[Renal amyloidosis secondary to post-traumatic chronic leg ulcer].
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Biomedical subjects
Publications and source records attributed to D Kleinknecht.
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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.
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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.
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The simultaneous occurrence of hepatitis B surface antigen (HBsAg) and antibody to HBsAg (anti-HBs) of different subtypes in the serum of a hemodiaylzed patient was studied. The w(a) subdeterminants were involved. The HBsAg belonged to the ayw3 subtype, and the anti-HBs exhibited monospecific anti-w2 activity. Both the HBsAg and the anti-HBs were detectable by counterelectrophoresis (CEP). The specificity of the antibody was demonstrated by CEP in tests against 128 sera containing HBsAg of 12 different subtypes and in absorption experiments with eight sera containing HBsAg of eight different subtypes, as well as by radioimmunoassay in the liquid phase. The monospecific antibody was selectively directed against the w2 subdeterminant of the adw2 subtype and was designated anti-w2.
Results obtained by thermography and angiography in surveying vascular access have been compared in 33 haemodialysis patients, including 23 with Cimino arteriovenous fistulae and 10 with homografts and heterografts. In 23 of 30 patients, blood flow stealing through collateral veins, or venous stenosis was detected by thermography and confirmed by angiography. Thermography seems a quick and simple method in routine conditions, restricting angiography to selected patients for whom a surgical revision of the fistula or of the graft is needed.
Data of the DIAPHANE Dialyse-Informatique system of the Society of Nephrology have been collected by patients just on a home dialysis program after training in the hemodialysis Unit of the Hospital of Montreuil. 35 patients have been using the computerized records since January 1978. A critical analysis of the first year has been made and results obtained have been compared with those obtained during the same period in patients dialysed in the Hospital. Results show that home dialysis patients are well able to fill in the computerized medical record concerning the dialysis session follow-up, and that the quality of the recorded information is similar to that recorded in hospital by nurses. Nevertheless few simplifications of home dialysis data sheet are considered. Computerized treatment of data collected on home dialysis program should allow useful comparisons required to improve the quality of care and expansion of this dialysis method.
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(1) AIN is the most frequent pattern of drug-induced immunologically mediated renal injury. A number of drugs may be responsible for AIN, namely methicillin and other penicillin derivatives, rifampicin, phenindione and sulfonamides. Particular clinical and pathological features often suggest an immune pathogenetic mechanism. IgG anti-TBM and IgE antibodies have been found in only a few cases and it is likely that antibody-mediated and cell-mediated injury may operate in the same patient. (2) Only few examples of drug-induced vasculitis and glomerulonephritis are known, and the pathophysiology of this kind of renal damage is poorly understood.
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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.
In a controlled study, the protection effect of hepatitis B immune globulin (HBIG) was evaluated in patients hemodialyzed for less than one month in two collaborating units. Fifteen randomly selected patients received HBIG at five to eight week intervals throughout the study, and 13 other control patients received no immunoglobulin. During a follow-up period of 14 to 30 months, none of the HBIG-treated and 12 of the control patients developed evidence of exposure to virus B hepatitis, including 10 with HBs Ag antigenemia (p is less than 0.001): five of these remained persistently antigen positive. Evidence of non-B hepatitis was found in 8 HBIG-treated and in 3 non-treated patients. Only two HBIG-treated patients developed active antibodies against hepatitis B surface antigen. Thus, HBIG seems effective in preventing hepatitis B in hemodialysis patients, provided the interval between two injections is not greater than two months. However, prolonged administration of HBIG may impair passive-active immunization to hepatitis B virus.
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