KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases

Kidney International, Journal Year: 2021, Volume and Issue: 100(4), P. S1 - S276

Published: Sept. 20, 2021

The Kidney Disease: Improving Global Outcomes (KDIGO) 2021 Clinical Practice Guideline for the Management of Glomerular Diseases is an update to KDIGO 2012 guideline on topic. aim assist clinicians caring individuals with glomerular disease, both adults and children. scope includes various diseases, including IgA nephropathy (IgAN) vasculitis (IgAV), membranous nephropathy, nephrotic syndrome in children, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), infection-related glomerulonephritis (GN), antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, lupus nephritis, anti-glomerular basement membrane (anti-GBM) GN. In addition, this will be first address subtype complement-mediated diseases. Each chapter follows same format providing guidance related diagnosis, prognosis, treatment, special situations. goal generate a useful resource patients by actionable recommendations valuable infographics based rigorous formal systematic literature review. Another propose research areas where there are gaps knowledge. targets broad audience treating while being mindful implications policy cost. Development followed explicit process evidence Treatment approaches reviews synthesis relevant studies, appraisal quality strength “Grading Recommendations Assessment, Development, Evaluation” (GRADE) approach. Limitations discussed, future also presented.

Language: Английский

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Dyslipidaemia in nephrotic syndrome: mechanisms and treatment

Nature Reviews Nephrology, Journal Year: 2017, Volume and Issue: 14(1), P. 57 - 70

Published: Nov. 27, 2017

Language: Английский

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Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

International Journal of Molecular Sciences, Journal Year: 2020, Volume and Issue: 21(7), P. 2632 - 2632

Published: April 10, 2020

Lipotoxicity is characterized by the ectopic accumulation of lipids in organs different from adipose tissue. mainly associated with dysfunctional signaling and insulin resistance response non-adipose tissue such as myocardium, pancreas, skeletal muscle, liver, kidney. Serum lipid abnormalities renal have been development kidney diseases, particular diabetic nephropathy. Chronic hyperinsulinemia, often seen type 2 diabetes, plays a crucial role blood liver metabolism abnormalities, thus resulting increased non-esterified fatty acids (NEFA). Excessive alters cellular homeostasis activates lipogenic glycogenic cell-signaling pathways. Recent evidences indicate that both quantity quality are involved damage to lipotoxicity activating inflammation, oxidative stress, mitochondrial dysfunction, cell-death. The pathological effects observed cells, promoting podocyte injury, tubular damage, mesangial proliferation, endothelial activation, formation macrophage-derived foam cells. Therefore, this review examines recent preclinical clinical research about potentially harmful kidney, metabolic markers these mechanisms, major pathways affected, causes excessive accumulation, types involved, well offers comprehensive update therapeutic strategies targeting lipotoxicity.

Language: Английский

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Lipid management in patients with chronic kidney disease

Nature Reviews Nephrology, Journal Year: 2018, Volume and Issue: 14(12), P. 727 - 749

Published: Oct. 25, 2018

Language: Английский

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Disorders of Lipid Metabolism in Chronic Kidney Disease

Blood Purification, Journal Year: 2018, Volume and Issue: 46(2), P. 144 - 152

Published: Jan. 1, 2018

Cardiovascular disease (CVD) is the leading cause of death in chronic kidney (CKD). One most important pathophysiological mechanisms for CVD patients with CKD widespread and possibly accelerated formation atherosclerotic plaques due to hyperlipidemia, uremic toxins, inflammation, oxidative stress, endothelial dysfunction. Recent studies showed that level oxidized low-density lipoprotein cholesterol increases, high--density dysfunction occurs as function declines inflammation becomes more prevalent. In this review, we aimed discuss effect dysfunction, on lipid -profile.

Language: Английский

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Combined Clinical Phenotype and Lipidomic Analysis Reveals the Impact of Chronic Kidney Disease on Lipid Metabolism

Journal of Proteome Research, Journal Year: 2017, Volume and Issue: 16(4), P. 1566 - 1578

Published: March 13, 2017

Chronic kidney disease (CKD) results in significant dyslipidemia and profound changes lipid lipoprotein metabolism. The associated dyslipidemia, turn, contributes to progression of CKD its cardiovascular complications. To gain an in-depth insight into the disorders metabolism advanced CKD, we applied UPLC-HDMS-based lipidomics measure serum metabolites 180 patients with 120 age-matched healthy controls. We found increases levels total free fatty acids, glycerolipids, glycerophospholipids CKD. directly correlated level triglyceride inversely cholesterol eGFR. A 126 species were identified from positive negative ion modes. Out 126, 113 significantly altered based on adjusted FDR method. These pointed disturbance acid metabolisms Logistic regression analysis showed strong correlations between methyl hexadecanoic acid, LPC(24:1), 3-oxooctadecanoic PC(20:2/24:1) eGFR creatinine (R > 0.8758). In conclusion, application lipidomic technique revealed observed increased levels.

Language: Английский

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The role of lipoprotein (a) in chronic kidney disease

Journal of Lipid Research, Journal Year: 2018, Volume and Issue: 59(4), P. 577 - 585

Published: Jan. 29, 2018

Lipoprotein (a) [Lp(a)] and its measurement, structure function, the impact of ethnicity environmental factors, epidemiological genetic associations with vascular disease, new prospects in drug development have been extensively examined throughout this Thematic Review Series on Lp(a). Studies suggest that kidney has a role Lp(a) catabolism, levels are increased association disease only for people large apo(a) isoforms. By contrast, those patients protein losses, as nephrotic syndrome continuous ambulatory peritoneal dialysis, is irrespective isoform size. Such acquired abnormalities can be reversed by transplantation or remission nephrosis. In Review, we focus relationship between Lp(a), chronic risk cardiovascular events. synthesized liver comprised single LDL particle linked to highly polymorphic (1.Berg K. A serum type system man–the LP system.Acta Pathol. Microbiol. Scand. 1963; 59: 369-382Crossref PubMed Google Scholar). Plasma vary widely individuals, from 0 >200 mg/dl, skewed distribution resulting most Europeans having <10 mg/dl (2.Kronenberg F. Utermann G. Lipoprotein(a): resurrected genetics.J. Intern. Med. 2013; 273: 6-30Crossref Scopus (261) Blood heritable chiefly determined copy number variation at LPA locus chromosome 6, well ethnically differences (3.Utermann The mysteries lipoprotein(a).Science. 1989; 246: 904-910Crossref Copy kringle IV 2 domain, encoding isoforms differing size, results varying copies identical repeats. inversely correlated genetically higher plasma being associated smaller sizes represented fewer also considerably among individuals given size (4.Berglund L. Ramakrishnan R. an elusive factor.Arterioscler. Thromb. Vasc. Biol. 2004; 24: 2219-2226Crossref (185) Epidemiological studies suggested raised with, causal in, coronary heart calcific aortic valve such (5.Nordestgaard B.G. Langsted A. Lipoprotein(a) cause disease: Insights epidemiology, genetics, biology.J. Lipid Res. 2016; 57: 1953-1975Abstract Full Text PDF (165) Scholar, 6.Thanassoulis genomics novel target stenosis.J. 917-924Abstract (44) 7.Erqou S. Kaptoge Perry P.L. Di Angelantonio E. Thompson White I.R. Marcovina S.M. Collins S.G. Danesh J. concentration stroke, nonvascular mortality.JAMA. 2009; 302: 412-423Crossref (926) Consequently, potential which treatments currently under development. Kidney both elevation levels. Furthermore, increases appear dependent review, will summarize complex inter-relationships consider insight offer into metabolism, importance (CKD), whether Lp(a)-lowering therapies might preventing patients. CKD defined presence damage (manifesting albuminuria, radiological histological evidence) decreased function [glomerular filtration rate (GFR) <60 ml/min/1.73 m2] least 3 months. characterized cause, stage (defined GFR), level worse GFR albuminuria each independently predicting renal prognosis (8.KDIGO Work Group KDIGO 2012 clinical practice guideline evaluation management disease.Kidney Int. Suppl. 3: 1-150Abstract (931) common affects 10–15% populations, but about 0.1% severe form, i.e., end-stage (ESRD), need dialysis (9.Hill N.R. Fatoba S.T. Oke J.L. Hirst J.A. O'Callaghan C.A. Lasserson D.S. Hobbs F.D. Global prevalence - systematic review meta-analysis.PLoS One. 11: e0158765Crossref (1021) Some high "nephrotic range" (urine albumin:creatinine ratio >220 mg/mmol). If accompanied low albumin edema, it termed syndrome" always caused glomerulus. venous arterial thrombosis (in part due loss anticoagulant factors urine), infection (due immunoglobulins marked hypercholesterolemia (with total cholesterol concentrations typically over 10 mmol/l). Diabetes leading many countries. Other causes include glomerular tubulointerstitial diseases, structural abnormalities, inherited conditions like polycystic disease. older age, hypertension, obesity (10.Levey A.S. Coresh Chronic disease.Lancet. 2012; 379: 165-180Abstract (1005) estimated (eGFR) events (11.Matsushita van der Velde M. Astor B.C. Woodward Levey de Jong P.E. Gansevoort R.T. Association all-cause mortality general population cohorts: collaborative meta-analysis.Lancet. 2010; 375: 2073-2081Abstract (2359) For example, meta-analysis observational 30% reduction eGFR increase major (12.Mafham Emberson Landray M.J. Wen C.P. Baigent C. Estimated mortality: 2011; 6: e25920Crossref reflect balance synthesis, occurs liver, thought involve less clearly understood (13.Albers J.J. Koschinsky M.L. Evidence mounts lipoprotein(a) catabolism.Kidney 2007; 71: 961-962Abstract (21) 14.Kronenberg Human genetics various diseases.Cardiovasc. Drugs Ther. 30: 87-100Crossref (75) 15.Frischmann M.E. Kronenberg Trenkwalder Schaefer J.R. Schweer H. Dieplinger B. Koenig P. Ikewaki vivo turnover study demonstrates diminished clearance hemodialysis patients.Kidney 1036-1043Abstract (73) 16.Oida Takai Maeda Takahashi Shimada Suzuki Tamai T. Nakai Miyabo Apolipoprotein(a) present urine excretion failure.Clin. Chem. 1992; 38: 2244-2248Crossref 17.Kostner K.M. Maurer Huber Stefenelli Steyrer Kostner G.M. Urinary fragments. Role catabolism.Arterioscler. 1996; 16: 905-911Crossref 18.Doucet Mooser V. Gonbert Raymond Chapman Jacobs Thillet syndrome: molecular analysis apolipoprotein(a) fragments urine.J. Am. Soc. Nephrol. 2000; 507-513Crossref 19.Kostner Clodi Bodlaj Watschinger Horl W. Derfler Decreased urinary apolipoprotein impaired function.Eur. Clin. Invest. 1998; 28: 447-452Crossref (24) 20.Reblin Donarski N. Fineder Brasen J.H. Thaiss Stahl R.A. Beisiegel U. Wolf Renal handling human rat.Am. Dis. 2001; 619-630Abstract 21.Kronenberg Lingenhel Friedrich Lhotta Schober Moes Konig Renovascular arteriovenous Lp[a] removal circulation.J. 1997; 1755-1763Abstract Higher observed reduced eGFR, even earliest stages impairment (22.Milionis H.J. Elisaf M.S. Tselepis Bairaktari Karabina S.A. Siamopoulos K.C. phenotypes failure.Am. 1999; 33: 1100-1106Abstract 23.Sechi L.A. Zingaro De Carli Sechi Catena Falleti Dell'Anna Bartoli Increased early failure.Ann. 129: 457-461Crossref 24.Catena Colussi Nait Pezzutto Martinis Early failure prothrombotic state.World 2015; 4: 374-378Crossref 25.Lin Reilly M.P. Terembula Wilson F.P. mild diabetics independent albuminuria.PLoS 2014; 9: e114397Crossref (15) 26.Kovesdy Longenecker J.C. level: third National Health Nutrition Examination Survey (1991–1994).Am. 2002; 40: 899-908Abstract (13) 27.Kronenberg Kuen Ritz Junker Kraatz Mann J.F. Muller G.A. Neyer et al.Lipoprotein(a) moderate failure.J. 105-115Crossref Penn Heart Study based 1,852 diabetes [but no evidence poor (eGFR m2)], were 60–90 m2) after adjustment (25.Lin involving 7,675 different ethnic backgrounds reported lower (based categories 15–59, 60–89, 90–149, >150 was weakly positively levels, particularly non-Hispanic blacks, suggesting (26.Kovesdy However, fixed may groups, unmeasured report explain some heterogeneity. one detailed date, al. (27.Kronenberg Scholar) 227 non-nephrotic Caucasian degrees impairment. significantly when compared age-, gender-, phenotype-matched controls [creatinine 2.02 (SD 1.16) versus 0.99 0.18) controls] not yet abnormal (i.e., >90 m2). worst highest primary seen subgroup isoforms, whom median varied 6.2 m2 18 <45 Despite mounting CKD, all replicated GFR. there significant 804 3–4 ranging 13 55 suggestion interaction (28.Uhlig Wang S.R. Beck G.J. Kusek J.W. Greene Sarnak Factors disease.Am. 2005; 45: 28-38Abstract (9) addition, 87 donors whose average 112 before donation 72 1 year later, showed difference result (18 19 donation, P = 0.07), albeit available examine specifically (29.Doucet Kaiser O. Hawley Isbel Live donor implications lipid parameters including lipoprotein a.Nephrology (Carlton). 21: 901-904Crossref (0) Numerous more ESRD), influence modality. ESRD undergoing shown healthy (30.Kronenberg Auinger Pribasnig Lang Reitinger Pinter Multicenter treated dialysis.J. 1995; 110-120Crossref 31.Dieplinger Schoenfeld P.Y. Fielding C.J. metabolism Difference treatment 1986; 77: 1071-1083Crossref 32.Shoji Nishizawa Y. Nishitani Yamakawa Morii High uremic dialysis.Clin. 271-276PubMed 33.Hirata Kikuchi Saku Jimi Zhang Naito Hamaguchi Arakawa maintenance with/without mellitus.Kidney 1993; 44: 1062-1070Abstract 34.Webb A.T. Reaveley D.A. O'Donnell O'Connor Seed Brown E.A. haemodialysis dialysis.Nephrol. Dial. Transplant. 8: 609-613PubMed 35.Gault M.H. Longerich L.L. Purchase Harnett Breckenridge Comparison effects hemodialysis, CAPD, transplantation, control literature.Nephron. 70: 155-170Crossref 36.Aggarwal H.K. Jain D. Lathar Yadav R.K. Sawhney Lipoprotein-A carotid intima media thickness disease.Ren. Fail. 32: 647-652Crossref (14) 37.Parsons Pavitt D.V. Misra weight apo remain proportion disease.Nephrol. 2003; 18: 1848-1853Crossref 38.Kronenberg 27: 1-25Abstract 39.Dieplinger Lackner Sandholzer Hoppichler Graf Elevated related polymorphism apolipoprotein(a).J. 91: 397-401Crossref 40.Gambhir J.K. Kalra O.P. Khaira Kaur advanced effect hemodialysis.Indian 23: 18-23Crossref (3) 41.Zimmermann Herrlinger Pruy Metzger Wanner Inflammation enhances 55: 648-658Abstract (1337) Scholar), regular five ten times (36.Aggarwal Similarly discussed above, elevations specific, showing than 30.Kronenberg This illustrated comparing 138 236 which, despite frequency, 2- 4-fold (39.Dieplinger (peritoneal dialysis) 42.Kronenberg Causes consequences disease.Clin. Exp. 234-237Crossref Milionis 47 79 found who had Table summarizes modalities levels.TABLE 1Summary Open table tab abnormality appears clearance. An stable isotopes fractional catabolic rates components, Lp(a)-apo(a) Lp(a)-apoB, these controls, thereby prolonged residence times; while production do differ (15.Frischmann suggests decrease rather production. further supported several 43.Mooser Seabra M.C. Abedin Landschulz K.T. H.H. 4-containing urine. Relationship lipoprotein(a).J. 97: 858-864Crossref (21.Kronenberg demonstrated vein ascending aorta angioplasty, removed circulation. (creatinine <70 ml/min) matched (44.Cauza Kletzmaier Dunky Herrmann non-LDL-bound apo(a), function.Nephrol. 1568-1572Crossref (17) involved clearing intact circulation, addition produced proteases tissues pre-renal degradation (45.Frank Hrzenjak Blaschitz Dohr fragmentation kidney.Eur. 31: 504-512Crossref Small particles [by contrast larger particles] directly secreted so declines, secretion falls small increases. correlates overall fraction cleared likely catabolism (43.Mooser While clear influences possible progression. prospective 862 diabetic prognostic factor (46.Yun J.S. Ahn Y.B. Song K.H. Yoo K.D. Park Y.M. Kim H.W. Ko S.H. predicts onset mellitus.Diabet. 639-643Crossref CRIC 3,939 adults however, half diabetes, baseline subsequent progression

Language: Английский

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A Comprehensive Update on the Chylomicronemia Syndrome

Frontiers in Endocrinology, Journal Year: 2020, Volume and Issue: 11

Published: Oct. 23, 2020

The chylomicronemia syndrome is characterized by severe hypertriglyceridemia and fasting predisposes affected individuals to acute pancreatitis. When due very rare monogenic mutations in the genes encoding enzyme, lipoprotein lipase, or its regulators, apo C-ll, -V, GPIHBP1, LMF1 CERBH, it referred as familial syndrome. Much more frequently, results from a cluster of minor genetic variants causing polygenic hypertriglyceridemia, which exacerbated conditions medications increase triglyceride levels beyond saturation point removal systems. This situation termed multifactorial These aggravating factors include common such uncontrolled diabetes, overweight obesity, alcohol excess, chronic kidney disease pregnancy several medications, including diuretics, non-selective beta blockers, estrogenic compounds, corticosteroids, protease inhibitors, immunosuppressives, antipsychotics, antidepressants, retinoids, L-asparaginase propofol. A third uncommon cause forms partial lipodystrophy. Development pancreatitis most feared complication syndrome, but risk cardiovascular well non-alcoholic steatohepatitis also increased. Treatment consists dietary fat restriction weight reduction combined with use lowering fibrates, omega 3 fatty acids niacin. Effective management improving diabetes control, discontinuing replacing reducing dose that raise essential. Importantly, many if not cases can be prevented effective identification people likelihood before starting may levels. Several new pharmacotherapeutic agents are being tested likely considerably improve treatment at risk.

Language: Английский

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Mechanisms of Primary Membranous Nephropathy

Biomolecules, Journal Year: 2021, Volume and Issue: 11(4), P. 513 - 513

Published: March 30, 2021

Membranous nephropathy (MN) is an autoimmune disease of the kidney glomerulus and one leading causes nephrotic syndrome. The exhibits heterogenous outcomes with approximately 30% cases progressing to end-stage renal disease. clinical management MN has steadily advanced owing identification autoantibodies phospholipase A2 receptor (PLA2R) in 2009 thrombospondin domain-containing 7A (THSD7A) 2014 on podocyte surface. Approximately 50–80% 3–5% primary (PMN) are associated either anti-PLA2R or anti-THSD7A antibodies, respectively. presence these used for diagnosis; antibody levels correlate severity possess significant biomarker values monitoring progression treatment response. Importantly, both causative MN. Additionally, evidence emerging that NELL-1 5–10% PMN PLA2R- THSD7A-negative, which moves us step closer mapping out full spectrum antigens. Recent developments suggest exostosin 1 (EXT1), EXT2, NELL-1, contactin (CNTN1) Genetic factors other mechanisms place regulate may contribute pathogenesis. This review will discuss recent over past 5 years.

Language: Английский

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Clinical Significance of Serum Albumin and Implications of FcRn Inhibitor Treatment in IgG-Mediated Autoimmune Disorders

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: June 1, 2022

Serum albumin (SA), the most abundant soluble protein in body, maintains plasma oncotic pressure and regulates distribution of vascular fluid has a range other important functions. The goals this review are to expand clinical knowledge regarding functions SA, elucidate effects dysregulated SA concentration, discuss relevance hypoalbuminemia resulting from various diseases. We potential repercussions dysregulation on cholesterol levels, liver function, processes that rely its homeostasis, as decreased concentration been shown be associated with increased risk for cardiovascular disease, hyperlipidemia, mortality. describe anti-inflammatory antioxidant properties well ability bind transport plethora endogenous exogenous molecules. is primary serum involved binding drugs such affect, or affected by, certain medications. Of current antibody-based inhibitors neonatal Fc receptor (FcRn), several which under development treat immunoglobulin G (IgG)-mediated autoimmune disorders; some have decrease concentration. FcRn acts homeostatic regulator by rescuing it, IgG, intracellular degradation via common cellular recycling mechanism. Greater understanding multifunctional nature impact needed; particular, treatments reduce may affect efficacy toxicity medications disease progression.

Language: Английский

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