Primary bronchogenic carcinoma in transplant recipients.
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Biomedical subjects
Publications and source records attributed to C Noël.
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Axillo-axillary angio-access can be an alternative device (bovine graft or synthetic graft) for dialysis patients among whom upper arm peripheral veins are impracticable or previous fistulas are thrombose. This procedure was used in seven dialysis patient (length of dialysis: 52.2 +/- 40.6 months) among whom forty one angio access were done. Except one immediate failure, these access were patent until, either the death of patients or the achievement of a cadaveric renal graft. The clinical and hemodynamic tolerance were perfect.
Reported cases of HUS/TTP (hemolytic uremic syndrome/thrombotic thrombopenic purpura) with cyclosporin (CsA) are more and more frequent, which led us to evaluate the incidence of microangiopathic process in kidney graft patients. In our first retrospective study we noted 9.4 percent of HUS/TTP among 117 patients. We tried to detect infraclinical hemolytic events prospectively in 40 new patients by systematic measurement of haptoglobin levels after introduction of CsA. The incidence of falls in haptoglobin levels was 25 percent. The immunological context was always noted: rejection crisis in 5 cases, cytomegalovirus infection in 3 cases, isolated markers of lymphocyte-activity in 2 cases. We never found a clinical or infraclinical form of microangiopathic process without a symptomatic or asymptomatic immunological complication. Monitoring haptoglobin levels make it possible to detect early endothelial injuries which could be linked to the future arteriolopathy described with CsA therapy.
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The incidence of cyclosporine (CsA) vascular toxicity is open to debate. We attempted to evaluate the incidence of hemolytic accidents in our series of patients taking all clinical forms into consideration. From January, 1989, to December, 1990, 117 patients received kidneys from cadaver donors and were treated with CsA. Five patients presented hemolytic uremic syndrome (HUS) accompanied by a rejection crisis; 6 patients presented hemolytic anemia associated in 2 cases with marked thrombocytopenia without any evidence of rejection. Cytomegalovirus (CMV) infection was diagnosed in 2 patients and bacterial infection preceded hemolysis in 2 other cases, suggesting a triggering factor. In addition, when we systematically determined haptoglobin levels after introduction of CsA treatment, we found asymptomatic hemolytic episodes more frequently. Our incidence of hemolytic accidents was approximately 10%. Hemolysis could indicate ischemic vascular damage leading to arteriolar medial hyalinosis preceding fibrosis in CsA nephrotoxicity. Thus, it would be interesting to detect asymptomatic forms of hemolysis by monitoring haptoglobin levels. This approach could lead to a reduction of the CsA dose in patients presenting low haptoglobin levels, even in the absence of evidence of nephrotoxicity.
We studied the relationship between circulating androsterone glucuronide, androstane-3 alpha, 17 beta-diol glucuronide and androstane-3 beta, 17 beta-diol glucuronide concentrations and adrenal as well as testicular C-19 steroids in men. Among the three 5 alpha-reduced steroid glucuronides, androsterone glucuronide is the predominant C-19 steroid glucuronide measured in plasma and its levels are markedly elevated compared to those of the non-conjugated steroid. The marked rise in testosterone during puberty was strongly correlated with the increase in both androsterone glucuronide and androstane-3 alpha, 17 beta-diol glucuronide, thus suggesting that testicular C-19 steroids are the main precursors of the steroid glucuronides. We also found that the presence of testicular androgen in plasma contributes to approx. 70% of plasma androsterone glucuronide and androstane-3 alpha, 17 beta-diol glucuronide. Our data suggest that the adrenal C-19 steroids remaining in circulation after castration in men are converted into potent androgen which are then glucuronidated by UDP-glucuronyltransferase. We also demonstrated that the human prostate cell line LNCaP is capable of converting to a large extent androstenedione into androsterone glucuronide. Our data further confirm that glucuronidation is a major pathway of steroid metabolism in steroid target tissues.
Relapsing polychondritis is a rare connective tissue disorder characterized by inflammation of cartilagenous structures such as ears, nose, joints, trachea and larynx. Renal disease is unusual. A 41 years old man presented with auricular chondritis, subacute renal failure and lung hemorrhage. A renal biopsy disclosed a diffuse proliferative glomerulonephritis with extensive crescents. Immunofluorescent studies suggested a GNRP type III so called "non immunologic disease". He was treated by prednisone and plasmapheresis with rapid disappearance of pulmonary hemorrhages and good renal functional improvement.
We review a series of 11 silicotic coal miners demonstrating a progressive renal failure with a syndrome of rapidly progressive glomerulonephritis. Renal biopsies reveal crescentic glomerulonephritides associated three times with angeitis. These cases confirm that silica induced glomerulonephritides can be an occupational hazard and warrant further clinical and epidemiological research.
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In a former study we have shown that 1 alpha OH vitamin D3 given to hemodialyzed patients taking A1(OH)3 at a constant dose increased their plasma concentrations of aluminium. Two mechanisms can explain this increase: increased intestinal absorption or decreased tissue storage of aluminium. We have, in the present study, given 1 alpha(OH)3 at the same dose (6 micrograms per week) and during the same duration (4 weeks) to 15 stable hemodialyzed patients after aluminium hydroxide has been discontinued 6 weeks before. Under A1(OH)3 treatment mean plasma aluminium was 2.33 +/- 2.36 mumol/l. After A1(OH)3 discontinuation, plasma aluminium decreased significantly as soon as the 2nd week of the control period (1.39 mumol/l). The decrease was maintained in plateau throughout the 5 weeks of the control period (1.38 mumol/l and, the 4 weeks of 1 OH Vit D3 administration (1.40 mumol/l). After 1 alpha OH D3 discontinuation there has been a non significant transient drop of aluminemia followed by a plateau at a level comparable to the previous plateau. Plasma calcium and phosphate concentrations increased significantly with 1 alpha(OH)3 and decreased thereafter confirming biological activity of 1 alpha(OH)3. Since 1 alpha(OH)3 increases plasma aluminium in hemodialyzed patients only when they are taking simultaneously A1(OH)3, it is suggested that this increase is mainly explained by an increase of the intestinal absorption of aluminium.
Over a 3 years period, PTH, 25 OHD, calcium and phosphate levels were measured in all patients admitted to a department of Internal Medicine with abnormal phospho-calcic metabolism or bone disease. The diagnostic value of iPTH was analysed, especially in cases of hyper- and hypocalcaemia. In hypercalcaemia, the iPTH did not differentiate between the two main differential diagnoses: hyperparathyroidism and cancer. In patients with a negative calcium balance, the iPTH level is often raised and many help towards diagnosis. However, it should first of all orientate the clinician towards the detection of renal failure which is a common cause of this condition.
Acute renal failure due to tubulo-interstitial nephritis accompanied by uveitis has been observed in 3 young women (TINU syndrome). In these 3 cases, the nephropathy was preceded (1-3 months) by asthenia, anorexia, weight loss and a major inflammatory syndrome. Nonsteroidal anti-inflammatory drugs (NSAID) administration was noted. In 2 cases, uveitis appeared after the nephropathy had subsided. Renal biopsies performed in the 3 patients revealed mainly interstitial changes with mononuclear cell infiltration; immunofluorescence studies were negative. Although the severity of renal failure varied among patients, renal function recovered completely, returning to normal within 2, 3 and 24 months respectively, on corticosteroid therapy. The TINU syndrome is a rare situation compared to drug-induced acute interstitial nephritis, including NSAID related-nephritis. However, the real incidence of this syndrome might be underestimated since the uveitis can appear a few weeks later and its origin may not be related to the renal episode.
Outer mitochondrial membrane was purified from rat liver. Its constituent proteins were analyzed by SDS-polyacrylamide gel electrophoresis and by electrophoretic immunoblotting employing antibodies raised against total outer mitochondrial membrane. Anti-outer mitochondrial membrane antiserum reacted with only one polypeptide (15 kDa) in rough microsomes, whereas no immunological cross-reactivity was observed with other mitochondrial compartments (intermembrane space, inner membrane, or matrix) or with lysosomes or total cytosol. The antiserum was employed to characterize precursors of outer mitochondrial membrane proteins synthesized in vitro in a rabbit reticulocyte cell-free system. One product (a 68 kDa polypeptide designated OMM-68) bound efficiently to mitochondria in vitro but did not interact with either dog pancreas or rat liver microsomes, either co-translationally or post-translationally. OMM-68 was synthesized exclusively by the membrane-free class of polyribosomes. Attachment of precursor OMM-68 to mitochondria was not accompanied by processing of the polypeptide to a different size.
Four cases of osteosclerosis were observed in patients with renal failure. All subjects presented with moderate reduction in renal function which had been stabilized for several years. Osteosclerosis appeared progressively but was clinically symptomatic in only one patient. Fluoride intoxication was ascertained on the basis of X-ray examination and bone biopsy. In addition, the source of fluoride intoxication was easily recognized as the drinking water (2 to 3 1/day), "Vichy Saint Yorre" commercial mineral water (fluoride concentration 9 mg/l) in 3 cases, and tap water in the fourth case. These observations emphasize the risk of high chronic fluoride intake in patients with renal failure, even with mild reduction of glomerular filtration rate.