Biomedical subjects
Publications and source records attributed to L Morel-Maroger.
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An unusual familial glomerular disease, characterized by the presence of diffuse round mesangial deposits of C3, is described in 2 siblings (1 male and 1 female) and their mother. The clinical picture in the 3 patients was a long-lasting proteinuria. An acute hemolytic uremic syndrome with malignant hypertension developed in the male at the age of 24 years, requiring bilateral nephrectomy. The glomerulonephritis recurred on a renal allograft. This disease is not HLA-linked and no characteristic abnormality of complement profile was seen in the 3 patients.
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The relation between the duration of bacterial infection and circulating immune complexes (CIC) level was evaluated using the C1q binding assay in a group of patients with well defined clinical sepsis. Fifty-four patients with endocarditis and 35 with post-open heart surgery mediastinitis were prospectively studied over a period of 2 years. CIC were detected in 42% of patients studied. Interindividual variations were observed but it was found that the level of CIC increased statistically with time (P less than 0.001). CIC were statistically linked with cryoglobulinemia (P less than 0.001), rheumatoid factor (P less than 0.001) and a decreased CH50 (P less than 0.05). CIC were more frequent in patients with endocarditis (53%) than in patients with mediastinitis (24%). However, when the duration of the infection was taken into account the difference was no longer significant. No relation could be evidenced between the incidence of CIC and clinical symptoms including prognosis and renal signs. In our experience, determination of CIC does not have a critical clinical value.
A 38 year-old man, operated upon two years previously for combined mitral and tricuspid valve disease of rheumatic origin, presented with signs of a severe biological inflammatory syndrome, and a mild proliferative glomerulonephritis (normal complement with exclusively mesangial deposits of IgM, Clq, and C3 on immunofluorescence), which developed slowly over a period of 3 years in the absence of any fever. Blood cultures were always negative, and prolonged antibiotic therapy on two occasions had no effect on the clinical or biological picture. Mitral prosthesis replacement was necessary 6 months after the onset of the affection, a second leakage 16 months later leading to rapidly fatal heart failure. Pathological examination confirmed the presence of an endocarditis at the zone of insertion of the prosthesis. The slow progression of the disorder in this case, and the absence of fever, emphasize diagnostic difficulties of certain cases of endocarditis, due to low virulence germs, that progress under cover of a generalized disease of renal expression. The value of renal biopsy, which provided almost specific indications in the present case, is also stressed.
A total of 32 patients with Plasmodium falciparum malaria were studied. Of these, 23 had benign infections, and 9 had typical cerebral malaria. Cryoglobulins, circulating immune complexes detected by a C1q-binding assay, and hypocomplementemia were found in eight of nine patients with cerebral malaria. Raised levels of complement component 3 breakdown products (C3d) were found in the seven patients tested. Peak levels of circulating immune complexes and C3d were associated with thrombocytopenia. In contrast, in patients with benign Plasmodium falciparum malaria, cryoglobulins and circulating immune complexes were found only in 3 of 23 patients. Similarly, hypocomplementemia was detected only in 5 of 23 patients. These observations suggest that the intensity of the immune response and of the associated complement activation may be important factors in the pathogenesis of cerebral malaria.
Suckling Swiss mice were injected daily for 8 days with either electrophoretically pure (EP) mouse interferon (s.a. 4.7 x 10(8) units/mg protein), major impurities obtained in the course of purification, or partially purified mouse interferon (s.a. 1.3 x 10(7) units/mg protein). Only EP or partially purified interferon inhibited growth, induced liver and kidney lesions, and killed mice. The authors conclude that interferon itself is responsible for these effects.
Immunopathological studies of the kidney, determination of circulating immune complexes and interferon blood levels were obtained in adult congenitally-athymic nude mice ((nu/nu) infected with lymphocyte choriomeningitis (LCM) virus as well as in their phenotypically-normal litter mates (nu/+). As previously reported, intracerebral or intraperitoneal infection in nu/nu mice did not induce any mortality and resulted in a carrier state characterized by persistently high levels of virus in the circulation. Interferon was present in the circulation for approximately 6 days. Circulating immune complexes were not detectable and glomerulonephritis assessed by light microscopy, electron microscopy and immunofluorescence, was either absent or very mild. These observations show that although a carrier state can be induced in adult nude mice, circulating immune complexes and glomerulonephritis do not develop. This situation is markedly different from that induced in normal Swiss mice infected at birth, which is characterized by raised levels of circulating immune complexes and development of glomerulonephritis in all infected mice.
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A 52 year old man was admitted to hospital for persistent back pain, fixed proteinuria of 6g/24 h that lead to the nephrotic syndrome (proteids 40 g/l, albumin 21,2 g/l). Two possible etiologies were envisaged: 1) Myeloma with K light chains as evidenced by biological findings (absence of normal Ig, presence of K light chains both in blood and urine, malignant medullary plasmocytosis) as well as x-rays (small punched out lesions). 2. Diabetes mellitus (blood glucose 2,4 g/l) with retinal and neurological involvement. Percutaneous renal biopsy revealed nodular glomerular sclerosis compatible with both diabetes and myeloma as well as homogeneous refringent thickening of tubular basement membranes more specific of myloma. No amyloid deposits, myelomatous casts were seen and anti-K light chain fixation was negative at immunofluorescence. An evolution of 33 months duration let to chronic renal failure (plasma creatinine 47 mg/l). The respective role of myeloma and diabetes in the genesis of this glomerular nephropathy are discussed.
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Glomerular lesions were studied in 41 patients with hepatic cirrhosis (32 cases) or steatosis (9 cases) by optical microscopy (38 cases) and immunofluorescence (22 cases) examinations of biopsy samples. The most frequently observed lesion on optical microscopy was a glomerulosclerosis (16 cases), arteriolar lesions being present in 15 cases, two-thirds of which had associated glomerular lesions. Immunofluorescence revealed the presence of immunoglobulin deposits in 17 cases, these possessing two main characteristics: the prevalence of IgA (14 cases), alone or in association with other immunoglobulins; and the predilection for the mesangium alone, or in association with parietal deposits. The glomerular nephropathy in the cirrhotic patients was completely latent in 3 out of 4 cases, renal signs, when they existed, being of mild intensity. Renal lesion can occur in the absence of severe hepatopathy, particularly in the presence of steatosis. IgA deposits in the mesangium, a fundamental feature of hepatic glomerulopathy, can be related to the presence of IgA deposits in the liver sinusoids, suggesting the development of IgA deposits in several organs during these affections. Their pathogenesis is still obscure but two hypotheses have been suggested: an immune disease with deposits of circulating immune complexes in the kidney; a non-immune disease, IgA deposits being a secondary and not a primary feature.
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We report on 4 cases of reversible acute renal failure (ARF), appearing within the first days after institution of a sulfinpyrazone treatment (600 mg p. day) early after a myocardial infarction. Urinary data were consistent with an acute tubular necrosis. A renal biopsy, performed in 3 patients, revealed only very discrete tubular and interstitial lesions, not helpful in the understanding of the ARF. Three pathogenetic mechanisms could be evoked. Data in favour of an acute tubular precipitation of uric acid or an immunologically induced acute interstitial nephritis are lacking. More probably this ARF is due to an inhibitory effect of sulfinpyrazone on the renal prostaglandin synthesis. Early after a myocardial infarction, renal prostaglandins could play an important protective role in maintaining the renal circulation. Renal function should be monitored closely when sulfinpyrazone is prescribed, especially early after a myocardial infarction.