Lautonnesen4173

In response to the HIV-AIDS pandemic, great strides have been made in developing molecular methods that accurately quantify nucleic acid products of HIV-1 at different stages of viral replication and to assess HIV-1 sequence diversity and its effect on susceptibility to small molecule inhibitors and neutralizing antibodies. Here, we review how knowledge gained from these approaches, including viral RNA quantification and sequence analyses, have been rapidly applied to study SARS-CoV-2 and the COVID-19 pandemic.

Recent studies have shown detection of SARS-CoV-2 RNA in blood of infected individuals by reverse transcriptase PCR (RT-PCR); and, as in HIV-1 infection, there is growing evidence that the level of viral RNA in plasma may be related to COVID disease severity. Unlike HIV-1, SARS-CoV-2 sequences are highly conserved limiting SARS-CoV-2 sequencing applications to investigating interpatient genetic diversity for phylogenetic analysis. Sensitive sequencing technologies, originally developed for HIV-1, will be needed to investigate intrapatient SARS-CoV-2 genetic variation in response to antiviral therapeutics and vaccines.

Methods used for HIV-1 have been rapidly applied to SARS-CoV-2/COVID-19 to understand pathogenesis and prognosis. Further application of such methods should improve precision of therapy and outcome.

Methods used for HIV-1 have been rapidly applied to SARS-CoV-2/COVID-19 to understand pathogenesis and prognosis. Further application of such methods should improve precision of therapy and outcome.

Despite ground-breaking innovations for most autoimmune diseases, the treatment of lupus nephritis has remained largely the same for decades because none of the tested drugs demonstrated superiority over standard-of-care in randomized controlled clinical trials.

Recently, the Belimumab in Subjects with Systemic Lupus Erythematosus - Lupus Nephritis trial tested belimumab, an inhibitor of B-cell activating factor, as an add-on therapy to steroids and either mycophenolate mofetil (MMF) or cyclophosphamide when given IV monthly over a period of 104 weeks at an effect size of 11% for a Primary Efficacy Renal Response. The NOBILITY trial reported positive results for the B-cell-depleting agent obinutuzumab as an add-on therapy to steroids and MMF when given IV every 6 months over a period of 76 weeks at an effect size of 22% for a complete renal response (CRR). The AURORA trial reported positive results for the calcineurin inhibitor voclosporin as an oral add-on therapy to low dose steroids and MMF when given twice daily over a period of 52 weeks at an effect size of 18.5% for a CRR.

These studies will change the treatment landscape of lupus nephritis. In which way is discussed in this article.

These studies will change the treatment landscape of lupus nephritis. In which way is discussed in this article.

Cardiovascular disease (CVD) is the leading cause of death in patients with chronic kidney disease (CKD). However, traditional CVD risk prediction equations do not work well in patients with CKD, and inclusion of kidney disease metrics such as albuminuria and estimated glomerular filtration rate have a modest to no benefit in improving prediction.

As CKD progresses, the strength of traditional CVD risk factors in predicting clinical outcomes weakens. buy Genipin A pooled cohort equation used for CVD risk prediction is a useful tool for guiding clinicians on management of patients with CVD risk, but these equations do not calibrate well in patients with CKD, although a number of studies have developed modifications of the traditional equations to improve risk prediction. The reason for the poor calibration may be related to the fact that as CKD progresses, associations of traditional risk factors such as BMI, lipids and blood pressure with CVD outcomes are attenuated or reverse, and other risk factors may become more malnutrition and polypharmacy. Machine learning over conventional risk prediction models may be better suited to handle the complexity needed for these CVD prediction models.

Severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) is the novel virus responsible for the current worldwide pandemic. The scientific and healthcare communities have made every effort to discover and implement treatment options at a historic pace. Patients with kidney disease are uniquely vulnerable to an infectious pandemic because of their need to be in frequent contact with the healthcare system for life-sustaining renal replacement therapy whether it be by dialysis or transplant.

The use of targeted viral therapies, extracorporeal therapies, immunosuppressive therapy and public health interventions are important in the management of patients with COVID-19 but require special consideration in patients with kidney disease because of the complexity of their condition.

Here, we discuss some of the major efforts made to prevent spread and emerging treatment options for this virus, as they pertain to patients with kidney disease.

Here, we discuss some of the major efforts made to prevent spread and emerging treatment options for this virus, as they pertain to patients with kidney disease.

Pendrin resides on the luminal membrane of type B intercalated cells in the renal collecting tubule system mediating the absorption of chloride in exchange for bicarbonate. In mice or humans lacking pendrin, blood pressure is lower, and pendrin knockout mice are resistant to aldosterone-induced hypertension. Here we discuss recent findings on the regulation of pendrin.

Pendrin activity is stimulated during alkalosis partly mediated by secretin. Also, angiotensin II and aldosterone stimulate pendrin activity requiring the mineralocorticoid receptor in intercalated cells. Angiotensin II induces dephosphorylation of the mineralocorticoid receptor rendering the receptor susceptible for aldosterone binding. In the absence of the mineralocorticoid receptor in intercalated cells, angiotensin II does not stimulate pendrin. The effect of aldosterone on pendrin expression is in part mediated by the development of hypokalemic alkalosis and blunted by K-supplements or amiloride. Part of the blood pressure-increasing effect of pendrin is also mediated by its stimulatory effect on the epithelial Na-channel in neighbouring principal cells.