[InspeCKD - Analysis of the use of diagnostics in patients at high risk for chronic kidney disease in German general practitioner (GP) practices]. / InspeCKD - Analyse zur Nutzung von Labordiagnostik im Kontext der chronischen Nierenerkrankung : Daten von Risikopatientinnen und -patienten in deutschen Hausarztpraxen.

BACKGROUND: Despite the high prevalence of chronic kidney disease (CKD) in Germany, only a small proportion of patients are currently diagnosed with CKD. Patients with hypertension, diabetes mellitus, and/or cardiovascular disease have a significantly increased risk of developing CKD and rapid disease progression and should therefore be screened and monitored in accordance with the guidelines. OBJECTIVES: The aim of this retrospective, cross-sectional study was to gain insights into appropriate diagnosis of patients at risk for CKD in German general practitioner practices. METHOD: For the analysis of the use of CKD-relevant diagnostics, electronic patient records from German general practitioner practices were analyzed. Adults with hypertension and/or diabetes mellitus and/or cardiovascular disease with a documented observation period of at least one year were included in the study. RESULTS: Data from a total of 448,837 patients from 1244 general practitioner practices were analyzed. 75.8% of patients had hypertension, 35.1% had cardiovascular disease, and 32.4% had diabetes mellitus. During a mean observation period of 1.7 years, serum creatinine was assessed at least once in 45.5% of patients. A urine dipstick test for albuminuria was performed in 7.9% of patients and in 0.4% of patients, urine albumin-to-creatine ratio (UACR) was measured. Laboratory diagnostics were initiated a little more frequently in high-risk patients compared to the overall cohort. CONCLUSIONS: The study highlights that despite known risk factors, guideline compliant CKD screening is rarely performed in German general practitioner practices, which implicates the need to increase the awareness of early diagnosis of CKD in patients at risk.

Off-label application of intravenous immunoglobulin (IVIG) for treatment of Cogan's syndrome during pregnancy.

We report the case of a woman with Cogan's syndrome concomitant with the wish to have children. After three major flares of the disease that led to unilateral deafness, immunosuppressive therapy with prednisolone and azathioprine was started. Because of the severe side effects, an off-label therapy with intravenous immunoglobulin (IVIG) was initiated, under which our patient has since given birth to three healthy children. To our knowledge this is the first report to describe Cogan's syndrome with multiple successful pregnancies under IVIG treatment.

Down-regulation of CD73 on B cells of patients with viremic HIV correlates with B cell activation and disease progression.

Recently, alterations of the T cell expression of the ectonucleotidases, CD39 and CD73, during HIV infection have been described. Here, peripheral (n = 70) and lymph nodal B cells (n = 10) of patients with HIV at different stages of disease as well as uninfected individuals were analyzed via multicolor flow cytometry with regard to expression of CD39 and CD73 and differentiation, proliferation, and exhaustion status. Patients with chronic, untreated HIV showed a significantly decreased frequency of CD73-expressing B cells (P < 0.001) compared with healthy controls. Decreased frequencies of CD39+CD73+ B cells in patients with HIV correlated with low CD4+ counts (P < 0.0256) as well as increased proliferation and exhaustion status as determined by Ki-67 and programmed death-1 expression. Down-regulation of CD73 was observed in naive and memory B cells as determined by CD27 and CD21. Neither HIV elite controller patients nor antiretroviral therapy-treated patients had significantly lower CD39 and CD73 expression on B cells compared with healthy controls. Of importance, low CD73+ expression on B cells was associated with modulated in vitro B cell function. Further in vivo studies are warranted to evaluate the in vivo role of phenotypic loss of CD73 in B cell dysregulation in HIV.