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J Cledes

Publications and source records attributed to J Cledes.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Dilatation of bile ducts in polycystic kidney disease in adults].

We report the cases of 4 adult patients with polycystic kidney disease and dilatation of bile ducts. Dilatation involved the extra-hepatic bile ducts in all 4 cases and also affected the intra-hepatic bile ducts in 3 cases. A prospective ultrasonographic study in search of biliary tract abnormalities was undertaken in 40 patients with dominant polycystic kidney disease. No bile duct dilatation was found in this series, which indicates that the lesion is rare. The 4 cases reported here increase the collection of hepatobiliary lesions associated with polycystic kidney disease of adults.

Bile Duct Diseases↗
PubMed1990

Captopril induces correction of postrenal transplant erythremia.

Kidney transplant patients may develop post-transplant erythremia (PTE), and in order to avoid thromboembolism venesection, anticoagulation and native kidney removal have been suggested. We propose captopril as an alternative therapy for PTE. Seven hypertensive PTE patients, aged 42 +/- 10 years with stable renal function, were investigated to exclude primary or secondary polycythemia. All patients manifested true erythrocytosis [red blood cells (RBC) mass greater than 20% of predicted level] with concomitant increases in hematocrit and hemoglobin levels. Captopril was introduced in gradually increasing doses up to 75 mg/day under careful monitoring of blood pressure and renal function. Weekly follow-up was arranged to evaluate drug efficacy. After captopril, a significant reduction with normalization of the RBC mass (42 +/- 4 vs 31 +/- 5 ml/kg: P less than 0.005) was observed. The RBC counts and hematocrit and hemoglobin levels also decreased. One patient had recurrent erythrocytosis after captopril withdrawal. Captopril may be a simple, effective, and non aggressive treatment for postrenal transplant erythremia.

Adult↗
PubMed1990

[Autosomal dominant polycystic kidney and genetic markers of chromosome 16].

The mutation for autosomal dominant polycystic kidney disease (APKD) has been mapped by linkage analysis on the distal part of the short arm of chromosome 16. We present in this study the results of linkage analysis using the two most tightly linked DNA markers (3'HVR and 24-1) in 183 members of 14 families of a same ethnic origin. We have constructed haplotypes using these two polymorphic probes, and compared the frequency of these on the normal and the affected chromosome. No evidence of linkage heterogeneity was found in our population.

Chromosome Mapping↗
PubMed1988

Anti-Ro-positive lupus and hereditary angioneurotic edema. A 7-year follow-up with worsening of lupus under danazol treatment.

A 24-year-old woman, having familial hereditary angioneurotic edema (HAE) treated with danazol, developed an anti-Ro-positive lupus featured by a mild erythematous eruption that seemed initially to decrease and then worsened under danazol, and dramatically improved after danazol was withdrawn. The relationship between lupus and HAE is discussed with special reference to the hormonal sensitivity of autoimmune diseases. It is possible that the responsibility of danazol as well as the immunogenetic background can explain the clinical course of this association.

Adult↗
PubMed1988

[Fatal acute pneumonopathies in disseminated lupus erythematosus].

Two cases of systemic lupus erythematosus (SLE) complicated by pneumonia which resulted in death are reported. The first patient, a 21-year old woman, died of acute diffuse lupus pneumonia; the initial and unusual radiological image of "multiple balloons" progressed within 2 months to terminal interstitial fibrosis. The second patient, a 60-year old woman, died of infection on an interstitial pneumonia which turned into severe fibrosis within 16 months. Acute or chronic lupus pneumonia is uncommon, but it may follow a very serious course. Clinically, true lupus pneumonia must be distinguished from all other types of lung involvement in SLE, such as infection, pulmonary haemorrhage or oedema, iatrogenic pathology, thromboembolic disease, etc. The pathogenetic mechanism of pulmonary lesions directly related to SLE is obscure, although some lung biopsy specimens have shown positive immunofluorescence. Concerning treatment, the initial response to corticosteroid therapy is usually very good, especially in the acute forms of the disease. However, in severe cases immunosuppressive drugs or even plasma exchanges must be added to steroids. For treatment to be rapidly initiated the diagnostic procedures must be completed in the early stages of the disease, involving, when necessary, surgical lung biopsy.

Acute Disease↗