Transplant renal artery stenosis (TRAS) is a well-recognized vascular complication after kidney transplant. It occurs most frequently in the first 6 months after kidney transplant, and is one of the major causes of graft loss and premature death in transplant recipients. Renal hypoperfusion occurring in TRAS results in activation of the renin–angiotensin–aldosterone system; patients usually present with worsening or refractory hypertension, fluid retention and often allograft dysfunction. Flash pulmonary edema can develop in patients with critical bilateral renal artery stenosis or renal artery stenosis in a solitary kidney, and this unique clinical entity has been named Pickering Syndrome. Prompt diagnosis and treatment of TRAS can prevent allograft damage and systemic sequelae. Duplex sonography is the most commonly used screening tool, whereas angiography provides the definitive diagnosis. Percutaneous transluminal angioplasty with stent placement can be performed during angiography if a lesion is identified, and it is generally the first-line therapy for TRAS. However, there is no randomized controlled trial examining the efficacy and safety of percutaneous transluminal angioplasty compared with medical therapy alone or surgical intervention.

Background: In animal studies, zinc supplementation inhibited phosphate-induced arterial calcification. We tested the hypothesis that higher intake of dietary zinc was associated with lower abdominal aortic calcification (AAC) among adults in the USA. We also explored the associations of AAC with supplemental zinc intake, total zinc intake and serum zinc level. Methods: We performed cross-sectional analyses of 2535 participants from the National Health and Nutrition Examination Survey 2013–14. Dietary and supplemental zinc intakes were obtained from two 24-h dietary recall interviews. Total zinc intake was the sum of dietary and supplemental zinc. AAC was measured using dual-energy X-ray absorptiometry in adults ≥40 years of age and quantified using the Kauppila score system. AAC scores were categorized into three groups: no AAC (AAC = 0, reference group), mild–moderate (AAC >0–≤6) and severe AAC (AAC >6). Results: Dietary zinc intake (mean ± SE) was 10.5 ± 0.1 mg/day; 28% had AAC (20% mild–moderate and 8% severe), 17% had diabetes mellitus and 51% had hypertension. Higher intake of dietary zinc was associated with lower odds of having severe AAC. Per 1 mg/day higher intake of dietary zinc, the odds of having severe AAC were 8% lower [adjusted odds ratio 0.92 (95% confidence interval 0.86–0.98), P = 0.01] compared with those without AAC, after adjusting for demographics, comorbidities and laboratory measurements. Supplemental zinc intake, total zinc intake and serum zinc level were not associated with AAC. Conclusions: Higher intake of dietary zinc was independently associated with lower odds of having severe AAC among noninstitutionalized US adults.

Metabolic acidosis is a common complication of chronic kidney disease. Accumulating evidence identifies acidosis not only as a consequence of, but as a contributor to, kidney disease progression. Several mechanistic pathways have been identified in this regard. The dietary acid load, even in the absence of overt acidosis, may have deleterious effects. Several small trials now suggest that the treatment of acidosis with oral alkali can slow the progression of kidney disease.

Background: 2019 novel coronavirus disease (COVID-19) has posed significant threats to public health. To identify and treat the severe and critical patients with COVID-19 is the key clinical problem to be solved. The present study aimed to evaluate the clinical characteristics of severe and non-severe patients with COVID-19. Methods: We searched independently studies and retrieved the data that involved the clinical characteristics of severe and non-severe patients with COVID-19 through database searching. Two authors independently retrieved the data from the individual studies, assessed the study quality with Newcastle-Ottawa Scale and analyzed publication bias by Begg’s test. We calculated the odds ratio (OR) of groups using fixed or random-effect models. Results: Five studies with 5,328 patients confirmed with COVID-19 met the inclusion criteria. Severe patents were older and more common in dyspnea, vomiting or diarrhea, creatinine >104 µmol/L, procalcitonin ≥0.05 ng/mL, lymphocyte count <1.5×10⁹/L and bilateral involvement of chest CT. Severe patents had higher risk on complications including acute cardiac injury (OR 13.48; 95% CI, 3.60 to 50.47, P<0.001) or acute kidney injury (AKI) (OR 11.55; 95% CI, 3.44 to 38.77, P<0.001), acute respiratory distress syndrome (ARDS) (OR 26.12; 95% CI, 11.14 to 61.25, P<0.001), shock (OR 53.17; 95% CI, 12.54 to 225.4, P<0.001) and in-hospital death (OR 45.24; 95% CI, 19.43 to 105.35, P<0.001). Severe group required more main interventions such as received antiviral therapy (OR 1.69; 95% CI, 1.23 to 2.32, P=0.001), corticosteroids (OR 5.07; 95% CI, 3.69 to 6.98, P<0.001), CRRT (OR 37.95; 95% CI, 7.26 to 198.41, P<0.001) and invasive mechanical ventilation (OR 129.35; 95% CI, 25.83 to 647.68, P<0.001). Conclusions: Severe patients with COVID-19 had more risk of clinical characteristics and multiple system organ complications. Even received more main interventions, severe patients had higher risk of mortality.

TLR7 has been linked to the pathogenesis of glomerulonephritis, but its precise roles are not clear. In this study, we evaluated the roles of TLR7 in IgA nephropathy (IgAN). TLR7 proteins were abundant in CD19 ⁺ B cells infiltrated in the kidneys of patients with IgAN. The intensities of both intrarenal TLR7 and CD19 proteins were closely associated with kidney function (estimated glomerular filtration rate [eGFR] and serum creatinine concentration) and renal histopathology (tubular atrophy, leukocyte infiltration, tubulointerstitial fibrosis, and global glomerulosclerosis) in patients with IgAN. Meanwhile, TLR7 mRNA levels were significantly increased in peripheral blood B cells of patients with IgAN. TLR7 ⁺ CD19 ⁺ B cells expressed inflammatory cytokines (IL-6 and IL-12) in kidneys and produced high levels of IgA1 and galactose deficient-IgA1 (Gd-IgA1) in peripheral blood of patients with IgAN. Mechanistically, TLR7 activated B cells to produce high levels of Gd-IgA1 via the TLR7-GALNT2 axis in IgAN. Protein levels of GALNT2 were increased by overexpression of TLR7, while they were reduced by TLR7 knockdown in B cells. GALNT2 overexpression augmented Gd-IgA1 production in B cells derived from patients with IgAN. Taken together, high TLR7 expression in B cells has dual roles in the development and progression of IgAN, by facilitating renal inflammation and Gd-IgA1 antibody synthesis.

The size of secondary calciprotein particles (CPP2) and the speed of transformation (T₅₀) from primary calciprotein particles (CPP1) to CPP2 in serum may be associated with vascular calcification (VC) in patients with chronic kidney disease (CKD). We developed a high throughput, microplate-based assay using dynamic light scattering (DLS) to measure the transformation of CPP1 to CPP2, hydrodynamic radius (R_h) of CPP1 and CPP2, T₅₀ and aggregation of CPP2. We used this DLS assay to test the hypothesis that a large R_h of CPP2 and/or a fast T₅₀ are associated with VC in 45 participants with CKD Stages 4–5 (22 without VC and 23 with VC) and 17 healthy volunteers (HV). VC was defined as a Kauppila score >6 or an Adragao score ≥3. CKD participants with VC had larger cumulants R_h of CPP2 {370 nm [interquartile range (IQR) 272–566]} compared with CKD participants without VC [212 nm (IQR 169–315)] and compared with HV [168 nm (IQR 145–352), P < 0.01 for each]. More CPP2 were in aggregates in CKD participants with VC than those without VC (70% versus 36%). The odds of having VC increased by 9% with every 10 nm increase in the R_h of CPP2, after adjusting for age, diabetes, serum calcium and phosphate [odds ratio 1.09, 95% confidence interval (CI) 1.03, 1.16, P = 0.005]. The area under the receiver operating characteristic curve for VC of CPP2 size was 0.75 (95% CI 0.60, 0.90). T₅₀ was similar in CKD participants with and without VC, although both groups had a lower T₅₀ than HV. R_h of CPP2, but not T₅₀, is independently associated with VC in patients with CKD Stages 4–5.