Search PubMed⌕ Search

Biomedical subjects

M Dhib

Publications and source records attributed to M Dhib.

At least 19 recordsLinked to original sources
PubMed1998

[Extracapillary glomerulonephritis secondary to D-penicillamine. Apropos of 1 case and review of the literature].

Extracapillary glomerulonephritis was diagnosed in a 51-year-old woman after 11 months of D-Penicillamine treatment given for systemic sclerosis. Antineutrophil cytoplasmic antibodies specific for myeloperoxydase were detected. Penicillamine was stopped and the patient was treated with plasma exchanges, cyclophosphamide and corticosteroids. The renal function progressively deteriorated leading to end stage requiring dialysis. Previous reports of extracapillary glomerulonephritis after D-penicillamine are analysed. Several cases with alveolar haemorrhage are consistent with the diagnosis of microscopic polyangiitis.

Adrenal Cortex Hormones↗
PubMed1997

Effect of the serotonin 5-HT4 receptor agonist cisapride on aldosterone secretion in corticotropic insufficiency and primary hyperaldosteronism.

Serotonin (5-HT) stimulates aldosterone secretion in man through activation of 5-HT4 receptors coupled to adenylyl cyclase via a Gs regulatory protein. In adrenocortical cells, the levels of expression of the Gs protein and ACTH receptor are decreased when the cells are deprived of ACTH and angiotensin II (ANG II). In order to examine the possible influence of ACTH and ANG II on the responsiveness of human glomerulosa cells to 5-HT, we have investigated the effect of cisapride, a 5-HT4 receptor agonist, on plasma aldosterone in patients with suppressed plasma ACTH, i.e. patients with corticotropic insufficiency (CI), and in patients with suppressed renin-ANG II activity, i.e. patients with primary hyperaldosteronism (PH) including both aldosterone-producing adenoma and idiopathic hyperaldosteronism. After 2 h of recumbency, all patients received a single oral dose of 10 mg cisapride. In the CI group, cisapride induced a 5-fold increase in plasma aldosterone levels without any modification of plasma renin, potassium or cortisol levels. Combined administration of cisapride and ACTH caused an increase in plasma aldosterone similar to that produced by ACTH alone. In the PH group, cisapride was still able to cause a 3.6-fold increase in plasma aldosterone levels while renin remained suppressed throughout the study. Taken together, these data show that cisapride stimulates aldosterone secretion in CI and PH patients, indicating that prolonged suppression of plasma ACTH or renin-ANG II activity does not affect the sensitivity of glomerulosa cells to 5-HT. The present study also demonstrates that the stimulatory effects of 5-HT and ACTH on aldosterone secretion are not additive.

Adrenocorticotropic Hormone↗
PubMed1996

[Nephrotic syndrome complicating treatment with interferon alpha].

UNLABELLED: We report two cases of nephrotic syndrome with minimal glomerular change complicating alpha-interferon therapy. CASE REPORTS: The first patient was a 60-year-old man with Waldenström's disease who was given 1 million units of alpha-interferon three times a week for 22 months. Acute renal failure developed when a second protocol was started. Renal biopsy revealed intraglomerular deposits and no cellular proliferation. Total remission could not be achieved with corticosteroids. The second case was a 46-year-old man given high dose alpha-interferon (15 million units 3 times a week) for lymph node metastasis of a malignant melanoma. A nephrotic syndrome without renal failure developed during the third month of treatment. Minimal glomerular involvement was seen. Symptomatic treatment led to resolution of the nephrotic syndrome. DISCUSSION: Nine other cases of nephrotic syndrome complicating alpha-interferon therapy have been reported in the literature.

Acute Kidney Injury↗
PubMed1996

Crescentic glomerulonephritis in juvenile chronic arthritis.

Juvenile chronic arthritis (JCA) was diagnosed in 2 young girls. In one of them, antinuclear antibodies (ANA) were strongly positive during the course of erosive polyarthritis. After 5 years followup, severe renal insufficiency occurred. Antineutrophil cytoplasmic antibodies (ANCA) were positive with a perinuclear pattern on indirect immunofluorescence (IIF) and antimyeloperoxidase (MPO) specificity. Renal biopsy showed severe crescentic glomerulonephritis without significant deposits on IIF. Treatment consisted of prednisone and monthly intravenous cyclophosphamide pulse. Renal failure worsened and hemodialysis was necessary. A 2nd patient was referred for polyarthritis with positive rheumatoid factors without positive ANA. The presence of microscopic hematuria led to the discovery of crescentic glomerulonephritis with positive ANCA of anti-MPO specificity. At latest examination, after prednisone for 10 months and azathioprine for 6 months, the patient had moderate proteinuria with normal renal function. These observations emphasize that in juvenile onset chronic polyarthritis, renal microscopic angiitis with ANCA of anti-MPO specificity may occur.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1996

[Light and heavy chain deposition disease with cutaneous and renal manifestations].

INTRODUCTION: Monoclonal light and heavy chain deposition disease is a rare syndrome distinct from light chain amyloid, which is defined by the presence of monoclonal deposits of immunoglobulins in various tissues. CASE-REPORT: A 65-year-old man presented with renal symptoms due to membranoproliferative glomerulonephritis, associated with urticarial papules located on the arms and back. Histological examination of a skin biopsy specimen showed lymphocytic vasculitis. Direct immunofluorescence examination of kidney and skin lesions using anti-gamma 2 and anti-Kappa monoclonal antibodies, showed a similar staining on the basement membrane zone and vessel walls. COMMENTS: As far as we know, this is the first documentation of monoclonal light and heavy chain deposition disease associated with a lymphocytic skin vasculitis and renal involvement caused by similar monoclonal deposits of immunoglobulins in the kidney and skin.

Aged↗
PubMed1994

Pharmacokinetics of sparfloxacin in patients with renal impairment.

The pharmacokinetics of sparfloxacin were studied in 14 renal failure patients (group I, 7 with creatinine clearance of > 10 to 30 ml/min; and group II, 7 with creatinine clearance of < or = 10 ml/min) after a single oral dose of 400 mg. Plasma and urine samples were collected up to 144 h postdosing for determination of parent and total (parent-plus-glucuronide-conjugated) sparfloxacin levels, by high-pressure liquid chromatography assay and UV detection. The elimination of the drug in patients compared with that in healthy volunteers was markedly impaired. The mean elimination half-lives of sparfloxacin were 34.9 and 38.5 h in group I and group II, respectively, versus 19.1 h in healthy volunteers. Conjugated drug half-lives were 23.7, 35.0, and 15.3 h, respectively. The renal clearance of the drug was markedly reduced in the patients, with values of 6.8, 4.8, and 21.2 ml/min determined for group I, group II, and healthy subjects, respectively, for parent sparfloxacin and with values of 31.5, 14.0, and 327 ml/min for conjugated sparfloxacin. The nonrenal clearance of sparfloxacin was moderately, but not significantly, decreased in group II renal failure patients. No difference between the two groups of patients was detected in sparfloxacin levels in plasma. A significant relationship between pharmacokinetic parameters and creatinine clearance was observed only for renal clearance of parent or conjugated sparfloxacin.

Adult↗
PubMed1994

[Pseudomembranous colitis revealing adult hemolytic-uremic syndrome].

A 33 year old woman presented with abdominal pain and bloody diarrhea. A subtotal colectomy was performed. Following surgery the haemolytic uraemic syndrome unmasked. Such surgical forms of haemolytic uraemic syndrome are rare. They demonstrate that the diagnosis is difficult at the initial abdominal period before renal insufficiency and anemia develop. Review of the literature confirms the severe nature of haemolytic uraemic syndrome associated lesions. Haemolytic uraemic syndrome and pseudomembranous colitis with capillary thrombosis would be two forms of a unique affection, i.e. thrombotic microangiopathy.

Adult↗
PubMed1994

[Thrombotic microangiopathy disclosing human immunodeficiency virus infection. Histological and ultrastructural study].

Thrombotic microangiopathy has recently been documented in association with human immunodeficiency virus infection. The authors present the clinical laboratory, histologic and electron microscopic kidney study features of one case of thrombotic microangiopathy revealing human immunodeficiency virus infection. They also review 28 previously reported cases of thrombotic microangiopathy associated with human immunodeficiency virus infection and discuss different pathogenic hypothesis which could be involved in genesis of human immunodeficiency virus-associated thrombotic microangiopathy.

Adult↗
PubMed1993

Pharmacokinetics and pharmacodynamics of zolpidem following repeated doses in hemodialyzed uraemic patients.

Zolpidem, an imidazopyridine derivative, is a chemically novel, non-benzodiazepine hypnotic agent. Many uraemic patients complain of sleep disorders and ask for hypnotic medication which is well tolerated both clinically and biologically in such patients. We studied the pharmacokinetics and pharmacodynamics of zolpidem in 12 end-stage renal patients regularly treated by hemodialysis three times a week. Zolpidem (10 mg) was given orally for 14 or 21 days. Pharmacokinetic and pharmacodynamic evaluations were repeated at the end of the study on day 14 or day 21. Cmax, Tmax, t1/2 and the area under the curve were not modified in hemodialyzed patients. After daytime dosing, zolpidem induced the same level of sleepiness after the first and last dose and was well tolerated as a hypnotic agent after the night-time dosing. From these results, it can be said that zolpidem may be administered safely to patients with severe renal impairment without any modification of the dosage regimen.

Adult↗
PubMed1992

[Drug-induced nephropathies].

Drug-induced nephropathies are frequent. Glomeruli, tubes, interstitium and arterioles may be altered. In this paper, we have tried to know if clinical, biological or histological signs of drug-induced nephropathies are similar or different from those observed in idiopathic nephropathies. We demonstrate that drug-induced nephropathies do not present any particular clinical or biological signs. We find that minimal changes and membranous glomerulopathies are the main lesions observed. In contrast, glomerular proliferations are very rare. Drug-induced tubulopathies are characterized by tubular necrosis with variable extension. Interstitial lesions are absolutely identical to those observed in immunologically mediated nephropathies. Vascular lesions are very rare. It should be noticed that evolution of drug-induced nephropathies differs completely from idiopathic nephropathies. Indeed, renal lesions are usually regressive when the drug administration is stopped. In conclusion, it appears that drug-induced nephropathies mimic other forms of nephropathies. It is important to know that some drugs are excellent experimental models to reproduce some aspects of human renal pathologies.

Animals↗
PubMed1992

[Should adult nephrotic syndrome secondary to idiopathic extramembranous glomerulonephritis be treated? An approach by decisional analysis].

Treatment of nephrotic syndrome (without renal insufficiency) due to idiopathic membranous glomerulonephritis in adults is not clearly defined. A decisional analysis was done from data published in literature in order to define the best therapeutic choice. Three therapeutic strategies were studied: corticosteroids (either 125 mg/48 h or 30 to 60 mg/24 h), alternate therapy according to Ponticelli protocol (corticosteroids and chlorambucil), abstention of therapy. The data were divided in two groups according to the time of follow-up. The first group allows a decisional analysis for a short period of time (16 to 37 months), the second group allows this analysis for a longer period of time (54 to 65 months). The results differed according to the length of post treatment follow-up. For the shorter follow-up, corticosteroids or the association corticosteroids and chlorambucil appeared to be better than no treatment. For longer follow-up, any treatment shows an advantage in comparison to abstention of therapy. Our tentative conclusion is to propose only symptomatic treatment for this disease.

Adrenal Cortex Hormones↗