Looking back at 2017, the field of kidney disease is also very profitable and has made many progress. Recently, Nature magazine gave a detailed overview of 5 major advances in kidney disease in 2017. Have you ever missed a chance?
Dr.Leo
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1.A new mechanism of hypertension and vascular dysfunction
In 2017, a number of basic and clinical studies published in the field of hypertension further deepen our understanding of the mechanism of blood pressure regulation. New discoveries include: immune mechanisms, the role of gut microbes, the adverse effects of perivascular fat and inflammation on the vascular system, and the effects of rare mutations in the renin-angiotensin-aldosterone system on salt sensitivity.
Important progress:
➤ The SGK1 signaling pathway in T cells upregulates Na + / K + / 2Cl-co-transporter 1 (NKCC1) and promotes phenotypic polarization of helper T-cell 17 (TH17) cells, resulting in Lead to salt-sensitive hypertension and end-stage ductal injury.
➤ A high-sodium diet alters the gut microflora in humans and mice, resulting in the depletion of lactobacilli, increasing the number of TH17 cells and increasing blood pressure.
➤ γδ T cells lead to angiotensin II-induced hypertension and endothelial dysfunction in mice and may also play important roles in human hypertension and end organ damage.
➤ AGTR1A and osteopontin are involved in the polarization of phenotypic macrophages in perivascular fat-inflammation, leading to inflammation and promoting aortic aneurysm formation.
➤ Rare mutations in the renin-angiotensin-aldosterone system (RAAS) -related gene (7 in total, including APLN and RENBP) are associated with salt-sensitivity to blood pressure.
2. glycolysis regulation, promote kidney disease progress
There is growing evidence that cellular metabolism is related to the fate of cells. In particular, glycolytic fluxes have become recognized as important drivers of self-renewal and cell proliferation and are crucial for angiogenesis and tumor growth. Several studies published in 2017 highlight the important role of glycolysis and mitochondrial function in kidney development and kidney function, as well as the impact on kidney disease progression.
Important progress:
➤ Increased glycolysis and mitochondrial respiratory function promote progenitor cell proliferation and self-renewal.
➤ Acute kidney injury and diabetic nephropathy are characterized by mitochondrial dysfunction and increased glycolytic intermediates - which can be metabolized to toxic metabolic end products.
➤ Coupling of glycolysis flux to mitochondrial respiratory function is becoming a potential treatment for ischemic and diabetic kidney damage.
3. Immune nephropathy mechanism and progress of treatment
In the past year, the research on the pathogenesis and treatment of immune-mediated glomerular diseases has been deepened and many progresses have been made. In the field of molecular transformation, two studies have found new pathogenesis and pathways, providing new treatments for the treatment of immune nephropathy - hormones may or may not be used in the future.
Important progress:
➤ The reason that HLA is associated with anti-glomerular basement membrane disease is that immunodominant epitope peptides bind to different HLA.
➤ Autoantigen DNA Methylation - Induced Antineutrophil Cytoplasmic Antibody (ANCA) -associated Vasculitis - May Be Associated with Disease Activity and Remission, and Predict Disease Activity and Remission.
➤ High-dose glucocorticoid treatment for IgA nephropathy has more side effects than potential benefits.
➤ Targeted Targeted Release Agent (TRF) Targeting Intestinal Immune Tissue - Budesonide is effective in treating IgA nephropathy and significantly reduces hormone use
➤ Small molecule C5a receptor inhibitors improve patient outcomes, meaning that complement plays an important role in ANCA-associated glomerulonephritis. Small molecule C5a receptor inhibitors are as effective as prednisone in inducing disease remission
Since 16 years ago IDNT and RENAAL studies have found no new drugs approved for use in patients with type 2 diabetes (T2DM) and kidney disease using the angiotensin II receptor blocker irbesartan and losartan Treatment of diabetic nephropathy. In 2017, however, studies have shown that the hypoglycemic agents sodium-glucose cotransporter 2 (SGLT2) inhibitors (enzaprine, canagliflozin) and glucagon-like peptide-1 (GLP- Liraglutide) has a protective effect on the kidney, bringing new hope for patients with diabetic nephropathy.
Important progress:
➤ CANVAS and EMPA-REG OUTCOME studies have reported that sodium-glucose cotransporter 2 (SGLT2) inhibitors are beneficial for renal outcomes, including proteinuria, and may reduce creatinine levels and reduce renal replacement therapy or kidney death.
➤ LEADER study shows that the GLP1 agonist liraglutide can reduce the incidence of diabetic nephropathy and delay the progression of the disease.
➤ Previous renal disease, estimated glomerular filtration rate of 30-60 ml / min / 1.73 m2 and / or large amounts of proteinuria, the use of enzapine can significantly reduce the risk of cardiovascular death, all-cause mortality risk and Heart failure hospitalization rate and all-cause hospitalization rate.
Effects of SGLT2 inhibitors and GLP1 agonists on diabetic renal hemodynamics; a: Hemodynamic changes due to hyperglycemia and diabetes; b: Effects of SGLT2 inhibitors and GLP1 agonists on hemodynamics; JGA: Golotrophore; NHE3: sodium-hydrogen exchanger 3; RAS: renin-angiotensin system; SNS: sympathetic nervous system
5. Uncover the mystery of the genetic structure of kidney disease
With the continuous development of gene sequencing technology, we have made a major breakthrough in understanding the genetic structure of kidney disease. In 2017, four major studies reveal the genetic basis of known diseases and novel diseases, providing new insight into the pathogenesis of glomerular diseases, kidney defects and clinical manifestations.
Important progress:
➤ SGPL1 recessive mutations lead to abnormal sphingolipid metabolism and are associated with steroid-resistant nephrotic syndrome.
Repeated loss of the 22q11.2 locus leads to DiGeorge syndrome, congenital kidney and urethral deformities; single-dose CRKL may also play a role.
➤ An unchallenged family history of autosomal dominant polycystic kidney disease has been a major clinical diagnostic difficulty, probably due to de novo lesions, germ cells or somatic chimeras, or mild disease due to PKD1 or PKD2 secondary morphological changes .
➤ Unidentified genomic diseases may impair the development of children's kidneys and neurocognitive development, and early detection can provide immediate intervention.
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