Urinalysis of individuals with renal hyperfiltration using ATR-FTIR spectroscopy.

Abnormal increased glomerular filtration rate (GFR), otherwise known as renal hyperfiltration (RHf), is associated with an increased risk of chronic kidney disease and cardiovascular mortality. Although it is not considered as a disease alone in medicine today, early detection of RHf is essential to reducing risk in a timely manner. However, detecting RHf is a challenge since it does not have a practical biochemical marker that can be followed or quantified. In this study, we tested the ability of ATR-FTIR spectroscopy to distinguish 17 individuals with RHf (hyperfiltraters; RHf (+)), from 20 who have normal GFR (normofiltraters; RHf(-)), using urine samples. Spectra collected from hyperfiltraters were significantly different from the control group at positions 1621, 1390, 1346, 933 and 783/cm. Intensity changes at these positions could be followed directly from the absorbance spectra without the need for pre-processing. They were tentatively attributed to urea, citrate, creatinine, phosphate groups, and uric acid, respectively. Using principal component analysis (PCA), major peaks of the second derivative forms for the classification of two groups were determined. Peaks at 1540, 1492, 1390, 1200, 1000 and 840/cm were significantly different between the two groups. Statistical analysis showed that the spectra of normofiltraters are similar; however, those of hyperfiltraters show diversity at multiple positions that can be observed both from the absorbance spectra and the second derivative profiles. This observation implies that RHf can simultaneously affect the excretion of many substances, and that a spectroscopic analysis of urine can be used as a rapid and non-invasive pre-screening tool.

Drug Induced Thrombotic Microangiopathy with Certolizumab Pegol

Background: Certolizumab pegol is used to treat ankylosing spondylitis, Crohn's disease, psoriatic arthritis, and rheumatoid arthritis. Unlike other monoclonal antibodies such as infliximab and adalimumab, certolizumab does not contain an Fc fraction and hence does not induce complement activation. In this report, we describe the case of a patient with thrombotic microangiopathy caused due to certolizumab pegol, with a brief description about the pathophysiological approach to thrombotic microangiopathy. Case Report: A-39-year-old man suffering from ankylosing spondylitis for the past 10 years presented with fatigue. He had been on certolizumab pegol treatment for 6 months, starting with 400 and 200 mg every 2 weeks. He had significant nonimmune hemolytic anemia and thrombocytopenia without a disseminated intravascular coagulopathy. Schistocytes were observed in more than 10% of the erythrocytes per field. Plasma exchange along with corticosteroid treatment was started. There was a dramatic improvement within a week, and after 10 sessions of plasma exchange, the patient was discharged on corticosteroids with a tapering plan. ADAMTS13 enzyme activity was determined to be normal. Conclusion: The development of drug-induced thrombotic microangiopathy may be either immune-mediated or dose-dependent toxicity-mediated Anti-drug antibodies and their immunological aspects are still unclear and yet to be elucidated.