite in myofibers is not enough to induce an inflammatory myositis with muscle cell necrosis. This suggests that immunological disturbances may contribute to the development of inflammatory myositis due to toxoplasma.

Adolescent↗

PubMed1999

Protective effect of L-arginine on hypercholesterolemia-enhanced renal ischemic injury.

The effects of hypercholesterolemia on ischemic renal failure were evaluated in rats subjected to 60 min of left renal artery clamping and contralateral nephrectomy. One group of rats (HC) was kept on a cholesterol-supplemented diet for 3 weeks before renal injury and compared to a group fed a regular diet (ND). Two days after renal ischemia, inulin clearance (C(in), ml/min per 100 g BW) was lower in HC-rats (0.033 +/- 0.011) than in ND-rats (0.227 +/- 0.037; P < 0.01). indicating that hypercholesterolemia potentiated renal ischemic injury. Twenty-one days after renal ischemia the C(in) of HC-rats did not differ from ND-rats, suggesting that hypercholesterolemia did not limit late recovery. Since nitric oxide production is impaired in HC, L-arginine (50 mg/kg BW i.v.) was administered immediately after ischemia. Two days after ischemia, L-arg did not protect ND-rats from ischemia, while the C(in) and renal blood flow were higher in L-arg-treated HC rats than in untreated HC rats (C(in) = 0.125 +/- 0.013 rats vs. 0.033 +/- 0.011; P < 0.001) (RBF = 3.96 +/- 0.64 vs. 2.40 +/- 0.20 ml/min per 100 g BW; P < 0.05), indicating that L-arg protects HC rats from renal ischemia. The administration of D-arginine to ND rats induced a significant decrease of the C(in) and a significant increase of FE H2O, FE Na and FE K compared to the L-arginine and not treated groups. Cultures of inner medullary collecting duct cells from ND rats were resistant to 24-h hypoxia. In contrast, IMCD cell cultures from HC rats showed higher LDH release after 24-h hypoxia than normoxic cells (69.2 +/- 3.4 vs. 30.9 +/- 3.6%, P < 0.001); 1 mM L-arg added to the medium attenuated LDH release (44.3 +/- 2.4%, P < 0.01). These data demonstrate that HC predisposes renal tubular cells to hypoxic injury and L-arg protects cells of HC.

Acute Kidney Injury↗

PubMed1999

Acute lung injury in leptospirosis: clinical and laboratory features, outcome, and factors associated with mortality.

Forty-two consecutive patients with leptospirosis and acute lung injury who were mechanically ventilated were analyzed in a prospective cohort study. Nineteen patients (45%) survived, and 23 (55%) died. Multivariate analysis revealed that 3 variables were independently associated with mortality: hemodynamic disturbance (odds ratio [OR], 6.0; 95% confidence interval [CI], 0.9-38.8; P=. 047), serum creatinine level >265.2 micromol/L (OR, 10.6; 95% CI, 0. 9-123.7; P =.026), and serum potassium level >4.0 mmol/L (OR, 19.9; 95% CI, 1.2-342.8; P=.009). These observations can be used to identify factors associated with mortality early in the course of severe respiratory failure in leptospirosis.

Acute Disease↗

PubMed1999

Beneficial and harmful effects of L-arginine on renal ischaemia.

BACKGROUND: The role of nitric oxide (NO) in acute renal failure (ARF) is not yet completely understood. L-Arginine (L-arg) is protective against different ARF models, while L-arg addition in isolated proximal tubules enhances hypoxia/reoxygenation (H/R) injury. The aim of this study was to evaluate the effects of L-arg on renal ischaemia. METHODS: In in vivo studies, Wistar rats were subjected to 60 min renal artery clamping, and renal function was evaluated 2 and 15 days after ischaemia. Four groups were studied: (1) control; (2) acute L-arg (50 mg/kg/bw i.v.); (3) L-nitro-arginine-methyl esther (L-NAME; 0.5 mg/kg/bw i.v.); and (4) chronic L-arg (L-arg 0.25% in drinking water/7 days). For the in vitro studies, proximal tubules (PTs), isolated by collagenase digestion and Percoll gradient, were studied from three groups: (1) untreated; (2) L-arg-treated (L-arg 0.25% in drinking water/7 days); and (3) L-NAME-treated rats (3 mg/kg in drinking water/7 days). PTs were kept oxygenated or subjected to 15 min hypoxia (H-15) and 35 min reoxygenation (R-35). In some experiments, additional doses of L-arg and L-NAME were administered. Cell injury was assessed by lactate dehydrogenase (LDH) release. NO production was evaluated by NO2-/NO3- measurement (Griess reaction) in both urine and isolation medium. RESULTS: After 2 days, L-arg infusion protected against ischaemia compared with control rats (0.4 vs 0.2 ml/min/100 g, P < 0.001), while neither L-NAME nor chronic L-arg supplementation ameliorated renal function. After 15 days, both acute and chronic L-arg groups showed a higher glomerular filtration rate (0.6 and 0.75 ml/min/100 g) compared with control rats (0.3 ml/min/100 g, P < 0.05) and L-NAME-treated rats (0.2 ml/min/100 g, P < 0.05). Despite similar recovery in both L-arg groups, the mortality rate was 25% in the chronic L-arg group. Tubular function was also better preserved in the acute L-arg group. PTs isolated from L-arg-treated rats were more sensitive to isolation injury. L-Arg addition enhanced H/R injury (44.9 vs 51.8%, P < 0.05), whereas L-NAME addition protected (44.9 vs 24%, P < 0.001) in untreated rats. In L-arg-treated rats, addition of L-arg did not enhance H/R injury (49.6 vs 53.5%, NS) and L-NAME was still protective (49.6 vs 32.3%, P < 0.001). In PTs from L-NAME-treated rats, L-arg addition also did not enhance H/R injury (50 vs 54%, NS) whereas L-NAME was protective (50 vs 27%, P < 0.001). NO2-/NO3- production paralleled L-arg and L-NAME supplementation. CONCLUSION: It was demonstrated that acute L-arg infusion was beneficial in in vivo renal ischaemia while it was harmful in isolated H/R tubules. In contrast, chronic L-arg supplementation was deleterious both in in vivo and in vitro renal ischaemia, suggesting that injurious effects had overcome the beneficial effects during excess NO exposure.

Acute Kidney Injury↗

PubMed1998

Hypercholesterolemia aggravates radiocontrast nephrotoxicity: protective role of L-arginine.

It is well known that the radiocontrast-induced ARF depends on risk factors often associated with compromised renal circulation. Since studies have shown that endothelium-dependent vasodilation is impaired in hypercholesterolemia (HC), we studied the effect of radiocontrast (RC) administration (6 ml/kg body wt, via femoral artery) in salt-depleted rats that were kept on a normal cholesterol (NC) or HC diet (4% cholesterol and 1% cholic acid). Inulin clearance (CIn, ml/min/100 g body wt), renal blood flow (RBF; electromagnetic flowmeter, ml/min/100 g body wt), and fractional excretions of sodium, potassium and water (FENa, FEK and FEH2O, respectively), cholesterol (mg/dl), and albumin (g/dl) were measured 24 hours after radiocontrast administration. The administration of RC to HC rats (RCHC) resulted in lower values of CIn compared with NC rats (RCNC) and control rats: 0.36 +/- 0.085 versus 0.76 +/- 0.13 (RCNC; P < 0.01), versus 0.84 +/- 0.03 (control HC; P < 0.01), versus 0.87 +/- 0.06 (control NC; P < 0.01). Hypercholesterolemia per se did not alter renal function, and control HC versus control NC was not significant. Renal blood flow was significantly lower in the RCHC when compared to RCNC (4.3 +/- 0.3 vs. 6.1 +/- 0.3; P < 0.001) and to control animals (control HC 8.2 +/- 0.3; P < 0.001), and control NC 7.5 +/- 0.33 (P < 0.001). To study the role of nitric oxide (NO), HC rats were treated with an infusion of L-arginine or D-arginine (150 mg via femoral artery) in a 50 mg bolus before RC administration and the remaining dose continuously for a period of one hour. The administration of L-arginine to RCHC rats resulted in significantly higher CIn (0.86 +/- 0.1; P < 0.001) when compared to the untreated rats (RCHC). D-arginine did not show a significant difference in CIn (0.49 +/- 0.08). There was a considerable difference between D-arginine RCHC and L-arginine RCHC (P < 0.05). The RBF fall was prevented by L-arginine in RCHC (8.4 +/- 0.23 vs. 4.3 +/- 0.3; P < 0.001), but it was not prevented by D-arginine (5.1 +/- 0.57; P < 0.001). Our data suggest that hypercholesterolemia aggravates nephrotoxicity, which is attenuated by L-arginine but not by D-arginine administration, suggesting that nitric oxide plays a significant role in this model of acute renal failure.

Acute Kidney Injury↗

PubMed1998

Renal potassium handling in aging rats.

Aging is often related to electrolyte disorders. This study was designed to evaluate the renal capacity for K+ handling of aging rats submitted to both extreme situations of K+ depletion and K+ loading. Aging rats were submitted to metabolic assessment, measurement of plasma aldosterone and determination of Na+,K+-ATPase and H+,K+-ATPase activity in the inner medullary collecting duct (IMCD). During K+ depletion, aging rats showed low values of urine K+ excretion. After 2 weeks of dietary K+ restriction, the plasma K+ levels of these animals reached 2.9+/-0.1 mEq/l without acid-base disorders. During K+ loading, aging rats showed a significant increase in urinary K+ excretion, with plasma K+ remaining at normal levels (4.7+/-0.1 mEq/l). Plasma aldosterone levels were low in control aging rats but K+ intake modulated the levels of this hormone, with K+ depletion reducing it and K+ loading significantly increasing it. Na+,K+-ATPase activity increased only in the initial portion of the IMCD of aging rats after 2 weeks of K+ depletion. In the distal portion of the IMCD, Na+,K+-ATPase activity did not change. H+,K+-ATPase remained unchanged in both the proximal and distal portions of the IMCD of aging rats. During K+ loading, there was no change in Na+,K+-ATPase or H+,K+-ATPase activity in the proximal or distal portions of the IMCD of aging rats. This study suggests that the senescent kidney responded to K+ conservation and excretion under the two extremes of low and high K+ intake.

Aging↗

PubMed1998

Acute disseminated encephalomyelitis: an unusual cause of encephalitic syndrome in childhood.

Acute disseminated encephalomyelitis is a rare central nervous system demyelinating disease that occurs most frequently in children. It usually runs a monophasic course, beginning with fever, headache, and meningeal signs and rapidly progressing to coma when appropriate diagnosis and treatment are not provided. We report a case of a 14-year-old patient to alert emergency physicians to consider acute disseminated encephalomyelitis when presented with any child with encephalitic signs with nonspecific cerebrospinal fluid findings, failure to detect any causative agent, and only mild alterations on computerized tomography scan. The role of magnetic resonance imaging for the diagnosis is emphasized.

Acute Disease↗

PubMed1997

L-Arginine and allopurinol protect against cyclosporine nephrotoxicity.

The role of nitric oxide (NO) and oxygen free radicals in cyclosporine (CsA) nephrotoxicity was investigated using L-arginine, an NO substrate, and allopurinol, a xanthine oxidase inhibitor (involved in the formation of oxygen radicals) in an experimental model with Wistar rats. CsA, administered at 15 mg/kg/body weight (BW) subcutaneously for 10 days, caused a decrease in glomerular filtration rate, with inulin clearance of 0.33+/-0.04 vs. 1.11+/-0.06 ml/min/100 g BW (P<0.01 vs. control). L-Arginine, 1.5% in drinking water 5 days before and during CsA administration, partially protected the animals against this fall in glomerular filtration rate, with inulin clearance of 0.68+/-0.03 ml/min/100 g BW (P<0.01 vs. CsA). Allopurinol, at 10 mg/kg/BW by gavage, also had a protective action, with inulin clearance of 0.54+/-0.04 ml/min/100 g (P<0.01 vs. CsA). CsA caused an elevation in NO production, as assessed by urinary excretion of its metabolites, nitrite and nitrate (NO2 and NO3; 0.836+/-0.358 vs. 0.107+/-0.019 nmol/microg creatinine). NO production was as much as threefold higher in the L-arginine group (1.853+/-0.206 nmol/g creatinine). This CsA effect is probably related to its vasoconstrictive stimulus. Supplementation with L-arginine, which provides more substrate for NO formation, may enhance vasodilatation and consequently reduce the impairment of renal function. The protection provided by allopurinol may be related to the reduced formation of oxygen radicals, preventing the deleterious effects of lipid peroxidation.

Allopurinol↗

PubMed1997

Nephrotoxicity of amphotericin B is attenuated by solubilizing with lipid emulsion.

Nephrotoxicity is the major adverse effect of conventional amphotericin B (AMB/D), often limiting administration of full dosage. The new liposomal amphotericin B seems to be less toxic. The new liposomal amphotericin B seems to be less toxic. In this study, it is proposed that solubilizing the standard AMB/D preparation with 10% lipid emulsion will attenuate nephrotoxicity. Rats were injected with either AMB/D (Fungizone), AMB, AMB/D plus lipid emulsion (AMB/D/LE), or sodium deoxycholate (D). Renal function studies were performed on day 5. To assess a direct tubular toxic effect, isolated rat proximal tubule suspensions and inner medullary collecting duct cells in culture were exposed to AMB/D, AMB, AMB/D/LE, liposomal amphotericin B, and D for 60 min in normoxia. Lactate dehydrogenase (LDH) release was assessed as an index of cell injury. Creatinine clearance (ml/min per 100 g) averaged 0.79 +/- 0.04 in control rats, 0.29 +/- 0.09 in AMB rats (P < 0.001 versus control), 0.38 +/- 0.04 in AMB/D rats, 0.46 +/- 0.05 in D rats, and 0.78 +/- 0.03 in AMB/LE rats. Renal blood flow (ml/min per 100 g) was 3.45 +/- 0.31 in control, 1.29 +/- 0.28 in AMB, 1.42 +/- 0.23 in AMB/D, 3.03 +/- 0.39 in D, and 2.71 +/- 0.21 in AMB/D/LE rats. The fractional excretion of potassium (%) was 27.3 +/- 1.18 in control rats, 61.6 +/- 7.00 in AMB/D rats, 58.4 +/- 15.32 in AMB rats, and 37.9 +/- 2.06 in AMB/D/LE rats. LDH release (%) in proximal tubules incubated with AMB/D and D was 43.6 +/- 3.39 and 58.6 +/- 4.20, respectively. Addition of lipid emulsion decreased LDH release: 21.6 +/- 1.22 for AMB/D/LE and 26.4 +/- 3.03 for deoxycholate plus lipid emulsion. AMB did not demonstrate any toxic effect in proximal tubule suspensions. D was not toxic to inner medullary collecting duct cells at 0.16 mg/ml, whereas D at a higher dose and AMB induced a significant LDH release. Addition of lipid emulsion did not affect the antifungal activity as assessed by the Etest method. In conclusion, an alternative way of administering standard AMB with reduced nephrotoxicity is proposed.

Amphotericin B↗

PubMed1997

Outcome of acute renal failure in meningococcemia.

We studied 28 consecutive patients (18 males and 10 females), 1-32 years of age, admitted to the intensive care unit from January 1989 to July 1995, with acute renal failure (ARF) due to meningococcal septicemia. All patients were treated with dexamethasone, penicillin, and/or chloramphenicol. Twenty-two patients presented septic shock and needed fluid replacement and vasoactive drugs. Acute renal failure was oliguric in 67.8%. Maximum levels of blood urea and serum creatinine were 210.3 +/- 26.6 mg/dL and 6.9 +/- 1.3 mg/dL, respectively. Metabolic acidosis was observed in 89.3% and hyperkalemia in 43%. The fractional excretion of sodium on day 1 was high (9.9 +/- 0.6%). The urinalysis did not show trace protein, but hematuria was positive in 81%. The mortality rate was 63.3%. In the 10 survivors, oliguria was present for a period of 12.7 +/- 2.4 days, and the period to reach a normal serum creatinine level was 20.2 +/- 4.7 days, although in two female patients, 7 and 17 years old, the elevated serum creatinine persisted. Renal biopsy was performed in one of these patients which revealed bilateral cortical necrosis. These data show that acute renal failure in meningococcemia presents high mortality rate associated to shock; 80% of the survivors recover renal function; and bilateral cortical necrosis occurred in one patient in this series.

Acute Kidney Injury↗

PubMed1997

Outcome of leptospirosis in children.

We conducted a retrospective analysis of 43 consecutive children (35 boys and 8 girls), 4-14 years of age and living in an urban area, who were hospitalized at the Instituto de Infectologia Emilio Ribas (Sao Paulo, Brazil) from January 1989 to December 1995 with an acute illness subsequently diagnosed as leptospirosis. Epidemiologic data indicated contact with contaminated water in most cases (88%). The patient sera reacted most strongly with Leptospira interrogans serovars copenhageni (45%) and icterohaemorrhagiae (32.7%). Jaundice was present in 70% of the patients, elevated transaminase levels in 56%, renal failure in 79%, meningitis in 23%, thrombocytopenia in 65%, and hemorrhagic manifestations in 11.6%. Three children had pulmonary hemorrhage with respiratory failure and one death occurred as a consequence of respiratory failure. We also observed that antimicrobial therapy reduced the extent of renal failure and thrombocytopenia. These data indicate that antibiotics benefit children with late, severe leptospirosis and that severe disease also occurs in children and should be considered in the differential diagnosis.

Acute Kidney Injury↗

PubMed1996

Peculiar electrolytic and hormonal abnormalities in acute renal failure due to leptospirosis.

Hypokalemia in leptospirosis acute renal failure (ARF) was studied in nine patients with severe leptospirosis ARF and five patients with moderate leptospirosis ARF and compared with five patients with severe acute tubular necrosis (ATN) and eight healthy individuals. Urinary volumes of both the severe and moderate leptospirosis groups were higher than those of the severe ATN group. Leptospirosis groups had serum potassium levels lower than those found in the healthy and severe ATN groups. Serum sodium levels were lower in the severe leptospirosis group than in the moderate leptospirosis, the severe ATN, and the healthy groups. There was a positive correlation between the fractional excretion of sodium and potassium in the severe leptospirosis group as well as between serum creatinine and potassium levels in the pooled leptospirosis groups. Urinary pH in the severe and moderate leptospirosis groups was lower than in the severe ATN group. Aldosterone levels were higher in the severe leptospirosis group than in the healthy individuals. Cortisol levels were higher in the leptospirosis groups than in the healthy subjects. These results strongly suggest that hypokalemia in leptospirosis ARF is due to renal potassium wasting potentialized by aldosterone and cortisol, requiring that special attention is given to potassium replacement as well as to volume repletion in the treatment of leptospirosis ARF.

Acute Kidney Injury↗