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Biomedical subjects

D Kleinknecht

Publications and source records attributed to D Kleinknecht.

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

[Toxic glomerulonephritis].

Most glomerulopathies are immunologically-mediated. Their pathogenesis is now better understood. The role of cell-mediated immunity has recently been envisaged. The role of circulating antibodies now seems to be more important than that of circulating immune complexes. Antibodies may recognize structural or "planted" antigens in the kidney, the latter being non-renal molecules that may bind renal structures for non-immune reasons. The linear or granular pattern observed at immunofluorescence depends upon the regular or irregular distribution of the antigen. In susceptible individuals, various toxins (heavy metals such as mercury or gold, drugs with an SH group, non-steroidal anti-inflammatory agents) may induce an immune glomerulopathy. It has recently been shown that Brown-Norway rats exposed to one of the above-mentioned agents develop anti-self class II T lymphocytes that are responsible for a polyclonal activation of B cells. Among the various autoantibodies that are produced, some have a nephritogenic potential. Other drugs are responsible for glomerular lesions due to a direct toxic effect of the compound. Doxorubicin induces a nephrotic syndrome in the rabbit, while mitomycin induces a haemolytic uraemic syndrome in humans. Finally, drug addiction often leads to glomerulosclerosis.

Animals↗
PubMed1989

Recurrent thrombosis and renal vascular disease in patients with a lupus anticoagulant.

In five patients suffering from recurrent thrombosis and/or fetal death, a lupus anticoagulant was associated with a renal vasculopathy. Ischaemic episodes also involved the skin, heart, eyes and/or central nervous system. All patients were hypertensive. Two had renal insufficiency, two had non-nephrotic proteinuria, and in the last patient renal cortical ischaemia was detected by a tomographic scan in the absence of proteinuria. Renal biopsy showed thrombosis and/or intimal fibrosis of intrarenal vessels, and normal or ischaemic glomeruli without proliferative lesions. High-titres of anticardiolipin antibodies were found in 3 of 3 cases, and persisted after steroid therapy even if the circulating anticoagulant factor disappeared. All patients received corticosteroid therapy, alone or in combination with immunosuppressive drugs; two patients had prolonged oral anticoagulation, but thrombotic episodes recurred after stopping the drug. One patient died; the remaining four survived 18 months to 11 years after diagnosis, with stable chronic renal insufficiency in one of them. These results show that a lupus anticoagulant may be associated with prominent renal vascular disease, in the absence of proliferative glomerular lesions, and suggest that continuous anticoagulation may be beneficial in these patients.

Adult↗
PubMed1989

[Renal cortex ischemia, right atrial thrombosis and coronary occlusion in anti-phospholipid antibody syndrome].

The presence of a lupus anticoagulant (LA) is paradoxically associated with a high incidence of arterial and venous thrombosis. In a patient with a lupus-like systemic disease, having received phenindione for 11 years, LA was discovered in association with recurrent deep venous thrombosis, a right atrial thrombus, coronary occlusion, arterial hypertension, thrombopenia, and anticardiolipin antibodies without anti-DNA antibodies. Renal cortical ischemia was detected by a tomographic scan. Renal biopsy showed glomerular ischemia and diffuse interstitial fibrosis. After a one-year anticoagulant and steroid therapy, LA has disappeared despite a high level of anticardiolipin antibodies, and renal function remains normal.

Autoantibodies↗
PubMed1988

[Acute granulomatous interstitial nephritis of drug origin].

Epithelioid cell granulomas within the renal interstitium are frequently found in drug-associated acute interstitial nephritis. Their presence is a strong argument in favour of an immunologically mediated nephropathy especially when extrarenal symptoms are absent and if the interstitial infiltrate does not contain eosinophils. They are probably due to a delayed hypersensitivity reaction. Unfortunately, there is no reliable experimental model. The high incidence of permanent renal damage observed in this type of nephritis indicates an early corticosteroid therapy, particularly when renal function does not rapidly improve after withdrawal of the offending drug.

Acute Disease↗
PubMed1988

[Acute interstitial nephritis caused by drug hypersensitivity. Current controversies].

Acute interstitial nephritis (AIN) due to drug hypersensitivity represents 0.8 to 8 p. 100 of all causes of acute renal failure. Two thirds of cases are due to antibiotics, mainly beta-lactamines, and to non-steroidal anti-inflammatory drugs. Blood hypereosinophilia, fever, arthralgias and/or hepatocellular damage are suggestive of an allergic drug reaction in patients with AIN, with a sensitivity of 0.75 and a specificity of 0.76. Examination of an early renal biopsy specimen is a clue to the diagnosis of AIN due to drug hypersensitivity if it discloses a diffuse or focal interstitial infiltration with lymphocytes, plasma cells, and mainly by eosinophils and/or epithelioid cell granulomas. These findings suggest a delayed hypersensitivity reaction, although many cases seem to be also mediated by humoral immune factors. Renal recovery is frequent when the responsible drug is promptly withdrawn. The value of steroid therapy in preventing residual renal damage has to be assessed by controlled studies.

Anti-Bacterial Agents↗
PubMed1986

Antihypertensive effects of tertatolol: 3-month comparative study against acebutolol.

Thirty-two hypertensive patients (mean age 52.9 +/- 1.7 years) with a supine diastolic blood pressure (DBP) between 95 and 130 mm Hg (mean 104.3 +/- 0.8) received, following a randomized allocation, either tertatolol 5 mg (n = 16) or acebutolol 400 mg (n = 16) in a single daily dose. The 2 drugs were administered during a 3-month treatment period (from day 0 to day 90) in a single-blind fashion. At rest (n = 32), the decrease of supine systolic blood pressure (SBP) reached 27.3 mm Hg after 1 month of tertatolol treatment (from day 0 to day 30; p less than 0.01); there was a further decrease of 5.1 mm Hg from day 30 (D30) to day 90 (D90) (NS). The corresponding decreases after acebutolol treatment reached respectively 22.3 mm Hg (p less than 0.01) and 5.7 mm Hg (p less than 0.05). Similar results were observed in the upright position. The decrease of supine DBP reached 14.0 mm Hg in patients treated with tertatolol from D0 to D30 (p less than 0.01); a further decrease of 2.9 mm Hg occurred from D30 to D90 (NS). The corresponding decreases in patients administered acebutolol reached respectively 7.6 mm Hg (p less than 0.01) and 5.2 mm Hg (p less than 0.01). Similar results were observed in the upright position. On submaximal exercise (ergometric bicycle; n = 18), the decrease of SBP reached respectively 31.3 mm Hg during tertatolol treatment from D0 to D30 (p less than 0.01) and 8.8 mm Hg from D30 to D90 (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Acebutolol↗
PubMed1986

Analgesic and non-steroidal anti-inflammatory drug-associated acute renal failure: a prospective collaborative study.

During a one-year period analgesic and non-steroidal anti-inflammatory drug-(NSAID) associated acute renal failure (ARF) was recorded in 147 of 398 patients registered in 58 nephrology units. This figure represented 36.9% of drug-associated ARF, and 6.8% of total patients with ARF hospitalized during the same period. Drugs involved were primarily glafenin (79), NSAID (62), paracetamol (5) and phenacetin (1 case). Hypersensitivity reactions were documented in 32 patients. Acute tubular necrosis was found in 20, and interstitial nephritis (AIN) in 9 of 34 biopsied patients. All patients in the glafenin group and 71.4% in the NSAID group recovered fully or regained previous renal function (p less than 0.01). Permanent renal damage (9.5% of total cases) was more frequent in patients with AIN than in those with other types of ARF (p less than 0.001). Preventive measures should be especially directed to older patients receiving NSAID, by avoiding the combined use of drugs potentiating their action and by correcting any predisposing factor to ARF.

Acetaminophen↗
PubMed1986

[Acute renal failure associated with drugs or iodinated contrast media. Results of a cooperative multicentric study by the Nephrology Society].

During a one-year period, drug-associated acute renal failure (ARF) was prospectively recorded in 398 patients, registered in 58 french nephrology Units. Drugs involved were primarily antibiotics, mainly aminoglycosides, glafenine, non-steroidal antiinflammatory drugs and contrast media. Hypersensitivity reactions were reported in 69 patients. Renal biopsy, performed in 81 instances, showed acute tubular necrosis in 42 and acute interstitial nephritis in 20 patients. Hypotension, sodium depletion and/or cardiac failure were predisposing factors in 198 cases. Fifty patients died, 251 recovered fully or regained previous renal function, and in 93 permanent renal damage remained. Advanced age, oliguria, severe ARF, and preexisting cardiac, hepatic or renal insufficiency were poor prognostic factors. Prevention of drug-associated ARF should be directed to high-risk patients, particularly those receiving aminoglycosides and contrast media.

Acute Kidney Injury↗
PubMed1984

[Acute pancreatitis caused by isolated involvement of the pancreas after closed abdominal injury].

Acute post-traumatic pancreatitis in unusual, accounting for no more than 1% of all cases of acute pancreatitis. The authors describe a case of acute pancreatitis in a patient who had a closed abdominal trauma during a football match. The recommended procedures for ensuring early diagnoses are described. Prognosis and management is dependent upon pathology and extension of lesions. Hemorrhagic and necrotic pancreatitis carries a poor prognosis, especially when diagnosis is delayed.

Abdominal Injuries↗