GFR increased 75 ± 24% ( = 0.016, = 3). PC-AKI developed following diatrizoate i.v. infusion (Cr 2.6 ± 0.7 baseline to 3.4 ± 0.6 at 24 h, < 0.01, = 3). LOTUS (starting 15 min prior to contrast and lasting for 90 min) prevented PC-AKI in the same animals 1 week later (Cr 2.5 ± 0.4 baseline to 2.6 ± 0.7 at 24 h, = ns, = 3). In patients with CKD ( = 10), there was an overall 25% increase in GFR in response to LOTUS ( < 0.01). LOTUS increased intrarenal NO, RBF, and GFR and prevented PC-AKI in a large animal model of CKD, and significantly increased GFR in patients with CKD. This novel approach may provide a noninvasive nonpharmacological means to prevent PC-AKI in high-risk patients. LOTUS increased intrarenal NO, RBF, and GFR and prevented PC-AKI in a large animal model of CKD, and significantly increased GFR in patients with CKD. This novel approach may provide a noninvasive nonpharmacological means to prevent PC-AKI in high-risk patients. Renal involvement was a common extra-articular manifestation of ankylosing spondylitis (AS). https://www.selleckchem.com/products/epacadostat-incb024360.html Few reports have investigated the pathological characteristics and renal outcomes of AS patients with kidney disease. The aim of this study was to investigate the pathological spectrums and the renal prognosis of AS patients with kidney disease. This retrospective and observational study was conducted working on 62 patients (47 males and 15 females) with a diagnosis of AS (ACR, 1984) and renal biopsies between 2008 and 2017. The histopathological findings and associated clinical manifestations were collected, and the renal prognoses of patients with kidney disease were evaluated too. Multivariate binary logistic regression analysis was performed to identify risk factors for the occurrence of IgA nephropathy (IgAN). Renal biopsy revealed that IgAN accounted for a majority (74.2%) of the kidney disease with AS, while membranous nephropathies, minimal change disease, focal segmental glomerulosclerosis, and other lesions accounted for a small minority. Multivariate analysis revealed that serum immunoglobulin A >3.45 g/L and immunoglobulin G >9.06 g/L were risk factors for the occurrence of IgAN. With a median follow-up time of 24.3 months, 28 patients (50.9%) reached complete remission, 9 patients (16.4%) had partial remission, and 1 patient had an eGFR decline >30%. No difference was found in prognosis between IgAN and non-IgAN. IgAN occurred in 76.4% of the kidney disease with AS, and higher serum immunoglobulin A and G increased the risk for the occurrence of IgAN. The renal prognosis of kidney disease in AS was good. IgAN occurred in 76.4% of the kidney disease with AS, and higher serum immunoglobulin A and G increased the risk for the occurrence of IgAN. The renal prognosis of kidney disease in AS was good. Serum phosphorus (SP) level is closely associated with overall mortality and cardiovascular events, while the role of SP controlled duration is not fully recognized. Here, we conducted a retrospective cohort study in our department to identify the relationship of SP controlled duration with clinical outcomes in patients undergoing peritoneal dialysis (PD). PD patients in our center from January 1, 2009, to June 30, 2019, were followed up at 2-month (the first year) or 5-month (the next follow-up period) intervals, and until death, until PD withdrawal, or until June 30, 2019. Data at each follow-up point were collected from their medical records. SP levels, changed degree of SP over baseline, and SP controlled duration were analyzed with overall mortality, PD withdrawal (including death, transferred to hemodialysis, and received renal transplantation), and combined endpoint (including death, acute heart failure, cardiovascular event, and stroke). A total of 530 patients entered the analysis. Of them, 456ion of SP control were tightly associated with overall mortality. We should control SP levels as early, as possible, and as long as we could. Levels of urinary microvesicles, which are increased during various kidney injuries, have diagnostic potential for renal diseases. However, the significance of urinary microvesicles as a renal disease indicator is dampened by the difficulty to ascertain their cell source. The aim of this study was to demonstrate that podocytes can release migrasomes, a unique class of microvesicle with size ranging between 400 and 2,000 nm, and the urine level of migrasomes may serve as novel non-invasive biomarker for early podocyte injury. In this study, immunofluorescence labeling, electronic microscopy, nanosite, and sequential centrifugation were used to purify and analyze migrasomes. Migrasomes released by podocytes differ from exosomes as they have different content and mechanism of release. Compared to podocytes, renal tubular cells secrete markedly less migrasomes. Moreover, secretion of migrasomes by human or murine podocytes was strongly augmented during podocyte injuries induced by LPS, puromycin amino nucleoside (PAN), or a high concentration of glucose (HG). LPS, PAN, or HG-induced podocyte migrasome release, however, was blocked by Rac-1 inhibitor. Strikingly, a higher level of podocyte migrasomes in urine was detected in mice with PAN-nephropathy than in control mice. In fact, increased urinary migrasome number was detected earlier than elevated proteinuria during PAN-nephropathy, suggesting that urinary migrasomes are a more sensitive podocyte injury indicator than proteinuria. Increased urinary migrasome number was also detected in diabetic nephropathy patients with proteinuria level <5.5 g/day. Our findings reveal that podocytes release the "injury-related" migrasomes during migration and provide urinary podocyte migrasome as a potential diagnostic marker for early podocyte injury. Our findings reveal that podocytes release the "injury-related" migrasomes during migration and provide urinary podocyte migrasome as a potential diagnostic marker for early podocyte injury. The syndrome of tubulointerstitial nephritis and uveitis (TINU) is an uncommon and multisystemic autoimmune disorder. This review reports a rare case of TINU being superimposed on thrombotic microangiopathy (TMA) and, by comparing with the available literature, also summarizes the clinical features, associated conditions, treatment, and outcome of patients with TINU. Herein, we report the case of a 37-year-old male patient with acute kidney injury (AKI) clinicopathologically identified as malignant hypertension-induced TMA superimposed by acute tubulointerstitial nephritis, which was suspected to be related to drug hypersensitivity. After treatment with oral prednisone combined with a renin-angiotensin system inhibitor, the patient achieved partial renal recovery and was withdrawn from hemodialysis. Recurrent AKI concomitant with new-onset asymptomatic uveitis was detected during routine clinical follow-up after cessation of prednisone. TINU was then diagnosed, and prednisone followed by cyclophosphamide was prescribed.