PubMed Health⌕ Search

Biomedical subjects

J M Suc

Publications and source records attributed to J M Suc.

At least 91 records · Page 5Linked to original sources
PubMed1988

Localization of a renal kallikrein immunoreactive-like substance in rat ureter.

An antibody against rat kallikrein was produced in rabbits and its localization was studied in various organs of the rat to confirm its specificity. The distribution of immunoreactive kallikrein was studied in rat ureter by use of immunochemical techniques. Ureteral tissue was fixed in Zamboni's-glutaraldehyde fixative and immunostained with indirect immunofluorescence and the peroxidase-antiperoxidase (PAP) method for light and electron microscopy. Preabsorption of the primary polyclonal antiserum with purified rat urinary kallikrein and substitution with normal serum were used as controls. By light microscopy, kallikrein was localized in the lamina propria and in the adventitial connective tissue surrounding the entire ureter. Immunoelectron microscopy confirmed this immunolocalization. Immunoreactive kallikrein was concentrated in fibroblasts of connective tissue and was not present in collagen fibers. Immunoreactivity was associated with the Golgi complex, free polyribosomes, and rough endoplasmic reticulum. No immunostaining was observed in other subcellular components of fibroblasts.

Animals↗
PubMed1988

[Arterial hypertension with hyperkalemia, tubular acidosis and normal renal function: Gordon syndrome and/or pseudohypoaldosteronism type II?].

Basic examination of Mr S., 45 years of age, short in stature and overweight (1.60 m, 76 kg), was carried out because of the mild hypertension (mean AP 125 mm Hg) from which he had suffered for 20 years. The results were as follows: (1) variable hyperkalemia: plasma potassium values were 5.3 to 6.9 mmol/l; (2) normal renal function: serum creatinine 91.5 mumol/l, clearance of inulin 136.6 ml/mn; (3) proximal tubular acidosis: plasma bicarbonate and chloride values were 18.4 and 109 mmol/l, respectively; urinary pH was 7.1 with negative H+ ions urinary excretion (-33 mumol/mn); when plasma bicarbonate level was raised to 26 mmol/l by acute loading, fractional excretion of bicarbonate increased to 19,5 p. 100 while plasma potassium value decreased to 4.2 mmol/l; (4) low PRA (0.29 ng/ml/h) and normal plasma aldosterone concentration (63 pg/ml) with a normal intake of sodium and in a recumbent position. Plasma atrial natriuretic factor (ANF) level was normal: 14 fmol/ml. Intravenous infusion of ANF for 2 h (1 microgram/mn) induced the expected increases in urinary flow rate, and sodium and potassium excretions (+226, +307 and +171 p. 100, respectively). Intravenous infusion of isotonic saline (2 l in 2 h) and oral administration of fludrocortisone acetate for 4 weeks (400 micrograms per day) resulted in a normal decrease in PRA and plasma aldosterone concentration, a normal rise in plasma ANF level (22 and 42 fmol/ml) while slightly increasing AP without improving bicarbonaturia and acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1988

[Segmental renal hypoplasia of an adult originating from pseudo-tumor hyperreninism].

A 38 year-old man was admitted for severe hypertension with hypokalemia. Blood pressure was 180-120 mmHg, funduscopic examination revealed grade II retinopathy and left ventricular hypertrophy was present. Laboratory data disclosed: natremia = 140 mmol/ml, kalemia = 2.8 mmol/l, chloride = 105 mmol/l, bicarbonate = 30 mmol/l, creatinine clearance = 100 ml/mn, natriuresis = 140 mmol/day, kaliuresis = 80 mmol/day. Intravenous pyelography was normal. Angiography revealed a defect in the mid third of the right kidney without arterial abnormalities. Study of renin angiotensin aldosterone system showed: plasma renin activity: peripheric blood = 36 ng/ml/h (normal range I to 2), right renal vein = 30 ng/ml/h. Left renal vein = 18 ng/ml/h, inferior cava vein = 19 ng/ml/h. Plasma aldosterone level = 86 ng/100 ml (normal range 10 to 15). Captopril acute administration was followed by a fall of BP to 70-50 mmHg at 2 hours. Right nephrectomy was performed and revealed an ischemic retracted cortical area without necrosis nor tumoral aspect. The day after BP was 140/80 mmHg. Eight days after, kaliemia was 4.2 mmol/l, PRA was 0.5 ng/ml/h. Light microscopy showed that affected area was sharply delimited from surrounding normal tissue. In this area, glomeruli were present and seemed more numerous as usual; interstitial fibrosis and infiltrates of inflammatory cells were also noted. The main fact was tortuosities of intralobular arteries, thickened, with intimal proliferation. There was a pelvic recess near this cortical tissue. Immunofluorescence findings: antirenin serum fixed on JGA but also on interlobular arterial walls and on peritubular interstitium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Lateralization of renin secretion in renovascular hypertension with bilateral arterial stenosis].

A retrospective analysis of peripheral and renal vein plasma renin activity has been performed in 9 patients with bilateral renal artery stenosis (3 fibromuscular dysplasia and 7 atherosclerosis). In all cases angiography showed a reduction of the arterial diameter of more than 70 p. 100. The renal artery was occluded in 3 cases. All patients received a constant sodium diet (100 mEq/day). Peripheral PRA values were classified as normal or low in 6 cases (less than 2.8 ng/ml/h) and high in one case (greater than 2.8 ng/ml/h): this values concerned 2 cases with renal artery occlusion and 1 case with a narrowing of 90 p. 100. Renal venous renin ratio of 1.5 or more has been found in 8 cases. In one case, the stenosis was quite symmetrical (70 p. 100) and the ratio less than 1.5. The secretion index has been calculated as the ratio between the venoarterial difference of both affected and unaffected side over the arterial value of PRA (V-A/A). On the more stenosed side, was found a V-A/A ratio of 0.5 or more. This ratio is particularly high in case of artery thrombosis, but there is no correlation between the ratio and the degree of stenosis. On the contralateral side, where the lesions were less important, the V-A/A ratio was low, ranging from 0 to 0.2; this estimation of renin secretion was found despite a significant stenosis on the angiography. 7 patients underwent PTA or surgery. 2 kidneys with arterial thrombosis were nephrectomized. In 5 cases the surgical treatment is performed on the 2 sides during the same procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

[Renal cholesterol embolisms: apropos of 6 case reports].

Often unrecognized, renal cholesterol embolization generally results in renal failure and a high rate of death. In the recent years, it was discovered only during autopsy, but now antemortem observations are not exceptional. In the most cases, the existence of a triggering factor may suggest a iatrogenic cause. We report six patients who developed cholesterol atheroembolic renal disease after aortic surgery and/or retrograde catheterization. Cholesterol embolism was demonstrated by the finding of cholesterol crystals in the arteriolar lumens: either on renal biopsies, or on skin biopsy. The five surviving patients required dialysis with recovery of renal function in only one case. Three of four patients on regular dialysis treatment died of unrelated complications. The responsibility of angiography in the origin of acute renal failure appeared major in this report. It is the rupture of an eroded atherosclerotic plaque caused by the catheter which causes the release of large quantity of cholesterol crystals in the circulation. Therefore, in the atheromatous patients, it appears safer to realize a computerized i.v. angiography.

Acute Kidney Injury↗
PubMed1988

[An exceptional cause of renal colic. Castleman's tumor. Lymphonodular angiofollicular hyperplasia].

The case of a 38-year-old man with renal colic due to compression by an abdominopelvic mass is reported. Histologic examination of the mass led to the diagnosis of giant lymph node hyperplasia or Castleman disease. Surgical removal of the lesion ensured complete recovery with no recurrence after 32 months follow up. Giant lymph node hyperplasia usually develops in the mediastinum, but superficial and abdominopelvic forms are seen occasionally. Pathogenic hypotheses are discussed. Outcome is usually favorable following surgical excision but rare multifocal forms with a potentially poor prognosis have been reported.

Adult↗
PubMed1987

Short lasting increase in urinary specific kallikrein activity during long term administration of furosemide.

Furosemide was administered for seven days to normal rats. Urinary kallikrein excretion showed a biphasic response during the seven consecutive days of study. During the initial three days only the kininogenase activity showed a significant increase without any variation in the excretion of the immunoreactive kallikrein. The specific urinary kininogenase activity was therefore enhanced. After three days of furosemide administration, both the urinary kininogenase activity and urinary immunoreactive kallikrein were augmented. The urinary specific kininogenase activity was that time no more different when compared to the basal value. Considering the delay time of three days, this second part of the response could be a mineralocorticoid mediated effect. In this respect, kidney level of immunoreactive and kininogenase activity of kallikrein are also increased after seven days of furosemide administration. However the short lasting increase in urinary specific kininogenase activity observed during the initial three days is due to a change in the ratio active versus inactive kallikrein without any variation of total kallikrein. It is possible that this immediate response results of a direct effect of furosemide acting either on the preferential excretion of the active form or on the activation of the prokallikrein in the urine.

Animals↗
PubMed1987

Direct radioimmunoassay of rat urinary kallikrein: its application to the determination of active and inactive kallikrein concentration after HPLC analysis.

Rat urinary kallikrein (RUK) was purified to apparent homogeneity by a three-step procedure and antibodies were raised in rabbits. Renal kallikrein exists as an active and an inactive form. A specific radioimmunoassay (RIA) was developed to measure directly the total kallikrein. The antibody used in this radioimmunoassay recognized both forms. No cross reactivity was detected with trypsin, esterase A or human urine. When iodinated rat urinary kallikrein was used, the detection range was between 0.125 and 16 ng with 6.5% intraassay variation and 8.1% between assay variation. Intrarenal kallikrein was measured in renal tissue after homogeneisation and solubilisation. Correlations between this RIA and the kininogenase activity or the amidolytic activity were highly significant. Since kallikrein exists as an inactive precursor the direct measurement of the total immunoreactive protein differs from activities determinations. An HPLC ion exchange system has been developed to separate active and inactive forms directly from urine, with a recovery of 79 +/- 11%. This procedure permits measurement of inactive forms. Rat urine contains as much inactive kallikrein as active kallikrein.

Animals↗
PubMed1987

Compared effects of a low and a high sodium diet on the renal and urinary concentration and activity of kallikrein in normal rats.

Different sodium intakes may affect or alter the urinary excretion of renal kallikrein. We have compared the renal and the urinary effects of sodium depletion and sodium loading with 1% NaCl on total kallikrein, using a direct radio-immunoassay against immunoreactive kallikrein and on active kallikrein assessed by a kininogenase assay with a kinin radio-immunoassay. Sodium depletion resulted in an increase in renal and urinary excretion of both the immunoreactive kallikrein and the kininogenase activity. Sodium loading resulted in a slight but significant decrease in renal tissue immunoreactive kallikrein content without any change in the kininogenase activity, while the urinary excretion of the kininogenase activity was greatly increased and the urinary immunoreactive kallikrein remained steady. This sodium depletion induces consistent effects at the renal and urinary level, resulting probably from a stimulation of biosynthesis. However, during sodium loading, renal and urinary measurements of kallikrein are dissociated. Furthermore, kininogenase activity and immunoreactive kallikrein are not correlated in either of the two studied compartments. Thus sodium loading seems to induce independent effects at the renal and urinary levels, possibly resulting from different mechanisms.

Aldosterone↗
PubMed1987

[First consultations in nephrology. Comparison of 2 multicenter studies conducted at a 5-year interval].

An investigation of "kidney outpatient" first consultations carried out in 1985 with the cooperation of 19 nephrological teams distributed all over France. Each team had taken part in a similar investigation in 1980. The work allowed to collect 1200 records. Analysis of the main results is presented. The comparison between the 1980th and the 1985th investigations shows a remarkable stability of the results, but suggests two new and interesting features: the progress of Dip-stick studies and serum creatinine concentration in general practice and the decreasing part taken by hypertension in "kidney disease out-patient" activity in 1985.

Adult↗
PubMed1986

Hydrolysis of rat high molecular weight kininogen by purified rat urinary kallikrein: identification of bradykinin as the kinin formed.

We have previously reported that, although human urinary kallikrein, like glandular kallikreins for other species, releases lysyl-bradykinin from homologous and heterologous substrates, rat urinary kallikrein released a kinin which migrated like bradykinin in CM-cellulose chromatography and polyacrylamide gel electrophoresis (BBA677, 471, 1981). In the study we definitively established the nature of the kinin produced by rat urinary kallikrein by using purified enzyme and substrate, HPLC, radioimmunoassay and N-terminal analysis. Rat urinary kallikrein was purified to apparent homogeneity by a procedure which included affinity chromatography on aprotinin agarose. The kinin produced by rat urinary kallikrein acting on either pure rat high molecular weight kininogen or rat plasma or semipurified bovine and dog plasma was identified as bradykinin. This observation provides the evidence of species differences in the specificity of glandular kallikreins acting on kininogens.

Animals↗
PubMed1986

Change in cortical active kallikrein during the onset of Goldblatt hypertension in the rat.

In two-kidney, one clip hypertensive rats renal cortical kallikrein was studied one and two weeks following induction of the hypertension in comparison with sham time controls. Cortical active kallikrein was lower in hypertensive rats only at week 2, although blood pressure was significantly higher one week after clipping. Total cortical kallikrein was however never different in sham control and in hypertensive rats. This results provide evidence for a change in the activation of prekallikrein during the onset of Goldblatt hypertension.

Animals↗