Anticancer Activity and Mechanisms of Action of MAPK pathway inhibitors

(B) The median (IQR) urine SG levels in anti-NMDAR antibody encephalitis patients with anti-NMDAR antibody <1:32 and anti-NMDAR antibody 1:32 were significantly lower than HCs, respectively (= 0

(B) The median (IQR) urine SG levels in anti-NMDAR antibody encephalitis patients with anti-NMDAR antibody <1:32 and anti-NMDAR antibody 1:32 were significantly lower than HCs, respectively (= 0.006 and < 0.001). of this article will be made available by the authors, without undue reservation. Abstract Objectives: The function of the N-methyl-D-aspartate receptor (NMDAR) in the kidney has been studied. However, the effect on the kidney from anti-NAMDAR antibody encephalitis has not been investigated thus far. Methods: Case data were collected from 82 Blasticidin S HCl Blasticidin S HCl patients with anti-NMDAR antibody encephalitis and 166 age- and sex-matched healthy controls (HCs). Clinical characteristics, urinalysis [including urine pH and urine specific gravity (SG)], serum creatinine (Scr), and estimated glomerular filtration rate (eGFR) based on Cr levels were evaluated. Results: At initial admission, urine pH levels and urine SG levels in anti-NMDAR antibody encephalitis patients were significantly higher and lower, respectively, than HCs (both < 0.001). There were no significant differences in Scr and eGFR between anti-NMDAR antibody encephalitis Rabbit Polyclonal to APLF patients and HCs. Urine pH levels in patients with anti-NMDAR antibody <1:32 were significantly lower than those in patients with anti-NMDAR antibody 1:32 (= 0.029). Urine pH levels were significantly lower (= 0.004) and urine SG levels were significantly higher Blasticidin S HCl (= 0.027) in a follow-up evaluation 3 months after treatment. Conclusions: The changes in urinalysis occur in patients with anti-NMDAR antibody encephalitis. The pathophysiological changes in anti-NMDAR antibody encephalitis were not limited to the CNS. Keywords: anti-N-methyl-D-aspartate receptor encephalitis, estimated glomerular filtration rate (eGFR), renal function, urinalysis, urine pH, urine specific gravity (USG) Introduction The anti-N-methyl-D-aspartate receptor (anti-NMDAR) antibody encephalitis is the most Blasticidin S HCl common antibody-mediated encephalitis (1) and is caused by the production of autoantibodies against the GluN1 subunit of NMDAR (2). It represents a severe neuropsychiatric manifestation characterized by seizures, memory decline, and behavioral deficits (3, 4). Microarray studies haveshown that all known NMDAR transcripts can be detected in the kidney (5), and there is now a consensus that activation of these receptors affects renal function, and in some cases may induce renal dysfunction (6). NMDARs are expressed in the renal cortex and medulla and appear to play a role in the regulation of renal blood flow, glomerular filtration, proximal tubule reabsorption, and urine concentration within medullary collecting ducts (6). Glomerular filtration, tubular reabsorption, and Blasticidin S HCl tubular excretion are three mechanisms through which kidneys accomplish the homeostasis of the internal environment (7). The glomerular filtration rate (GFR) is a universal marker of renal function (8) and classically used for evaluating individual’s kidney function and for scoring disease stages in chronic kidney disease (CKD) patients (9). Urine specific gravity (SG) correlates with urine osmolality and reflects the concentrating ability of the kidneys (10). Urine pH is generally used to provide an overall estimate of a patient’s acid-base status and reflects the pH of body fluids (11). In patients with anti-NMDAR antibody encephalitis, it is not clear whether anti-NMDAR antibodies could lead to damage in the kidney resulting in abnormal urinalysis and renal function. To the best of our knowledge, no studies have been conducted to analyze the urinalysis and renal function in patients with anti-NMDAR antibody encephalitis. The objective of this study is to evaluate the results from urinalysis and renal function between anti-NMDAR antibody encephalitis and HCs, including urine SG, pH, serum creatinine (SCr), and estimated GFR (eGFR). Methods Study Design and Samples This study is approved by the Medical Ethics Committee of the Third Affiliated Hospital of Sun Yat-sen University. All study participants have provided written consent for research and publication. We recruited 82 Chinese Han patients with anti-NMDAR antibody encephalitis from the Department of Neurology at the Third Affiliated Hospital of Sun Yat-sen University during March 2015 to November 2019. Diagnosis criteria for anti-NMDAR antibody encephalitis were based on the diagnostic criteria by Graus et al. (12): (1). The presence of one or more of the six major groups of symptoms: (i) Abnormal (psychiatric) behavior or cognitive dysfunction; (ii) Speech dysfunction (pressured speech, verbal reduction, mutism); (iii) Seizures; (iv) Movement disorder, dyskinesias, or rigidity/abnormal postures; (v) Decreased level of consciousness; and (vi) Autonomic dysfunction or central hypoventilation. (2). Anti-NMDAR antibody testing in cerebrospinal fluid (CSF) was positive. (3). Reasonable exclusion of other disorders. Additionally, none of the patients had urinary tract infections, stones in the kidney or urinary tract, or obviously abnormal thyroid function at initial admission or at follow-up. Anti-NMDAR antibodies in CSF, or both CSF and serum,.