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Biomedical subjects

A Kanfer

Publications and source records attributed to A Kanfer.

At least 55 records · Page 3Linked to original sources
PubMed1989

Physiological significance of increased levels of endogenous atrial natriuretic factor in human acute renal failure.

In twelve patients with acute renal failure, mean plasma levels of atrial natriuretic factor (ANF) and of its second messenger cGMP were found elevated at the early phase of the disease, but tended to return towards normal values at recovery. Variations of plasma ANF and cGMP were correlated significantly (p less than 0.05) with those of total blood volume. At the early phase of the disease, plasma ANF was also correlated with the excreted fraction of filtered sodium (FENa) (r = 0.95). Moreover, plasma ANF and FENa peaked concomitantly at the onset of the diuretic phase in the five patients who were not treated by diuretics or dialysis and were studied sequentially during the course of the disease. It is suggested that enhanced plasma ANF levels might reflect one of the mechanisms of adaptation controlling body fluid balance in acute renal failure.

Acute Kidney Injury↗
PubMed1988

[Hypokalemias].

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Humans↗
PubMed1987

[Interstitial nephropathies induced by meticillin: demonstration of distal tubule functional anomalies].

Renal tubular dysfunction was investigated in two patients with meticillin-induced interstitial nephritis. Some degree of renal failure persisted after the acute episode in both cases. The first patient was investigated 10 weeks after the onset of the nephropathy. Nephrogenic diabetes insipidus and distal tubular acidosis were demonstrated. The second patient was investigated 7 months after the onset of the nephropathy. A major impairment in urinary concentration ability was demonstrated. Neither patient had proximal tubular dysfunction. These data show that meticillin-induced interstitial nephritis may be responsible for distal tubular abnormalities, namely nephrogenic diabetes insipidus and distal tubular acidosis, which may persist long after the onset of the nephropathy.

Adult↗
PubMed1987

Enhanced glomerular procoagulant activity and fibrin deposition in rats with mercuric chloride-induced autoimmune nephritis.

The mechanism involved in glomerular fibrin deposition was investigated during mercuric chloride (HgCl2)-induced autoimmune glomerulonephritis in the Brown Norway rat. To ascertain whether the local hemostatic system was activated secondarily to the immunological conflict, the ability of glomerular lysates to induce coagulation in vitro was assessed in treated and control rats. Glomerular procoagulant activity (PCA) of HgCl2-injected rats was measured on day 12 (latent phase of the disease), day 20 (acme), and days 32 and 42 (recovery phase) after the first mercury injection. PCA rose 3-fold (p less than 0.02) at day 20 and then almost returned to control values. Proteinuria, PCA, and the incidence of glomerular fibrin deposits peaked concomitantly at day 20. Glomerular PCA was characterized as thromboplastin. The number of Ia positive cells detected by monoclonal OX-6 antibody was not different from the control number at any phase of the disease; the number of macrophages per glomerular section detected by electron microscopy at day 20 in HgCl2-injected rats was 1.80 +/- 0.60, versus 0.30 +/- 0.11 in the controls. No correlation was found between glomerular PCA and either the number of monocytes/macrophages or of Ia-positive cells present in the glomeruli. Since glomerular PCA was maximal at the onset of fibrin formation in the glomeruli and then decreased toward its basal level, and since the fibrin disappeared, it is concluded that increased production of thromboplastin by glomeruli, with activation of the extrinsic coagulation pathway, may contribute to intraglomerular fibrin deposition in HgCl2-induced glomerulonephritis.

Animals↗
PubMed1987

Changes in erythromycin pharmacokinetics induced by renal failure.

As erythromycin ototoxicity appears to be favored by renal insufficiency, its pharmacokinetics were assessed in chronic uremic patients treated by maintenance hemodialysis in comparison with normal subjects. Two groups of 8 patients each were studied, the first one on an interdialytic day, the second immediately after the end of an hemodialysis session. All subjects ingested a single dose of 1 gram of erythromycin ethylsuccinate. Times of peak serum concentration and biological half-lifes were similar in patients and in controls. Maximum serum concentrations and areas under the serum concentration time-curve were higher in patients than in controls whereas apparent oral clearances were lower in the former. The differences between the two groups of patients were not significant. These pharmacokinetic changes are suggestive of an enhanced bioavailability of erythromycin in chronic renal failure which might predispose uremics to the ototoxicity of the drug.

Adult↗
PubMed1984

Relative contribution of intrinsic lung dysfunction and hypoventilation to hypoxemia during hemodialysis.

Two mechanisms have been proposed to explain hemodialysis (HD)-induced hypoxemia: reversible lung damage due to intrapulmonary leukostasis as a consequence of the contact of blood with the dialyzer membrane, or alveolar hypoventilation due to the loss of carbon dioxide through the dialyzer. To assess the role of these factors, seven chronically uremic patients were studied before and during 4-hr HD sessions using a cuprophane membrane and either acetate (AHD) or bicarbonate (BHD) dialysate. In AHD only we observed, by comparison with predialysis values, a significant hypoxemia, and a decrease of alveolar ventilation (VA), lung carbon dioxide output, and respiratory exchange ratio. In both the AHD hypoxemic group and BHD nonhypoxemic group, there was a similar decrease in lung carbon dioxide diffusing capacity (DLCO) and of white blood cells (WBC), and a positive correlation between arterial oxygen pressure and VA without modification of alveolo arterial PO2 difference, an argument against the existence of ventilation-perfusion or ventilation-diffusion mismatching. We conclude that, although WBC sequestration induced a lung damage evidenced by DLCO impairment, the key factor of hypoxemia observed in AHD was the hypoventilation.

Acetates↗
PubMed1983

Acute interstitial nephritis due to drug hypersensitivity. An up-to-date review with a report of 19 cases.

The clinical, biologic, and pathologic features and the course and treatment of acute interstitial nephritis (AIN) due to drug hypersensitivity are reviewed. The authors report 19 additional cases of AIN, outlining some particular and unusual features. The drugs most often responsible now are penicillins and cephalosporins, cotrimoxazole, thiazide diuretics, glafenin and its derivatives, and nonsteroid anti-inflammatory agents. Diagnosis of AIN should be considered in any case of rapidly progressive renal failure occurring during drug therapy, especially when fever, skin rash, arthralgias, macroscopic hematuria, and blood or urinary eosinophilia are present. In the absence of the preceding symptoms, systematic early renal biopsy may be helpful to detect intersitial infiltrates containing lymphocytes, plasma cells, and eosinophils and/or granulomas with epithelioid cells. Immunologic tests are inconstantly positive. Their sensitivity and specificity often are doubtful in the absence of precise knowledge of the pathogenetic factors involved. Recovery may be hastened in some cases by corticoid therapy. Recurrence of the disease will be avoided by definitive suppression of offending and related drug(s).

Acute Disease↗