Tumor necrosis factor alpha (TNF-α) is considered to play an important role in the pathogenesis in IgA nephropathy (IgAN). The correlations between serum TNF-α and disease severity in patients with IgAN remain controversial. Concentrations of serum TNF-α of 147 patients with IgAN and 126 healthy subjects were measured by chemiluminescence immunoassay. Correlations with clinicopathological features of patients with IgAN were evaluated. Serum levels of TNF-α [9.20 (7.70–10.60) pg/mL vs. 6.04 (5.11–7.23) pg/mL, P < 0.0001] were higher in patients with IgAN than that in healthy subjects. Receiver operating characteristic curve analysis revealed that TNF-α had better discrimination between patients with IgAN and healthy controls than estimated glomerular filtration rate [TNF-α: (AUC, 0.87; 95% CI, 0.83–0.91; P < 0.0001) vs. estimated glomerular filtration rate: (AUC, 0.76; 95% CI, 0.71–0.82; P < 0.0001), P = 0.007]. Multivariate linear regression analyses showed that serum levels of TNF-α were positively correlated with 24-h urine protein excretion (r = 0.33, P = 0.04), urinary protein to serum creatinine ratio (r = 0.33, P = 0.03), serum creatinine (r = 0.46, P < 0.0001) and Cystatin C (r = 0.59, P < 0.0001) in IgAN and negatively correlated with estimated glomerular filtration rate (r = − 0.49, P < 0.0001) after adjustment for sex, systolic blood pressure and diastolic blood pressure. Patients with higher mesangial hypercellularity or tubular atrophy/interstitial fibrosis score according to Oxford classification showed higher serum levels of TNF-α. Our data showed that serum levels of TNF-α detected by chemiluminescence immunoassay was a potential biomarker for evaluating the disease severity in IgAN.

The coronavirus disease-19 (COVID-19) has spread over many countries and regions since the end of 2019, becoming the most severe public health event at present. Most of the critical cases developed multiple organ dysfunction, including acute kidney injury (AKI). Cytokine storm syndrome (CSS) may complicate the process of severe COVID-19 patients. This manuscript reviews the different aspects of blood purification in critically ill patients with AKI and increased inflammatory factors, and examines its potential role in severe COVID-19 treatment. Continuous renal replacement therapy (CRRT) has been practiced in many sepsis patients with AKI. Still, the timing and dosing need further robust evidence. In addition to the traditional CRRT, the high-throughput membrane with adsorption function and cytokine adsorption column are two representatives of recently emerging novel membrane technologies. Their potential in removing inflammatory factors and other toxins prospects for the treatment of severe COVID-19.

Objective.: Renal thrombotic microangiopathy (TMA) is an uncommon pathological finding in lupus nephritis (LN), and its clinical significance remains to be defined.Methods.: Twenty-four patients with lupus nephritis (LN) and renal TMA were selected from a retrospective review of 677 biopsy-proven LN patients, and compared with 48 LN controls without TMA (1:2 ratio) matched according to demographics and treatments.Results.: Renal TMA was noted in 3.5% of kidney biopsies of LN. TMA was associated with a higher prevalence of anti-Ro (45.8% vs 18.8%; p = 0.016), higher Systemic Lupus Erythematosus Disease Activity Index scores (21.4 ± 8.5 vs 10.8 ± 2.3; p < 0.001), lower estimated glomerular filtration rate (eGFR; 16.8 ± 11.7 ml/min vs 77.8 ± 28.6 ml/min; p < 0.001), and a higher percentage of patients who required dialysis (37.5% vs 2.1%; p < 0.001) at the time of kidney biopsy. Activity and chronicity indices [median (range)] were higher in the TMA group [11 (2–19) and 3 (1–8), respectively, compared with 7 (0–15) and 1 (0–3) in controls; p = 0.004 and p < 0.001; respectively]. Patients with TMA showed inferior 5-year renal survival and higher incidence of chronic kidney disease at last followup (70% and 66.6%, respectively, compared with 95% and 29.2% in controls; p = 0.023 and 0.002, respectively). The TMA group also showed lower median eGFR compared with controls [50.1 (IQR 7–132) ml/min vs 85.0 (IQR 12–147) ml/min; p = 0.003]. Five-year patient survival rate was similar between the 2 groups (87% and 98% in TMA and control group, respectively; p = 0.127).Conclusion.: TMA in kidney biopsy was associated with more severe clinical and histological activity, and significantly inferior longterm renal outcome in LN.

Chronic kidney disease patients have an increased prevalence of subclinical cerebrovascular diseases. Dialysis patients have severe vascular diseases burden. The cerebral small vessel diseases (CSVD) are difficult to find by clinical assessment. The evaluation of CVSD needs MRI. Cognitive impairment is a consequence of CVSD which is diagnosed by cognitive testing. These limited the study of CVSD and cognitive function in dialysis patients. Peritoneal dialysis (PD) patients are minority of dialysis population. We know even fewer about the CVSD in this special population. In this cross-sectional study, we enrolled 72 PD patients who received care at the Peking Union Medical College hospital peritoneal dialysis center. CSVD were assessed by brain MR images. Cognitive function was evaluated with the Chinese version of the MMSE and MoCA. In our PD patients, the brain MRI showed the prevalence different signs of CSVD were: lacunar infarcts 38.9%, microbleeds 36.1%, abnormal brain white matter hyperintensities (WMHs) 48.6%, and intracerebral hemorrhage 4.2%. 25% and 86.8%of our patients could be diagnosed as cognitive impairment, according to the MMSE and MoCA test, respectively. nPCR was lower in patients with a lacunar infarct or intracerebral hemorrhage, and relative to the MMSA/MoCA score; hsCRP was higher in patients with lacunar infarct or abnormal WMHs and negative relative to the MMSA/MoCA score. In logistic regression analyses, nPCR was an independent risk factor for lacunar infarcts and impaired cognitive function. The presence of lacunar infarct was an independent risk factor for cognitive function decline. We demonstrated a high prevalence of CSVD and cognitive impairment in our PD patients. Lacunar infarct was the main kind of CVSD responsible for PD patients cognitive function decline. Our novel observation also revealed an association between malnutrition-inflammation and CSVD.

Objective.: To investigate the characteristics and outcomes of patients with systemic lupus erythematosus (SLE)–associated thrombotic microangiopathy (TMA) based on their ADAMTS13 inhibitor profiles.Methods.: The medical data of 31 SLE patients with clinically diagnosed TMA were analyzed. ADAMTS13 activity and ADAMTS13 inhibitor were measured in all patients.Results.: TMA was attributable to active SLE in 19 patients. ADAMTS13 inhibitor and severe ADAMTS13 deficiency were detected in 6 of them. Patients with ADAMTS13 inhibitor (n = 6) exhibited a lower platelet count (7.3 ± 5.1 vs 25.0 ± 17.8 × 10⁹/l, p = 0.005) and more prevalent central nervous system (CNS) involvement (100.0% vs 23.1%, p = 0.003) than patients without ADAMTS13 inhibitor (n = 13). Patients with ADAMTS13 inhibitor also had mild renal involvement characterized by a higher estimated glomerular filtration rate (112.7 ± 18.0 vs 21.6 ± 12.0, p < 0.001), lower proteinuria level [0.6 (0.2–2.5) vs 8.1 (5.2–14.0) g/d, p = 0.011], and lower mean arterial pressure (95.3 ± 13.6 vs 117.5 ± 13.1 mmHg, p = 0.008) than was observed in patients without ADAMTS13 inhibitor. All patients with ADAMTS13 inhibitor achieved complete remission within 18.6 ± 8.7 days, while 3 patients (23.1%) without ADAMTS13 inhibitor achieved complete remission during a median followup of 5.0 months, even though more patients in this group received therapeutic apheresis (100.0% vs 50.0%, p = 0.021). The chance of complete remission increased by 10.8-fold (HR 10.8, 95% CI 1.8–65.5, p < 0.001) when ADAMTS13 inhibitor was present in SLE-associated TMA.Conclusion.: Acquired ADAMTS13 deficiency is associated with more severe thrombocytopenia and CNS involvement, mild renal involvement, rapid resolution, and relatively good treatment response in SLE-associated TMA.