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Biomedical subjects

D Ganeval

Publications and source records attributed to D Ganeval.

At least 37 records · Page 2Linked to original sources
PubMed1982

[Light chain or monoclonal immunoglobulin deposition disease: physiopathogenic concepts].

Although recently identified, this disease is by no means exceptional. It is characterized by the deposition in various organs of an amorphous substance which differs from the amyloid substance and contains monoclonal immunoglobulin determinants: either a light kappa or lambda chain, or a light and a heavy chain. The severity of the disease is due to various organs being involved, notably the kidneys. There is in every case a monoclonal plasmocytic or lymphoplasmocytic proliferation which may appear as benign. In almost one-third of the cases no monoclonal immunoglobulin can be detected in the serum. In a study of immunoglobulin biosynthesis, 6 out of 8 patients showed striking structural abnormalities. The relationship between these very unusual lg's and tissue deposition is discussed in detail.

Chemical Phenomena↗
PubMed1982

Glaphenine-induced acute renal failure in the rat: a new experimental model.

Glaphenine, a nonsteroid analgesic compound, administered by gastric gavage in rats (800 mg/kg), induced nonoliguric reversible acute renal failure (ARF). Intratubular deposits were found in medullary collecting ducts. Intratubular hydrostatic pressure (Pt) increased from 11.7 +/- 0.7 to 30.0 +/- 0.9 mmHg. Renal failure was almost completely prevented by concomitant high water and solute diuresis, achieved by furosemide infusion in Wistar rats and by high salt intake in Brattleboro rats with diabetes insipidus. In the latter protected animals, Pt was only slightly elevated (17.0 +/- 0.5 mmHg). Urinary excretion of prostaglandin E2 (PGE2) dropped dramatically after glaphenine administration in Wistar rats; the fall was slight in Brattleboro rats in which PGE2 excretion was normally low. We conclude that tubular obstruction plays a prominent role in glaphenine-induced ARF in the rat. High water and solute diuresis prevented tubular obstruction. Reduced renal PGE2 synthesis is probably not involved in the pathophysiology of this ARF model, inasmuch as Brattleboro rats on a high salt intake were protected despite low basal urinary excretion of PGE2.

Acute Kidney Injury↗
PubMed1982

Diabetes mellitus following pentamidine-induced hypoglycemia in humans.

Four patients, treated with pentamidine because of Pneumocystis carinii pneumonitis, displayed severe fasting hypoglycemia during this treatment. Diabetes mellitus appeared later, requiring insulin therapy in the three of them who survived more than a few weeks. The metabolic study, performed in two cases during the hypoglycemic period, demonstrated inappropriately high insulin levels in the postabsorptive state. 28 +/- 1 microunits/ml (blood glucose 41 +/- 4 mg/dl) and 86 +/- 5 microunits/ml (blood glucose 15 +/- 5 mg/dl) vs. 15 +/- 3 microunits/ml in 10 control subjects and 55 +/- 3 microunits/ml in 6 patients with a verified B-cell tumor, respectively. Poor B-cell secretory responses followed the stimulations by oral glucose (maximal increment over basal: +5 microunits/ml vs. + 40 microunits/ml in control group and +77 microunits/ml in the insulinoma group), by i.v. arginine (maximal increment + 10 and +28 microunits/ml, respectively, vs. +55 in the controls and +90 microunits/ml in the insulinoma group) and by i.v. glucagon (+10 and +23 microunits/ml, respectively) vs. +40 microunits/ml in both the control and the insulinoma groups). Plasma cortisol and glucagon, and the A-cell response to arginine were higher than normal. These high, nonsuppressible, nonstimulable insulin levels and the sequence of hypoglycemia followed by insulin-dependent diabetes mellitus is consistent with the hypothesis of a selective toxicity turned towards the B-cells. In vitro incubation of islets with pentamidine 10(-10) M produced a passive release of insulin, followed by a significant decrease in B-cell response to glucose + theophylline. It is suggested that pentamidine can induce hypoglycemia because of an early cytolytic release of insulin, and then diabetes mellitus because of B-cell destruction and insulin deficiency.

Adult↗
PubMed1981

Systemic lambda light-chain deposition in a patient with myeloma.

Systemic lambda light-chain deposition occurred in a 73-year-old man with myeloma. An initial renal biopsy specimen showed the features of myeloma kidney. When he died 22 months later lambda light chains were detected by immunofluorescence in kidneys, liver, spleen, and heart. They were probably responsible for cardiac dysfunction and the fatal arrhythmia. It is suggested that in this patient deposition was due to a structural alteration of the light chains, possibly induced by cyclophosphamide.

Aged↗
PubMed1979

Immunologically-mediated acute renal failure of nonglomerular origin in the course of systemic lupus erythematosus [SLE]. Report of two cases.

Acute anuric renal failure was observed in two patients with systemic lupus erythematosus (SLE) during the clinical and serologic active phase of the disease. Renal biopsies, performed during the acute episodes, showed only mild and focal mesangial cell proliferation without deposits. In contrast, tubulointerstitial lesions were predominant. Intense granular immune deposits along the tubular basement membrane, or immunofluorescence examination, were suggestive of immune complex deposition. One of these patients had severe high blood pressure and vascular lesions likely induced by immune complexes. In both, renal function was recovered. Immunologically-mediated tubular and vascular lesions in the course of SLE are discussed.

Acute Kidney Injury↗
PubMed1977

[Nephrotoxicity of gentamicin. Conditions for the use of this antibiotic in the elderly and in the patient with renal insufficiency].

Reversible acute renal failure was observed in 13 patients after combined antibiotic therapy using gentamicin. High and prolonged doses were used in 7 patients whose initial renal function was normal, while 6 other patients with preceding chronic renal insufficiency received usual doses of gentamicin. Precipitating factors were: increasing age, previous renal impairment, and combined use of other antibiotics, mainly cefalotin (8 patients). The nephrotoxicity of gentamicin is poor but well established, and may be prevented by checking the initial renal function, adjusting the dosage subsequently, and monitoring the renal function and gentamicin serum levels during therapy.

Acute Kidney Injury↗
PubMed1976

Furosemide in acute oliguric renal failure. A controlled trial.

A randomized study was conducted on 66 patients with acute established oliguric renal failure. Intravenous doses of furosemide ranging from 1.5 to 6.0 mg/kg were given every 4 h to 33 of the patients; the remaining 33 patients served as controls. A persisting diuretic response was observed in 5 treated patients and in 2 controls. Hemodialyses were required in most of them. Furosemide did not significantly modify in cured patients the mean oliguric period, the number of dialyses and the mean period of renal insufficiency.

Acute Kidney Injury↗