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A 42-year-old male was referred to the internal medicine department because of renal failure and persistent malaise after a recent SARS-CoV-2 infection. Blood results showed anemia and severe renal insufficiency (hemoglobin of 10.3 g/dL and a creatinine of 2.19 mg/dL). Additional tests revealed a type I cryoglobulinemia with a cryoprecipitate composed of dual IgM (kappa and lambda). Further investigations on the cryoprecipitate revealed that the immunoglobulins were directed against SARS-CoV-2 antigens. In the meanwhile, our patient noticed improvement of his symptoms accompanied by resolution of laboratory abnormalities. Three months later, the cryoglobulin could no longer be detected.Type 1 cryoglobulinemia is usually associated with lymphoproliferative disorders and is characterized by various symptoms caused by cryoprecipitates occluding small blood vessels. This is, to our knowledge, the first case of type I cryoglobulinemia with proven precipitation of SARS-CoV-19 antibodies. COVID-19 induced cryoglobulinemia appears to have a mild disease course and to be self-limiting upon viral clearance.

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BACKGROUND: Hantavirus infection is an uncommon cause of acute renal failure with massive proteinuria. Serology tests to support a presumptive diagnosis usually take a few days. During the initial work-up, autoimmune causes including anti-glomerular basement membrane (GBM) glomerulonephritis need to be excluded, because these require urgent therapy. In this case the delay in serological testing caused a dilemma in treatment initiation. CASE PRESENTATION: An 18-year-old patient was admitted to the hospital with acute renal failure, erythrocyturia and massive proteinuria. Routine blood analysis showed leucocytosis (40,5 × 109/l) and a serum creatinine of 233 µmol/l. Infectious causes, e.g. leptospirosis or hantavirus infection, or an autoimmune disease, e.g., AAV or anti-GBM glomerulonephritis was the most feasible underlying diagnosis. Before hantavirus serology results were known, anti-GBM antibodies were positive. Treatment for anti-GBM glomerulonephritis was withheld, because of the absence of other signs and symptoms of the disease and slight improvement of renal function. The diagnosis of acute hantavirus infection was later on confirmed, by seroconversion of a follow-up serum sample. Without further intervention renal function recovered and anti-GBM antibodies disappeared. CONCLUSION: Hantavirus infection may induce anti-GBM antibodies, falsely suggestive of anti-GBM glomerulonephritis. Anti-GBM antibodies are supposed to be 100% specific. No earlier reports of false positive anti-GBM titers were reported. Nevertheless, the anti-GBM antibodies in this case were seen as an innocent bystander effect. Considering the need of urgent initiation of plasmapheresis and administration of immunosuppressants it may lead to diagnostic dilemmas with crucial therapeutic consequences. Knowledge of this anomaly when diagnosing acute renal failure, is very important.

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Measuring anti-dsDNA levels could support treatment adjustment during follow-up of patients with systemic lupus erythematosus (SLE). We investigated whether patients with exacerbations of SLE showed changes in anti-double-stranded DNA (anti-dsDNA) levels prior to the exacerbation using the Farr and EliA assay and examined which assay showed highest specificity and predictive value for exacerbations. Changes in anti-dsDNA of ≥ 25% prior to exacerbation were considered of clinical significance. Exacerbations were retrospectively abstracted from medical records. Eighteen of 48 patients showed one or more exacerbations. We found 22 exacerbations with complete lab work-up, all accompanied by ≥ 25% change in anti-dsDNA in one or both assays. Only 10 exacerbations showed concordant changes in anti-dsDNA in both assays. Changes in anti-dsDNA had a low predictive value for exacerbations of SLE, but the specificity of anti-dsDNA changes for patients with exacerbations was higher for EliA than Farr. We conclude that despite the limited relation between anti-dsDNA changes and exacerbations of SLE, anti-dsDNA testing could still support clinical decision making when used in the correct setting. We conclude that EliA is preferable over Farr for assaying anti-dsDNA during follow-up of patients with SLE because of higher specificity, less "hands-on" time and absence of radioactivity.

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The interpretation of specific IgE test results in patients with suspected food allergies is not always straightforward. In fact, specific IgE test results for food allergens can provide physicians with more questions than answers. Based on the description of two patient cases, we discuss the interpretation of specific IgE test results for food allergens; the description includes the diagnostic process, cross-reactivity and component-resolved diagnostics.

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BACKGROUND: Dexamethasone is a synthetic glucocorticoid and is analogous to cortisol. It is used in the low-dose overnight dexamethasone suppression test (LDODST) to diagnose hypercortisolism in patients suspected to be suffering from Cushing's syndrome (CS). Measuring plasma dexamethasone in conjunction with measuring the amount of cortisol following the LDODST may allow clinicians to improve the diagnosis of CS. METHODS: Plasma samples were cleaned up by solid-phase extraction before analysis. Liquid chromatographic separation was carried out under reversed-phase conditions prior to detection by tandem mass spectrometry. The analytes were determined in the presence of deuterated internal standards cortisol-d4 and dexamethasone-d4. RESULTS: Limit of quantitation (LOQ) was 1.89 nmol/L for dexamethasone and <0.02 µmol/L for cortisol. Recoveries of both analytes ranged from 80.2% to 114.4%. Intra- and interassay coefficients of variation were <15%. The concentration of dexamethasone and cortisol was determined in 62 patients after performing LDODST. Dexamethasone concentrations ranged from 3.0 to 21.5 nmol/L (median 7.4 nmol/L) for 57 of these samples. For five patients the concentration was 0.22 µmol/L). CONCLUSIONS: A method for the simultaneous measurement of dexamethasone and cortisol in human plasma by liquid chromatography/tandem mass spectrometry has been developed and validated. The method is suitable for controlling the compliance to the LDODST and for determining the cortisol plasma concentration after the test. The interpretation of LDODSTs was improved by the simultaneous determination of both analytes.

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Background: Influenza vaccination is recommended for patients with B-cell chronic lymphocytic leukaemia (CLL). Because response rates are often low, we decided to evaluate antibody response to single and booster vaccinations with influenza A and B virus vaccine in these patients. Methods: Twenty patients with B-CLL received two subunit virus vaccine injections 21 days apart. Antibody titres were determined before and 21 days after the single and booster vaccinations. The serological response was expressed using the following criteria: (1) response rate, i.e. the proportion of subjects with at least a 4-fold titre increase; (2) the protection rate, i.e. the proportion of subjects exceeding the threshold of 100 (influenza A) or 200 (influenza B); and (3) the mean fold increase (MFI), i.e. the difference between the log-adjusted geometric mean titres of pre- and post-vaccination sera. Results: Response rates were 5% for influenza A and 15% for B after the single vaccination and 15% for A and 30% for B after the booster vaccination. Protection rates were 0% for influenza A and 25% for B after the single vaccination; they were 5% (H1N1) and 10% (H3N2) for influenza A and 30% for B after the booster. The MFI+/-S.D. (range) after the booster vaccination was 0.26+/-0.33 (0-1.00), 0.17+/-0.34 (0-1.00) and 0.35+/-0.34 (0-1.20) for H1N1, H3N2 and influenza B, respectively. Conclusion: In this study with B-CLL patients, immune response to influenza vaccination was poor. Thus, single and booster vaccinations with influenza virus vaccine do not appear to be of great value to patients with B-cell CLL.