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The risk of dialysis following contrast exposure is unclear. We aimed to examine the overall risk of contrast induced nephropathy and the need of dialysis based on a systematic review with random-effects meta-analysis. We searched the electronic database including PubMed, Medline, Embase, and Cochrane Library from inception to 31 October, 2020 with predetermined search term to identify relevant studies. Observational studies investigating the association between contrast induced nephropathy after angiography and the need of dialysis were included, and summary risks were estimated. Two independent reviewers extracted the data, followed with random effects model to calculate the overall pooled incidence of contrast induced nephropathy and the need of dialysis after angiography. Subgroup-analysis and meta-regression were performed to assess heterogeneity of incidence across studies. Of 2,243 identified articles, 259 met our inclusion criteria were included in the meta-analysis after screening. Pooled effect estimates had the following summary incidence proportion for contrast induced nephropathy after angiography: 9.06% (95% CI: 8.53-9.58%; derived from 120 studies) and 0.52% (95% CI: 0.37-0.70%; derived from 110 studies) for the need of dialysis, respectively. The stratified summary incidence proportion of contrast induced nephropathy after contrast administration intra-arterial route was 9.60% (95% CI: 9.0-10.2%; derived from 106 studies) and was 0.6% (95% CI: 0.40-0.80%; derived from 100 studies) for the need of dialysis, respectively. Our meta-regressions found that the amount of contrast medium exposure was associated with contrast-induced nephropathy. The potential risk of dialysis needs to be communicated to patients undergoing procedures requiring contrast, especially intra-arterial exposure. [https://reurl.cc/8Wrlry], identifier [CRD42020170702].

Patients with end stage renal disease (ESRD) are at high risk of developing upper tract urothelial carcinoma (UTUC). Due to high recurrence rate of UTUC in contralateral kidney and ureter, and high risk of complications related to surgery and anesthesia, whether it’s necessary to remove both kineys and ureters at one time remains in debate. We utilized Taiwanese UTUC Registry Database to valuate the difference of oncological outcomes and perioperative complications between patients with ESRD with unilateral and bilateral UTUC receiving surgical resection. Patients with ESRD and UTUC were divided into three groups, unilateral UTUC, previous history of unilateral UTUC with metachronous contralateral UTUC, and concurrent bilatetral UTUC. Oncological outcomes, perioperative complications, and length of hospital stays were investiaged. We found that there is no diffence of oncological outcomes including overall survival, cancer specific survival, disease free survival and bladder recurrence free survival between these three groups. Complication rate and length of hospital stay are similar. Adverse oncological features such as advanced tumor stage, lymph node involvement, lymphovascular invasion, and positive surgical margin would negatively affect oncological outcomes.

Dyslipidemia is associated with glomerular injury. However, the effect of statins on chronic kidney disease (CKD) progression remains controversial. We aimed to investigate the efficacy of statins for renal protection in patients with CKD. The retrospective cohort study comprised 3441 patients diagnosed with CKD in multiple medical centers. We divided the patients into two cohorts based on statin prescription, and compared proportions and risks of CKD progression events between the two groups. CKD progression event was defined as an average annual decline of eGFR >5 mL/min/1.73 m 2 or advancement to the dialysis stage. The result revealed that among all incident patients with CKD, 28.7% and 30.3% of the users and nonusers demonstrated CKD progression, respectively. The crude odds ratio (OR) of CKD progression was 0.93 [95% confidence interval (CI) 0.78–1.10]. After adjustment for baseline characteristics, the adjusted OR was 0.80 (95% CI 0.63–1.01). The sensitivity analysis results showed consistent OR for CKD progression, stratification by age, sex, Charlson score, and statins use within 1 year before index date. The effect of statins was significant in patients with CKD stage 3B-5 (OR 0.68, 95% CI 0.48–0.95), but not statistically significant in those with CKD stage 1–3A (OR 0.97, 95% CI 0.68–1.38). The effect of statins was significant in patients with proteinuria ≥1000 mg/day (OR 0.63, 95% CI 0.43–0.92), but not statistically significant in those with proteinuria <1000 mg/day (OR 1.02, 95% CI 0.74–1.41).

PurposeMammalian target of rapamycin (mTOR) inhibitors were previously considered a potential therapy for autosomal dominant polycystic kidney disease (ADPKD), but prior studies remained controversial about their efficacy. We performed an updated meta-analysis regarding the therapeutic and adverse effects of mTOR inhibitors in patients with ADPKD.MethodsWe systematically searched Cochrane Library, PubMed, EMBASE, and Medline for randomized controlled trials (RCTs) comparing mTOR inhibitors to placebo in ADPKD patients up to August 2019. We calculated weighted mean differences (WMDs) for total kidney volume (TKV), estimated glomerular filtration rates (eGFRs), and weighted odds ratios (ORs) for treatment-related complications between the treatment and the placebo groups, using the random effects model.ResultsWe retrieved a total of 9 RCTs enrolling 784 ADPKD patients receiving rapamycin, sirolimus, or everolimus between 2009 and 2016. The WMDs of TKV and eGFR from baseline to the last measurement were − 31.54 mL (95% confidence interval [CI] − 76.79 to 13.71 mL) and 2.81 mL/min/1.73 m2 (95% CI − 1.85 to 7.46 mL/min/1.73 m2), respectively. Patients receiving mTOR inhibitors had a significantly increased risk of any adverse effects (OR 5.92, 95% CI 3.53–9.94), with the most common ones being aphthous stomatitis (OR 15.45, 95% CI 9.68–24.66) and peripheral edema (OR 3.49, 95% CI 1.31–9.27) compared to placebo users.ConclusionsmTOR inhibitors did not significantly influence renal progression in patients with ADPKD, but were associated with a higher risk of complications. Whether mTOR inhibitors can be an add-on option or second-line agents remain undetermined.

Benign prostate hyperplasia (BPH) refers to the nonmalignant enlargement of the transition zone of the prostate gland. While holmium laser enucleation of the prostate and open simple prostatectomy are effective in the management of patients with large prostates, they have some limitations. Thus, this study aimed to analyze the efficacy and safety of the sandwich method of bipolar transurethral resection of the prostate (B-TURP) and GreenLight photoselective vaporization of the prostate (GLPVP) in patients with large prostates. Patients diagnosed with BPH who underwent the sandwich method with B-TURP and GLPVP from 2015 to 2020 were included. Efficacy analyses included the change in the uroflowmetry results in both group A (prostate volume < 80 g) and group B (prostate volume ≥ 80 g), and complication analyses included perioperative complications, early postoperative complications at three months and late postoperative complications at 12 months. The cohort comprised 188 and 44 patients in groups A and B, respectively. The prostate volume of groups A and B were 50.83 ± 14.14 g and 102.03 ± 19.36 g (p < 0.001), respectively. The peak (Qmax) and average (Qavg) flow rates were comparable between the two groups. The only significant difference noted was in the postoperative post-void residual (PVR) urine. Improvement was seen in all the variables including the Qmax, Qavg and PVR urine in each group. No patient experienced perioperative complications. Analysis of the overall one-year complication rate showed no significant difference between the two groups. The sandwich method of B-TURP and GLPVP may be feasible for the management of patients with large prostate.

End-stage renal disease (ESRD) has a major impact on health and affects more than 600,000 people in the USA. The current mainstay treatments include dialysis and kidney transplantation (KT), and patients who have received KT have a higher quality of life and a lower mortality risk than those on chronic dialysis. Therefore, KT is considered the more preferred treatment modality for patients with ESRD. However, even though KT results in a higher long-term survival rate, the use of immunosuppressants is associated with various complications, including opportunistic infections and malignancies, which may lead to a higher risk of death in the first year after transplantation. Progressive multifocal leukoencephalopathy (PML) is a rare complication following KT, with an incidence of 0.027% in KT recipients. We present a case of PML following immunosuppressant therapy in a patient who received KT.

The frequency of stroke mimics among stroke patients has been reported to be up to 30%, and that in patients who receive thrombolytic therapy ranges between 1% and 16%. Atlantoaxial dislocation with myelopathy mimicking stroke is extremely rare. An 83-year-old man with a history of old cerebellar infarction presented to the emergency department with acute left hemiplegia after a chiropractic manipulation of the neck and back several hours before symptom onset. Mild hypoesthesia was observed on his left limbs. No speech disturbance, facial palsy, or neck or shoulder pain was observed. Intravenous thrombolytic treatment was given 238 min after symptom onset. Brown–Sequard syndrome subsequently developed 6 h after thrombolysis with a hypoesthetic sensory level below the right C5 dermatome. An emergent brain magnetic resonance angiography did not reveal an acute cerebral infarct but rather an atlantoaxial dislocation causing upper cervical spinal cord compression. Clinical symptoms did not deteriorate after thrombolysis. He received successful decompressive surgery 1 week later, and his muscle power gradually improved, with partial dependency when performing daily living activities 2 months later. A literature review revealed that only 15 patients (including the patient mentioned here) with spinal disorder mimicking acute stroke who received thrombolytic therapy have been reported. Atlantoaxial dislocation may present as acute hemiplegia mimicking acute stroke, followed by Brown–Sequard syndrome. Inadvertent thrombolytic therapy is likely not harmful for patients with atlantoaxial dislocation-induced cervical myelopathy. The neurological deficits of patients should be carefully and continuously evaluated to differentiate between stroke and myelopathy.

This study examined the involvement of fibroblast growth factor-23 (FGF-23) in primary aldosteronism (PA), a condition characterized by elevated aldosterone levels and hypertension. We recruited patients with unilateral PA (uPA) and observed increased levels of C-terminal FGF-23 (cFGF-23) and C-terminal to intact FGF-23 (iFGF-23) in patients with uPA compared with essential hypertension control participants. Elevated preoperative cFGF-23 levels were associated with adverse outcomes, including mortality and cardiovascular or kidney events. Plasma cFGF-23 levels demonstrated a nonlinear rise with aldosterone, but iFGF-23 levels were not correlated with plasma aldosterone concentration. Higher cFGF-23 levels independently predicted hypertension remission after adrenalectomy for patients with uPA. Patients with uPA, who exhibited elevated cFGF-23 levels, had decreased levels after adrenalectomy. In cell cultures, aldosterone enhanced cleavage of iFGF-23, leading to increased levels of cFGF-23 fragments, an effect mitigated by silencing of family with sequence similarity 20, member C (FAM20C). However, the enhancement of cFGF-23 levels remained unaffected by the furin inhibitor. The study suggests that aldosterone influences FGF-23 phosphorylation by interacting with FAM20C, with docking experiments indicating aldosterone's binding to FAM20C. This work highlights that patients with uPA with elevated cFGF-23 levels are associated with cardiovascular risks, and adrenalectomy reduces cFGF-23. Aldosterone likely promotes cFGF-23 production through FAM20C-mediated phosphorylation of iFGF-23.

Familial tooth agenesis (FTA), distinguished by developmental failure of selected teeth, is one of the most prevalent craniofacial anomalies in humans. Mutations in genes involved in WNT/β-catenin signaling, including AXIN2 WNT10A, WNT10B, LRP6, and KREMEN1, are known to cause FTA. However, mutational interactions among these genes have not been fully explored. In this study, we characterized four FTA kindreds with LRP6 pathogenic mutations: p.(Gln1252*), p.(Met168Arg), p.(Ala754Pro), and p.(Asn1075Ser). The three missense mutations were predicted to cause structural destabilization of the LRP6 protein. Two probands carrying both an LRP6 mutant allele and a WNT10A variant exhibited more severe phenotypes, suggesting mutational synergism or digenic inheritance. Biallelic LRP6 mutations in a patient with many missing teeth further supported the dose-dependence of LRP6-associated FTA. Analysis of 21 FTA cases with 15 different LRP6 loss-of-function mutations revealed high heterogeneity of disease severity and a distinctive pattern of missing teeth, with maxillary canines being frequently affected. We hypothesized that various combinations of sequence variants in WNT-related genes can modulate WNT signaling activities during tooth development and cause a wide spectrum of tooth agenesis severity, which highlights the importance of exome/genome analysis for the genetic diagnosis of FTA in this era of precision medicine.

Diabetes-related brain complications have been reported in clinical patients and experimental models. The objective of the present study was to investigate the neuroprotective mechanisms of Lactobacillus reuteri GMNL-263 in streptozotocin (STZ)-induced diabetic rats. In this study, three different groups, namely control group, STZ-induced (55 mg/kg streptozotocin intraperitoneally) diabetic rats (DM), and DM rats treated with Lactobacillus reuteri GMNL-263 (1 × 10 9  CFU/rat/day), were utilized to study the protective effect of GMNL-263 in the hippocampus of STZ-induced diabetic rats. The results demonstrated that GMNL-263 attenuated diabetes-induced hippocampal damage by enhancing the cell survival pathways and repressing both inflammatory and apoptotic pathways. Histopathological analysis revealed that GMNL-263 prevented structural changes in the hippocampus in the DM group and decreased the level of inflammation and apoptosis in the hippocampus of DM rats. The IGF1R cell survival signaling pathway also improved after GMNL-263 treatment. These results indicate that probiotic GMNL-263 exerts beneficial effects in the brain of diabetic rats and has potential ability for clinical application. Graphical abstract