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Biomedical subjects

A Meyrier

Publications and source records attributed to A Meyrier.

At least 109 records · Page 6Linked to original sources
PubMed1984

Paraneoplastic hypercalcemia associated with bladder carcinoma: report of 2 cases.

Hypercalcemia associated with bladder carcinoma is rare. We report on 2 patients with hypercalcemia and bladder tumor without bone metastases. In both patients serum calcium returned to normal after removal of the tumor. Serum immunoreactive parathyroid hormone levels were normal in both patients. In 1 case a high gradient of immunoreactive parathyroid hormone across the tumor was demonstrated but the secretion of nephrogenous cyclic adenosine monophosphate was normal. Urinary excretion of prostaglandins also was normal in this case. These data show that hypercalcemia was caused by the tumoral production of some humoral factor different from parathyroid hormone.

Adult↗
PubMed1984

Rapidly progressive ('crescentic') glomerulonephritis and monoclonal gammapathies.

In 3 patients rapidly progressive glomerulonephritis revealed plasma cell dyscrasia in 2 cases and Waldenstrom's macroglobulinemia in the 3rd. Renal biopsy showed proliferative glomerulonephritis with marked endo- and extracapillary (crescentic) proliferation. In case 1, corticosteroids and cyclophosphamide favorably influenced the course of the disease. The 2nd patient was not treated and went on to maintenance hemodialysis. In the 3rd case, plasma exchange and cytotoxic drugs allowed discontinuation of hemodialysis. Thirteen other cases of proliferative glomerulonephritis associated with monoclonal gammapathies have been described in the literature, including 3 with crescents. B-cell dyscrasia should be considered a possible etiology in a patient with crescentic glomerulonephritis. In such case we show that treatment of the hematologic disorder can be followed by a dramatic improvement of renal function.

Aged↗
PubMed1984

[Serous otitis and necrotizing angiitis].

Three cases are reported of necrotizing angiitis of otologic origin (one polyarteritis nodosa and two wegener's disease). Data in the published literature are reviewed and necrotizing angiitis classified. Two features resulting from this review are emphasized. Firstly, form the pathogenic point of view the fact that specific lesions were detected in the ear in one of these patients means that this localization may be a possible visceral manifestation, as are rhinologic and pulmonary lesions. Otologic sites may be an isolated, or in association, further type of pathogenic mechanism. From the practical point of view, any unexpected serous otitis in adults should suggest the need for an erythrocyte sedimentation test, very high values requiring investigation of etiology. This will avoid unnecessary medical and surgical treatments and the institution of immunosuppressant therapy active against all visceral lesions and the only effective means of treating the otitis. Early treatment could avoid the catastrophic prognosis observed short-term in the 3 cases reported.

Adult↗
PubMed1984

[Hypocomplementemic urticarial vasculitis with glomerulopathy and renal venulitis].

A 58 year-old woman had atypical chronic urticaria, arthralgias and abdominal pain. Attacks of angioneurotic edema occurred. Proteinuria was discovered. She had clinical and biological signs of inflammation, leukoneutropenia , antileukocyte antibodies and low CH 50, C1q and C4 levels without functional C1 esterase deficiency. C1q precipitins were not detectable. Skin biopsy disclosed angiitis and by immunofluorescence a lupus band test was positive. Serologic investigations in search of SLE were negative. Renal biopsy showed mesangial deposits, capillary loop thickening and mesangial fixation of anti-IgG, C3 C1q and C4 antisera. In the interstitium, voluminous perivenular inflammatory infiltrates were visible. With corticosteroid treatment clinical manifestations subsided and proteinuria disappeared. This observation of McDuffie 's angiitis with renal venulitis leads to a review of the literature with discussion of the mechanisms of hypocomplementemia.

Biopsy↗
PubMed1983

Immunopathological studies of polyarteritis nodosa and Wegener's granulomatosis: a report of 43 patients with 51 renal biopsies.

Although it is generally considered that vasculitis of the polyarteritis nodosa (PAN) group and Wegener's granulomatosis (WG) is immune complex (IC) mediated, there are no simultaneous data on circulating IC, complement levels and deposits of Ig and complement in the kidney. Therefore we have performed a retrospective study of 43 patients suffering from PAN and WG. Ig glomerular deposits were uncommon and scanty, except in two patients with WG; C3 deposits were detected in 12 patients, whereas fibrinogen was constantly found when lesions were recent and active. Similar data were obtained for the renal vessel walls. Contrasting with these results, rheumatoid factors and cryoglobulins, suggestive of the presence of circulating IC, were detected respectively in nine of 39 and seven of 37 patients, and IC 'activity' assessed by the Raji cell assay and the Clq binding assay was found respectively in six of 17 and nine of 10 patients before treatment, and in none of 10 and five of seven patients in remission. Haemolytic complement activity and complement components were never decreased, but the C3d breakdown product of C3 was elevated in all the eight patients studied before treatment. Signs of persistent hepatitis B virus (HBV) infection were detected in five of 25 patients of the PAN group, whereas three of eight patients with WG had only anti-HBV antibodies. Furthermore, cytomegalovirus (CMV) could be isolated from the blood in a case of WG before the treatment was started. Persistent interferonaemia was detected in one of five patients. These results suggest either that renal deposition of CIC is transient, the paucity of Ig deposits being due to rapid clearance of IC by phagocytic cells; or alternatively that vascular and glomerular lesions are not caused by CIC, as in some cases of experimental vasculitis induced by infectious agents.

Adolescent↗
PubMed1983

[Acute hematogenic interstitial nephritis of urinary origin: an unrecognized factor in the exacerbation of chronic kidney failure].

Hypertension, phosphate retention, hyperfiltration hyalinosis and the natural course of the underlying are well known factors leading to progression of chronic renal failure. Acute bacterial interstitial nephritis occurring in a previously diseased kidney, although well documented in experimental animals, has not been shown to aggravate chronic renal failure in man. We report on 3 cases of acute suppurative interstitial nephritis, due to E. coli urinary infection complicated by septicemia. All had rapid aggravation of previously mild renal failure secondary to chronic interstitial nephritis. Sepsis originated from the urinary tract which in 2 instances had been temporarily obstructed. Renal biopsy disclosed a diffuse interstitial infiltrate containing numerous polymorphonuclear leukocytes. This was superimposed on chronic tubular and interstitial lesions. In 1 case there were glomerular lesions with crescents and mesangial C3 deposits. A 2nd biopsy performed in 2 cases was of prognostic interest. In one case it showed active lesions and the necessity of continuing the treatment and in the other a satisfactory healing allowing cessation of therapy. Treatment was guided by antibiograms, the clinical and urinary signs of activity, renal biopsy findings and antibiotics known to be concentrated in renal tissue. The duration of treatment seemed important for the regression of acute renal lesions. Hematogenous bacterial interstitial nephritis should be considered as a possible cause of aggravation in chronic renal failure.

Acute Disease↗
PubMed1983

[Myxoma of the left atrium and advanced renal failure].

A 34 years old woman with a history of childhood rheumatic fever presented with a number of episodes of systemic embolism over a 10 years period attributed to mitral stenosis despite long-term anticoagulant therapy. All preoperative electrocardiograms showed sinus rhythm. After one episode of recurrent embolism (brain, limbs) requiring femoral embolectomy, she developed oligo-anuric renal failure and needed 21 days of hemodialysis. She made a full recovery. Several years later, she presented with chronic progressive renal failure. The diagnosis of left atrial myxoma was eventually made at echocardiography: surgical excision was successful. Periodic hemodialysis was started six months later. The authors use this case to illustrate unusual presentations of myxoma and above all their vascular complications; the possibility of embolic renal disease leading to advanced renal failure is discussed, a complication of left atrial myxoma which seems to be very rare.

Adult↗
PubMed1981

Minor haemoglobin fractions in uraemic and in diabetic patients.

Using a high resolution automated chromatographic method, the levels of the different minor haemoglobins Hb A1a, A1b, and A1c were measured in 20 healthy controls, in 20 patients with chronic renal failure, in 20 uraemic patients on intermittent haemodialysis, and in 20 insulin-dependent diabetic patients. In uraemic non haemodialysed patients, the levels of the three minor fractions were increased significantly. The two fractions Hb A1b and A1c were normalised subsequent to haemodialysis, whereas the level of Hb A1a was higher in the haemodialysed than in the uraemic non haemodialysed group. In both groups of uraemic patients, no correlation was found between the minor Hb fractions and the corresponding serum creatinine, uric acid, urea, phosphorus, bicarbonate and blood glucose levels. In diabetic patients, the three minor fractions were increased. As expected, Hb A1c and glucose concentrations were tightly correlated. No correlation was found between blood glucose levels and Hb A1a, whereas a correlation existed between blood glucose levels and Hb A1b. It is concluded that the increase of minor haemoglobin fractions in renal failure does not only reflect the glucose intolerance. Renal failure itself causes an increase of the three minor fractions. Overall assay of the minor haemoglobin components (Hb A1) may lead to misinterpretation in case of diabetic patients with chronic renal failure.

Adult↗