Biomedical subjects
Publications and source records attributed to K Andrassy.
In 4 consecutive cases of Wegener's granulomatosis with glomerulonephritis, antibodies against the extractable nuclear antigen SSA (Ro) could be demonstrated with counterimmunoelectrophoresis. Antibodies were demonstrable on admission and paralleled disease activity while patients were under therapy. This potential serological marker may be of value for diagnosis and follow-up of patients with Wegener's granulomatosis.
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IgA-glomerulonephritis represents the most frequent glomerulonephritis (GN; 20%) among our patients. In contrast to data from the literature the prognosis is not benign. Renal insufficiency developed in 17 out of 50 investigated patients within 4 to 96 months, 3 of these patients had to undergo dialysis. Eleven of the 17 patients still had a normal renal function at the time of diagnosis. Malignant hypertension was present in 5 patients. An unfavourable course was predictable in cases of male gender, proteinuria, hypertension, age above 30 years, and histological changes indicating glomerulosclerosis, tubular atrophy, interstitial fibrosis and vascular lesions. Increased serum IgA levels, circulating IgA complexes, association with certain HLA-B or -Dr antigens as well as clinical symptoms and signs of haematuria, dysuria and kidney pains were not helpful either for diagnosis or for prognosis. The value of skin biopsy was comparatively small. Positive IgA demonstration was possible in 12 out of 41 cases with IgA-GN, however, also in 4 out of 21 patients with non-IgA-GN. None of 50 probands without renal disease showed IgA. Five out of 7 skin biopsies demonstrated IgA2, one IgA1 and one both IgA1 and IgA2. Increased serum IgA levels were found in a high percentage (21 out of 38 patients). The same applied to circulating IgA-complexes (8 out of 33 patients).
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Two new beta-lactam antibiotics, moxalactam and cefotaxime, were administered to two groups of patients with clinical indications for cephalosporin therapy and bacteriologically confirmed infection. The ten patients receiving moxalactam included five patients with impaired renal function; the ten receiving cefotaxime included seven with impaired renal function (serum creatinine greater than 1.3 mg/dl). Antibiotics were administered for seven days in dosages adjusted to the level of renal function. Serum trough levels, measured by microbiological assay, were within the therapeutic range: moxalactam median, 3 micrograms/ml (range, 0.6-20 micrograms/ml) and cefotaxime median, 2.9 micrograms/ml (range, 0.5-16 micrograms/ml).
IgA-glomerulonephritis (IgA-GN) accounts for approximately 20 per cent of all glomerulonephritis in our unit. Seventeen out of 50 patients with IgA-GN developed renal failure, which appeared in 11 out of 17 over the course of a mean follow-up of 68 months. Haemodialysis was required in three patients. Twenty-two out of 50 patients had hypertension, five with malignant hypertension. Perivascular IgA deposits were found in skin biopsies of 29 per cent of patients with IgA-GN and also in 19 per cent of patients with other GN, but not in healthy controls. Mucosal (salivary and nasal) secretory IgA concentrations were normal. In cutaneous and glomerular IgA/IgM deposits, IgA1 was demonstrated using monoclonal antibodies. No excess of HLA-A, B or DR antigens and no relation of clinical course and HLA-Bw35 were found.
Antibody response to vaccination with hepatitis B vaccine (HB-Vax) was evaluated in 43 staff, 81 dialysis patients and 12 non-dialysed uraemic patients. We confirmed less frequent seroconversion and lower concentration of antibody to hepatitis B surface antigen (anti-HBs) in dialysis patients despite a higher dose (40 micrograms vaccine). However, more frequent vaccination (5 times vs 3) increased anti-HBs concentration to almost normal. Concomitant administration of hepatitis B immunoglobulin (HBIG) and hepatitis B vaccine (passive/active) did not interfere with vaccination success. Antibody response was equally poor in dialysed non-dialysed uraemic patients.
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Heparin dose requirements for s.c. heparin prophylaxis were investigated in control individuals and in uremic patients. Heparin levels (neutralisation of factor Xa activity, neutralisation of Xa amidolytic activity; PTT and thrombin time) at timed intervals after single and repetitive s.c. doses of 5,000 or 7,500 IU were measured in 11 uremic patients and 9 individuals with normal renal function. At a dose of 2 x 5,000 IU/d heparin s.c. no difference between controls and uremic individuals was found. In contrast, in uremic patients, peak concentrations and area under the curve (AUC) were significantly lower and plasma half life shorter after 3 x 5,000 IU heparin s.c. After repeated administration of heparin, heparin concentrations (24 hrs) had fallen to nil in uremic patients whereas in controls measurable activity was still demonstrable. After i.v. bolus injection of heparin, peak concentrations were identical in controls and in uremic patients, but elimination half life was prolonged in uremic patients. It is therefore suggested that lower plasma heparin concentration after heparin s.c. is the result of diminished net absorption from the subcutaneous depot. It is concluded that in order to achieve a given plasma activity, higher s.c. doses of heparin must be administered to uremic patients than to non-uremic individuals. But further studies are required to demonstrate safety and efficacy of heparin prophylaxis in uremic individuals.
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A patient was observed with interstitial nephritis which resulted in renal tubular acidosis (distal type), tubular proteinuria and defective urinary concentrating ability in the absence of edema, elevated arterial blood pressure, glomerular proteinuria or abnormal urinary sediment. The presence of interstitial nephritis was established by renal biopsy which showed dense infiltrates in the interstitium, interstitial fibrosis and thickening and splitting of the pericapillary basal membranes. Immunofluorescence was non contributory. Extrarenal symptoms were discrete (arthralgia of both hands, Raynaud's syndrome upon cold exposure). Mixed connective tissue disease (MCTD) was suspected because of a positive ANF test (speckled pattern), which was completely abolished by ribonuclease pretreatment. However, in hemagglutination tests, no antibodies against ribonuclear protein (ENA) could be demonstrated. The diagnosis of Sjögren's syndrome was established by demonstration of antibodies against SSA and SSB antigens. The observation suggests that in patients with interstitial nephritis the diagnosis of Sjörgren's syndrome must be considered even if extrarenal symptoms of Sjögren's disease are minimal or lacking. The diagnosis can be established with recent serological techniques.
In 40 patients with non-metastasising (n = 31) and metastasising (n = 9) renal cell carcinoma, evidence of Stauffer's syndrome (increase in alkaline serum phosphatase and prolongation of prothrombin time) was found in 18 patients. Prolongation of prothrombin time was not due to depletion of vitamin K-dependent coagulation factors or manifest fibrinolysis, but due to the presence of circulating fibrinogen fibrinmonomer-FDP complexes. Ethanol gelation test was found to be positive in 28/40 subjects and soluble fibrin monomer complexes were increased in 38/40 patients. The resulting disturbance of fibrinogen-fibrin conversion was reflected by an increase in thrombin coagulase time and reptilase time. These findings suggests a state of latent compensated intravascular coagulation (presumably triggered within the vascular tumor). For diagnostic purposes the most sensitive indicator is thrombin coagulase time. Thrombin coagulase time normalised after tumor resection and was positive in patients with recurrent metastases. The increase in alkaline serum phosphatase was due to an increase in the hepatic isoenzyme. Such an increase was much more common than the elevation of total alkaline serum phosphatase. Regan's isoenzyme was only found in 1 subject. In parallel, gamma-GT was elevated in 24 patients. The study shows that Stauffer's syndrome occurs more frequently than commonly assumed when thrombin coagulase time, gamma-GT and the hepatic isoenzyme of alkaline serum phosphatase are determined in patients with renal cell carcinoma. DIC and low grade fibrinolysis may account for the coagulation abnormalities of the syndrome.
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