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Biomedical subjects

M Marcondes

Publications and source records attributed to M Marcondes.

At least 37 records · Page 2Linked to original sources
PubMed1993

Nephrotoxicity of human Bence Jones protein in rats: proteinuria and enzymuria profile.

The effect of intravenous administration of 80 mg purified human Bence Jones protein twice weekly for 5 weeks was investigated in male Wistar rats (N = 7; 2 months old). A state of immunological tolerance was demonstrated by the absence of a B-cell response (plaque-forming cells and hemagglutination titers) and by the absence of detectable antigen or antibody deposition in glomeruli, as indicated by light and electron microscopy. No rise in blood urea level was detected (33.9 +/- 4.3 vs 32.8 +/- 1.3 mg%). There was an increase in proteinuria (5.3 +/- 0.9 vs 32.8 +/- 4.0 mg/day), mainly due to Bence Jones protein excretion (0 vs 29.2 +/- 5.2 mg/day), with a slight but significant increase in albuminuria (0.2 +/- 0.1 vs 1.0 +/- 0.2 mg/day). There was a significant increase of lysosomal N-acetyl-beta-D-glucosaminidase in the urine (6.1 +/- 1.3 vs 72.7 +/- 18.8 mU/mg in creatinine). Lysosomal accumulation of Bence Jones protein in proximal tubular cells was evidenced by immunoelectronmicroscopy with protein A-gold. These results clearly showed proximal tubular dysfunction induced by chronic Bence Jones protein administration, without interference of autologous immune response as demonstrated by immunological state of tolerance.

Animals↗
PubMed1993

[Effect of treatment with chlorthalidone on reduction of left ventricular mass in patients with systemic arterial hypertension].

PURPOSE: To evaluate the effects of the use of chlorthalidone on left ventricular mass of patients with mild and moderate systemic arterial hypertension (SAH). METHODS: Twenty-nine patients with mild and moderate SAH were studied with mean age of 48.4 years and 16 men. Clinical evaluation, systolic (SBP) and diastolic (DBP) blood pressure and heart rate (HR), in supine and standing positions, were obtained before and every 3 weeks, after 2 with placebo, during 12 weeks of treatment with 50mg of chlorthalidone each 48 hours. Laboratory data (hemogram, sodium, potassium, urea creatinine, glucose, hepatic aminotransferases and urinalysis) were done before and at end of study. Echocardiographic study was performed by M-mode before and after 6 and 12 weeks of treatment, and obtained the following data: diastolic diameter (DdLV), diastolic septum (DSTLV) and posterior wall thickness (PWTLV) of left ventricle. The left ventricular mass (LVM) was calculated by the formula: LVM = (DSTLV+PWTLV+DdLVE)3 - (DdLV)3 x 1.05/body surface, in g/m2. RESULTS: A significant reduction of SBP (p < 0.0001), DBP (p < 0.001) in supine and standing positions. HR did not show statistical difference. At echocardiographic study, M-mode, was observed a significant reduction of LVM after 12 weeks of treatment (181 +/- 67 to 156 +/- 34 g/m2, p < 0.01). CONCLUSION: Chlorthalidone was effective to control blood pressure and to reduce LVM of patients with SAH.

Adult↗
PubMed1992

Higher salt consumption, digoxin-like factor, and nifedipine response are associated with salt sensitivity in essential hypertension.

In addition to demonstrating evidences of increased sympathetic nervous system activity and marked left ventricular hypertrophy in salt-sensitive hypertensives, our group has also reported increased weight gain with salt overload in these patients. The increased weight gain suggests volume expansion, a situation already shown to increase plasma levels of a Na, K-ATPase inhibitor. Therefore, in the present study, digoxin-like factor (DLF) serum levels, spontaneous salt ingestion, nifedipine hypotensive effect, and plasma renin activity were evaluated in essential hypertensive subjects. Thirteen essential hypertensive outpatients were studied sequentially on an ad lib diet, a low salt diet (LSD = 30 mEq Na/day), and a high salt diet (HSD = LSD + 171 mmol/L NaCl/day), 1 week each. On the seventh day of LSD and HSD, DLF levels, mean blood pressure (MBP) response to nifedipine (10 mg sublingual), and plasma renin activity were measured. The MBP percent change from the seventh day of LSD to the seventh day of HSD (salt sensitivity) ranged from -13.7 to 20.9%. A positive correlation (r = 0.64, P < .01) was observed between salt sensitivity and 24-h urinary sodium excretion with an ad lib diet. The DLF serum levels correlated with the salt sensitivity both on LSD (r = 0.50, P < .05) and on HSD (r = 0.53, P < .05). Salt sensitivity was positively correlated with the difference of response to nifedipine between HSD and LSD (r = 0.78, P < .001). Plasma renin activity correlated inversely with DLF on LSD (r = -0.51, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Nodular diabetic glomerulosclerosis without diabetes mellitus.

A 66-year-old white man presented with severe chronic renal failure. He had no past or present symptomatic glucose intolerance nor a family history of diabetes mellitus. Several fasting plasma glucose determinations, hemoglobin Alc and an oral glucose tolerance test were normal. Funduscopic ophthalmoscopy and retinal fluorescein angiography did not demonstrate diabetic retinopathy. The kidney biopsy showed nodular diabetic nephropathy, with increased mesangial matrix, thickened glomerular basement membrane, and afferent and efferent glomerular arteriolar hyalinization. The diagnosis of nodular diabetic nephropathy was made in this patient in the absence of past or present or familial evidence of diabetes mellitus.

Aged↗
PubMed1992

Late evaluation of glomerular filtration rate, proteinuria, and urinary acidification after acute tubular necrosis.

Fourteen patients were studied 2 to 36 months after acute tubular necrosis. It was observed that 43% of the patients had decreased glomerular filtration rate. These patients were older and had lower urinary excretion of ammonium and titratable acidity. Proteinuria greater than 150 mg/day, without reaching a nephrotic level, was found in 92% of the patients. The presence of oliguria, the demand of dialysis, and the acute tubular necrosis etiology were not statistically different among the patients who recovered their glomerular filtration rate either totally or partially.

Adult↗
PubMed1992

IgA nephropathy: acute renal failure, acute tubular necrosis, and features of postinfectious acute glomerulonephritis.

From 1976 to 1987 on our Nephrological Unit, 57 patients with IgA nephropathy (IgAN) proven by renal biopsies were found. Three of those presented with acute tubular necrosis (ATN) and glomerulitis, without extrarenal predisposing cause in two; and showed, as prominent manifestation, a severe acute renal failure syndrome (ARFS), needing dialytic treatment. All three had hematuria, which was macroscopic in two and microscopic in one. Thus the prevalence of the association of glomerulitis and ATN was about 5.2%. There was complete recovery of renal functions in all three patients, but the usual symptomatology of IgAN. Two patients presented polymorphonuclear neutrophils infiltration of glomerular capillaries and in one of them, electron-dense deposits on the epithelial side of glomerular basement membrane ("humps") were observed, as well as those identified in the mesangial area. The glomerular polymorphonuclear neutrophils infiltration and endothelial cells proliferation (cases 1 and 3), the presence of "humps" (case 1), high antistreptolysin O (ASO) titers (cases 1 and 2), and low serum complement levels (case 1), suggest the possibility that antigens able to cause postinfectious glomerulonephritis (streptococcal or not) could induce in some individuals, by another immunopathogenetic route, mixed histopathological and clinical features of IgAN and postinfectious glomerulonephritis.

Acute Disease↗
PubMed1992

Use of dextran 70 to estimate peritoneal lymphatic absorption rate in CAPD.

Peritoneal lymphatic absorption rate (LAR) in 15 patients on a CAPD program was measured by estimation of the disappearance of dextran 70 from the peritoneal cavity. The LAR was 1.03 +/- 0.45 ml/min. The cumulative lymphatic absorption, cumulative net transcapillary ultrafiltration, calculated net ultrafiltration (CUF) and measured net ultrafiltration (MUF) at 4 h exchange were respectively: 261 +/- 127 ml, 694 +/- 134 ml, 446 +/- 135 ml and 409 +/- 136 ml. Calculated and measured net ultrafiltration didn't differ significantly. An inverse correlation between MUF and LAR and a positive correlation between MUF and the ratio for dialysate glucose concentration at 4 hand dialysate glucose at 0 h (G4/G0) were observed (r = -0.522 and 0.547, respectively, p < 0.05). The multiple correlation coefficient between the MUF and LAR plus G4/G0 was higher (r = 0.617, p < 0.05). Peritonitis and the presence of diabetes didn't interfere with LAR. We have concluded that lymphatic absorption plus peritoneal transfer rate of glucose are important determinants of intraperitoneal volumes and that dextran 70 is a useful marker to measure lymphatic absorption.

Absorption↗
PubMed1991

Left ventricular hypertrophy is more marked in salt-sensitive than in salt-resistant hypertensive patients.

Besides the duration and severity of hypertension, several other factors have been shown to be related to left ventricular hypertrophy (LVH) in essential hypertension. The present study was conducted to examine the influence of salt sensitivity on LVH. Fifteen essential hypertensive ambulatory patients were submitted to a low-salt (30 mEq of Na/day for 7 days) and a high-salt (200 mEq of Na/day for 7 days) diet after 12 weeks on placebo. Daily urine collection was obtained during the whole study. After the placebo period, all patients were submitted to a complete clinical and laboratory investigation that included an echocardiogram (M-mode and two-dimensional). Five patients were salt-sensitive (mean blood pressure (BP) increase from the seventh day of the low- to the seventh day of the high-salt diet greater than 10%). No differences in weight, sex ratio, and duration of hypertension were obtained between salt-sensitive and -resistant patients. The initial BP was higher in the salt-sensitive patients. However, the difference was small and without statistical significance. The left ventricular weight was higher in the salt-sensitive than in salt-resistant patients (148 +/- 51 vs. 109 +/- 32 g/m2, p less than 0.05). The left ventricular end-diastolic diameter was also higher in the salt-sensitive patients (50 +/- 10 vs. 43 +/- 6 mm, p less than 0.05). The interventricular septum and posterior wall thicknesses were higher in salt-sensitive patients, although they did not reach statistical significance. In conclusion, salt-sensitive essential hypertensive patients are at a higher risk to develop LVH.

Adult↗
PubMed1989

Essential hypertension and histocompatibility antigens. A linkage study.

It is well established that genetic and environmental factors are involved in the etiology of essential hypertension. The presence of genes predisposing to essential hypertension in the human leukocyte antigen (HLA) complex is controversial because studies of an association between HLA antigens and essential hypertension have failed to yield consistent results. Our aim in the present study was to further investigate this issue through the method of linkage analysis. Analysis of 96 hypertensive siblings distributed in 31 families indicated a significant distortion (p = 0.0009) of the normal segregation pattern of inheritance of HLA haplotypes. Thus, our data indicate that at least one of the genes responsible for genetic predisposition to essential hypertension is located very near or within the HLA complex.

Adolescent↗
PubMed1989

Salt sensitivity in human essential hypertension: effect of renin-angiotensin and sympathetic nervous system blockade.

We studied the acute effect of oral captopril (25mg) and clonidine(300 micrograms) on blood pressure (BP) in patients with essential hypertension successively maintained on a low (LSD) and high (HSD) salt diet. Seven patients were salt sensitive (SS) and seven were salt resistant (SR). The maximal decrease in diastolic BP caused by captopril in patients on the LSD was greater in SS than SR individuals. Baseline urinary norepinephrine levels did not change from LSD to HSD (p greater than 0.05) in SS patients and decreased in SR patients (p less than 0.05). The maximal decrease in mean BP during the clonidine test was the same for both diets (p greater than 0.05) in SS patients and was lower (p less than 0.05) for the HSD in SR patients. SS patients on the HSD presented a higher decrease in systolic BP than SR patients (p less than 0.05) during the clonidine test. These data suggest overactivity of the renin-angiotensin system in SS patients on the LSD and of the sympathetic nervous system in SS patients on the HSD and that the clonidine test could be a good indicator for identifying SS and SR patients.

Adult↗
PubMed1989

Effect of posture and physical activity on urinary protein excretion by patients with glomerular proteinuria diseases.

The rate of urinary protein excretion (Uprot.V) was evaluated in 20 patients with massive proteinuria caused by various histopathological types of glomerular disease. Measurements were made during five consecutive periods: period A (overnight bed rest) and periods B, C, D and E corresponding to normal everyday upright physical activity. Mean Uprot.V was significantly lower during period A (8.2 +/- 1.3 mg/min, mean +/- SEM) than during all the periods of physical activity (11.8 +/- 1.8 mg/min). For 5/20 patients, physical activity induced a mean percent increase of 340 +/- 200% and for 11 an increase of 51 +/- 7% was observed. Only in 4 patients was the rate of urinary protein excretion unaffected or decreased on the average by -20 +/- 9% during physical activity.

Exercise↗
PubMed1988

Prolonged inhibition of angiotensin II attenuates glycerol-induced acute renal failure.

1. A lipophilic competitive angiotensin II antagonist (octanoyl-[8-leucine]-angiotensin II, OCTLEU A-II) was used to partially block the renin-angiotensin system in rats with glycerol-induced acute renal failure. The rats, which were maintained either on a normal or on a low-sodium diet, were dehydrated for 24 h before injection of glycerol. Daily intramuscular injections of OCTLEU A-II in peanut oil were started 48 h before glycerol administration to assure an angiotensin II blockade up to 48 h after glycerol administration. 2. In the low-sodium group (N = 23), acute renal failure was significantly attenuated in OCTLEU A-II-treated rats (N = 9) when compared with the controls (N = 14). The following values (means +/- 1 SD) for renal function parameters were obtained for the treated and control groups: urine volume, 15.2 +/- 11.7 vs 1.4 +/- 2.0 ml/24 h (P less than 0.01); plasma creatinine 5.5 +/- 1.3 vs 8.6 +/- 1.3 mg/dl (P less than 0.01); creatinine clearance 0.23 +/- 0.16 vs 0.03 +/- 0.03 ml min-1 kg-1 (P less than 0.01); plasma potassium 6.6 +/- 1.5 vs 10.1 +/- 1.9 mEq/1 (P less than 0.01); and sodium excretion fraction 3.0 +/- 4.0 vs 21.6 +/- 17.4% (P less than 0.02). Mean arterial blood pressure was 107 +/- 23 mmHg for the OCTLEU A-II-treated animals and 102 +/- 18 mmHg for the controls. 3. The rats on a normal sodium diet (N = 16) developed moderate non-oliguric renal insufficiency. The OCTLEU A-II-treated (N = 8) and control (N = 8) groups did not differ in any of the parameters measured. 4. The present results show that sodium restriction aggravates glycerol-induced acute renal failure and that the renin-angiotensin system participates, since its inhibition at the level of the angiotensin II receptor attenuates the extreme loss of renal function and prevents anuria.

Acute Kidney Injury↗
PubMed1988

Nephritis blunts urinary kallikrein excretion and aggravates DOCA/NaCl hypertension in rats.

1. Normal rats and passive Heymann membranous glomerulonephritic rats were chronically treated with DOCA/NaCl for 9 weeks. Normal and untreated nephritic rats were used as controls. Urinary kallikrein excretion (UKE), proteinuria and tail blood pressure (BP) were determined in awake rats. Glomerular filtration rate (GFR), plasma renin activity (PRA), and plasma potassium (PK) concentration were measured at the end of the experiment. 2. Comparison between basal and 9th-week measurements indicated that DOCA/NaCl administration significantly increased (P less than 0.05) UKE (3.96 +/- 0.30 vs 7.60 +/- 1.51 U/24 h) and BP (118 +/- 2 vs 135 +/- 6 mmHg) in normal rats, whereas in nephritic DOCA/NaCl-treated rats, UKE was unaltered (3.80 +/- 0.50 vs 3.40 +/- 0.30 U/24 h) and BP increased to higher levels (117 +/- 2 vs 152 +/- 3 mmHg) than in the normal DOCA/NaCl group (P less than 0.05). Passive Heymann nephritis alone did not affect UKE (3.56 +/- 0.40 vs 3.60 +/- 0.80 U/24 h) or BP (124 +/- 2 vs 125 +/- 2 mmHg). 3. At the end of the study, PK was decreased and PRA totally suppressed in both normal and nephritic DOCA/NaCl-treated rats. Proteinuria was more pronounced in nephritic DOCA/NaCl-treated rats (44.8 +/- 5.2 mg/day) than in control nephritic animals (15.1 +/- 2.4 mg/day) and GFR was increased equally in both DOCA/NaCl-treated groups. 4. The failure of nephritic rats to respond to DOCA/NaCl by increasing UKE was not associated with any significant derangement of renal function or structure and may have been related to the aggravation of arterial hypertension in this group.

Animals↗
PubMed1986

Acute glomerulonephritis: three episodes demonstrated by light and electron microscopy, and immunofluorescence studies--a case report.

The patient, a white boy, had 3 episodes of recurrent acute glomerulonephritis at 7, 12 and 17 years of age. The episodes were preceded by impetigo and there was a good clinical and laboratorial recovery after all of them. Renal biopsies were performed during the acute episodes, and the light, immunofluorescence and electron microscopy studies showed only lesions typical of acute glomerulonephritis. Four months after the third episode another renal biopsy demonstrated only lesions compatible with the subsiding stages of acute glomerulonephritis.

Acute Disease↗
PubMed1986

Sodium handling and renal hemodynamics in euvolemic and volume-expanded nephrotic rats.

Normal (N) rats and rats with nephrotoxic serum nephritis (NSN) were used in whole-kidney and micropuncture studies while being kept euvolemic by homologous plasma infusion and after isotonic volume expansion (VE). During euvolemia, whole kidney and single nephron (SN) glomerular filtration rate (GFR), as well as urinary sodium excretion (UNa X V), were significantly lower in NSN rats (GFR = 0.40 +/- 0.06 ml/min; SNGFR = 14.4 +/- 1.9 nl/min; UNa X V = 0.05 +/- 0.02 microEq/min) than in controls (GFR = 1.14 +/- 0.06 ml/min; SNGFR = 32.7 +/- 2.0 nl/min; UNa X V = 0.05 +/- 0.02 microEq/min); fractional proximal and "distal" (beyond the proximal convoluted tubule) sodium reabsorption rates were significantly higher than N, further depressing urinary sodium output. Saline expansion significantly elevated GFR and decreased renal vascular resistance (RVR) in both N and NSN rats. In the latter, however, GFR remained below, and RVR above, levels observed in N rats. Urinary sodium excretion increased markedly with saline expansion in N rats, reaching 26.9 +/- 1.31 microEq/min. NSN rats exhibited a blunted natriuretic response to expansion (UNa X V = 3.85 +/- 1.02 microEq/min); however, despite a still depressed GFR and increased RVR, urinary sodium excretion in NSN rats reached levels well above euvolemic control. Fractional proximal and "distal" tubular sodium reabsorption rates were depressed by VE in both N and NSN rats. However, this depression was less evident in NSN rats, particularly in the "distal" nephron, suggesting that the stimulus for sodium reabsorption in these segments was somehow enhanced in NSN rats. Fractional potassium excretion was increased to a much greater extent in NSN than in N rats. This finding, associated with the small depression of fractional sodium reabsorption in the "distal" nephron of NSN rats, suggests a participation of elevated levels of circulating aldosterone in the sodium retention observed in this model.

Animals↗