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Biomedical subjects

D Kleinknecht

Publications and source records attributed to D Kleinknecht.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1983

Drug-induced granulomatous interstitial nephritis.

Among 22 cases of drug-induced acute interstitial nephritis (AIN), noncaseating interstitial granulomas were found in eight cases (36%). Acute renal failure (ARF), oliguric in three patients, appeared within 1-20 days after the beginning of therapy. Clinical symptoms suggesting a hypersensitivity reaction were unusual, marked blood eosinophilia was absent, and immunologic tests were inconstantly positive. The discovery of interstitial granulomas may be a clue to the diagnosis of drug-induced AIN, especially when the inflammatory infiltrates do not contain eosinophils. Since significant residual renal impairment may be observed the benefit of early steroid therapy must be debated.

Adolescent↗
PubMed1982

[Rhabdomyolysis with acute renal failure and malignant neuroleptic syndrome].

Seven episodes of rhabdomyolysis with acute renal failure (ARF) have been observed in 6 patients treated with various short-acting tranquilizers and antidepressants. Clinical features usually included severe hyperthermia, diffuse hypertonicity with or without coma, circulatory failure or unstable blood pressure, and often acute respiratory failure. Serum CPK were always elevated. The type of ARF was prerenal failure without oliguria in 5/7 episodes, and acute tubular necrosis in 2/7 episodes, requiring hemodialyses in one patient. Three patients died. In any case, the tranquilizers and antidepressants responsible for this syndrome were stopped, and electrolyte disorders and acidosis were corrected. Associated acute circulatory failure, septicemia and/or acute hepatic failure required prompt therapy, and artificial ventilation was required in 4 instances. The further use of phenothiazines, butyrophenones, sulpiride and their derivatives should be avoided in any patient having developed such an accident, whose pathophysiology is similar to that described in malignant hyperthermia of various origin.

Acute Kidney Injury↗
PubMed1981

[Acute respiratory distress syndrome of tuberculous origin in an intensive care unit. Clinical presentation and course (author's transl)].

The authors have observed 6 cases of acute respiratory distress syndrome (ARDS) of tuberculous origin. The condition presented as pulmonary oedema in 4 cases and as extensive bilateral pneumonia in 2. Pulmonary oedema was treated by artificial ventilation with intermittent positive pressure in 2 patients who died, and by continuous positive airway pressure in 2 patients who survived. The 2 patients with pneumonia survived without respiratory assistance. In these patients with atypical symptoms, early diagnosis (which may involve liver and bone marrow biopsies) and immediate therapeutic measures are life-saving. The diagnosis of tuberculosis should be systematically considered in adult ARDS, especially i patients with pulmonary oedema of unknown origin.

Acute Disease↗
PubMed1980

Antiglomerular basement membrane nephritis after solvent exposure.

A rapidly progressive glomerulonephritis with definitive anuria was observed after solvent inhalation in two young women, aged 22 and 17 years. In both cases the renal biopsy specimen showed diffuse epithelial crescents in all glomeruli, with linear deposits of IgG along the glomerular basement membrane (GBM). High circulating anti-GBM antibody levels were found in sera by indirect immunofluorescence and radioimmunoassay. No anti-alveolar basement membrane antibodies were detectable by immunofluorescent microscopy in one patient. It is suggested that the solvent inhalation resulted in a chemical alteration of the alveolar basement membrane giving rise to anti-basement membrane antibodies, some of which may have cross-reacted with the GBM and initiated the glomerulonephritis.

Adolescent↗
PubMed1980

Dense deposit disease with rapidly progressive renal failure in a narcotic addict.

A girl aged 17 developed a nephrotic syndrome with renal insufficiency after narcotic abuse. Renal biopsy showed a diffuse glomerulonephritis with crescents and dense deposits within the glomerular basement membrane; glomerular C3 deposits were present without immunoglobulin. The serum complement profile was typical of activation via the alternative pathway, and tests for C3 nephritic factor were strongly positive. Terminal renal failure occurred within 6 months and required chronic hemodialysis. It is likely that the narcotics used or their contaminants were responsible for the renal damage, presumably by activating the complement system via the alternative pathway.

Adolescent↗