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D Kleinknecht

Publications and source records attributed to D Kleinknecht.

At least 37 records · Page 2Linked to original sources
PubMed1993

[Cardiac manifestations of phospholipid antibody syndrome. Study of 2 cases].

Cardiac manifestations of phospholipid antibody syndrome may include mitral and/or aortic valve disease, pseudo-infectious endocarditis, thrombi of the right atrium, myocardial infection, pulmonary artery hypertension and cardiomyopathy with global or segmental left ventricular dysfunction. The authors report two patients showing evidence simultaneously of a circulating anticoagulant, dissociated syphilis serology and cardiolipin antibodies at a very high level. They had the majority of cardiac complications described in phospholipid antibody syndrome. Both also had renal involvement and one of them had recurrent venous thromboses and a cerebrovascular accident. Prolonged corticosteroid treatment, combined with anticoagulants in one patient, was accompanied by stability of lesions with follow-up of five years and ten months respectively.

Adult↗
PubMed1993

Acute reversible renal failure with macroscopic haematuria in IgA nephropathy.

Macroscopic haematuria is common in IgA nephropathy, but its significance and influence on prognosis remains uncertain. We compared the clinical and pathological features of 11 adult patients with primary IgA nephropathy who had had a renal biopsy during or shortly after a bleeding episode. Six patients developed transient acute renal failure (ARF) (group 1) and five did not (group 2). Patients of group 1 had a higher percentage of tubular red-blood-cell (RBC) casts (P < 0.05) and of glomerular crescents (P < 0.001). However, crescents were focal and involved less than 50% of glomeruli. Acute tubular necrosis was only present in patients of group 1, and ARF was attributed to the acute tubular changes rather than to the glomerular lesions. Despite a prolonged duration of ARF (mean: 38 days), further outcome did not differ in patients of both groups. We suggest that acute tubular damage and/or tubular obstruction by RBC casts should be considered in any patient who develops ARF soon after a haematuric episode.

Acute Kidney Injury↗
PubMed1992

Acute renal failure after the use of angiotensin-converting-enzyme inhibitors in patients without renal artery stenosis.

During a 4-year period, acute renal failure was observed in 27 patients (mean age 65 years) treated by various angiotensin-converting-enzyme (ACE) inhibitors for hypertension, heart failure, or a combination of both. None had significant renal artery stenosis on angiography. Overt volume depletion was present in 21 and hypotension in 12 cases. All patients received diuretic therapy and/or a low-salt diet. Other facilitating factors included cardiac failure, pre-existing chronic renal insufficiency, combined therapy with non-steroidal anti-inflammatory drugs, and diabetes mellitus. Twenty-two patients had two or more of these factors at presentation. A renal biopsy performed in 10 cases showed severe arteriosclerosis of small renal arteries in eight and acute tubular necrosis in five instances. Therapy comprised volume expansion, and withdrawal of diuretics and, except in two patients, of ACE inhibitors. Twenty-one patients recovered normal renal function, two died, and permanent renal damage remained in four. These results suggest that sodium depletion has a critical role in inducing acute renal failure, whose outcome is not always benign. A combination of diuretics and ACE inhibitors should be prescribed with caution, especially in older patients with small as well as with large renal vessel disease.

Acute Kidney Injury↗
PubMed1992

[Liddle syndrome (or pseudo-hyperaldosteronism). Long-term development and erythrocyte potassium flow study in 4 cases].

BACKGROUND: Liddle's syndrome (or pseudoprimary aldosteronism) is a rare hereditary disease; only 18 cases have been reported since 1963. Its cause remains unclear, but one of its features is increased cell membrane permeability to ions. PATIENTS AND METHODS: A diagnosis of Liddle's syndrome was made in 4 new cases, all female, two of them sisters (cases n0 3 and 4), at the ages of 2, 12, 5 and 4 years. The first manifestations were dehydratation with hypokalemia at 6 months (case n0 1), hypertension at 2 years (case n0 2), polydipsia with poor weight and height gain at 5 and 4 years of age (cases n0 3 and 4). At diagnosis, all the patients had severe hypertension, metabolic alkalosis, hypokalemia and hyperkaliuria, low plasma renin activity and serum aldosterone levels. Administration of antihypertensive agents was without effect, but the hypertension was reduced when triamterene and low-sodium diet were used. Hypercalciuria was observed in 2 cases and nephrocalcinosis in 2 (case n0 1 had both hypercalciuria and nephrocalcinosis). The 2 oldest patients (n0 3 and 4) developed progressive kidney failure, possibly due to reno-vascular disease secondary to hypertension. Patient n0 3 underwent kidney transplantation 18 years after the first symptoms of the disease. This resulted in the complete disappearance of her hypokalemia and hypertension. The red blood cell membrane permeability to K+ and Cl- was studied in all 4 cases before triamterene treatment. The passive permeability to K+ and (K+/Cl-) cotransport were both elevated. A second study, 3 years (cases n0 2 and 3) and 8 years (cases n0 1 and 4) later, of patients treated with triamterene showed low values for passive K+ permeability and (K+/Cl-)-cotransport. CONCLUSIONS: The 4 new cases of Liddle's syndrome had the classic features of the disease, except for hypercalciuria and nephrocalcinosis in 2 of them. The cell membrane permeability data are difficult to interpret. Hypokalemia and hypertension were immediately corrected after kidney transplantation in one case and remained so for 4 years, suggesting that this disease is tubular in origin.

Aldosterone↗
PubMed1991

[Glomerulonephritis of infectious origin].

Glomerulonephritis may complicate infections due to various microorganisms. These microorganisms are bacterial, fungal, viral or parasitic. Considerable clinical and experimental evidence has accumulated to indicate that glomerular injury is due to in situ immune complex deposition. In France, renal lesions are more often due to focal skin infection and sinus or visceral abscesses, with or without endocarditis, rather than to pharyngeal streptococcal infection. Staphylococcal infections are a frequent cause, especially in intravenous illicit drug users. Recovery requires suppression of the infective agent. However, in severe forms, after initial acute glomerular damage the evolution may be characterized by the development of chronic glomerulonephritis.

Glomerulonephritis↗
PubMed1991

Chronic effects of tertatolol on renal function in hypertensive patients with mild chronic renal failure.

To assess the potential benefit of drug-induced renal haemodynamic changes in patients with chronic renal failure, we have evaluated the effects of the beta-blocking agent tertatolol on blood pressure, glomerular filtration rate, and renal plasma flow. Inulin and PAH clearances were performed before and after 3 months treatment and oral tertatolol, 5 mg daily in eight hypertensive patients with moderate chronic renal failure. After 3 months of treatment, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) increased significantly by 10% and 13% respectively, whereas renal vascular resistance decreased by 16% and the filtration fraction was unchanged. These results indicate that tertatolol possesses novel renal haemodynamic properties in hypertensive patients with chronic renal failure. However, the long-term benefit of such a therapy is yet to be confirmed.

Adrenergic beta-Antagonists↗
PubMed1991

Renal complications of intravesical bacillus Calmette-Guérin therapy.

We report 3 patients who developed signs of systemic infection and renal insufficiency after intravesical bacillus Calmette-Guérin (BCG) instillations for a bladder cancer. Renal biopsy showed tubulo-interstitial nephritis with or without epithelioid granulomas in 2 cases, and mesangial glomerulonephritis in the last case. All patients had granulomatous hepatitis in association. It seems that hematogenous dissemination via a traumatic instillation of BCG and/or an immune-complex mechanism may have contributed to the renal damage, which was only partially reversible in 2 patients.

Administration, Intravesical↗
PubMed1991

[Extramembranous glomerulonephritis induced by lithium].

We report the case of a patient who developed a nephrotic syndrome after lithium carbonate therapy. The nephrotic syndrome disappeared after withdrawal of therapy and recurred when the patient was rechallenged with the same drug. This seems a convincing argument to believe that lithium was the causal agent. Renal biopsy specimens showed membranous nephropathy, suggesting that immune-complex formation was involved in the reaction to the drug. Membranous nephropathy is an exceptional and benign hazard during lithium therapy, and underlines the need for periodic urinalysis in patients treated with the drug.

Glomerulonephritis, Membranous↗
PubMed1990

Transjugular renal biopsy.

A novel technique to obtain renal biopsy specimens from patients in whom percutaneous renal biopsy is contraindicated is described. After adaptation of equipment used for transjugular liver biopsy, 50 such patients underwent transjugular renal biopsy: specimens of renal tissue were obtained from 44 patients, and glomeruli were found in 38 specimens. No major complications were observed and histological examination of the biopsy specimens led to changed diagnosis or management in 13 patients. Transvenous renal biopsy should be considered when percutaneous biopsy is contraindicated or has failed.

Aged↗