China
Africa
Explore chapters and articles related to this topic
Metabolic Syndrome
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Endothelial dysfunction causes the glomerulus of the kidney to allow larger molecules to enter, and excessive albumin leaks into the tubules. Not all of it is reabsorbed, so albumin can be found in the urine as microalbuminuria or macroalbuminuria. The presence of albuminuria is well related to other endothelial dysfunction tests. Albuminuria is also a marker for atherosclerosis. When the glomerulus is more permeable to albumin, the endothelium will be more permeable to lipoproteins. Microalbuminuria is an independent risk factor for cardiac events as well as highly predictive for coronary artery disease, likely due to the link between metabolic syndrome as well as endothelial dysfunction. The lower the albumin: creatinine ratio in the urine, the lower the risks for cardiovascular events. The cutoff point is 30 mg albumin:1 g creatinine. However, for cardiovascular risks, the threshold is not as high, only 7 mg albumin:1 g creatinine. Albuminuria in metabolic syndrome can be decreased by TZDs, carvedilol (a beta blocker), and RAAS inhibitors.
Nephrology
Published in Miriam Orcutt, Clare Shortall, Sarah Walpole, Aula Abbara, Sylvia Garry, Rita Issa, Alimuddin Zumla, Ibrahim Abubakar, Handbook of Refugee Health, 2021
Albuminuria is measured with a spot urine sample: an albumin:creatinine ratio can be calculated if laboratory support permits. Urine test strip protein is more feasible in most humanitarian aid and low-resource settings – it approximates albuminuria as follows: negative-trace = normal to mildly increased; trace-1+ = moderately increased; >1+ = severely increased (respectively categories A1–3 in the Kidney Disease: Improving Global Outcomes chart in Figure 11.5.1).1,2,3
2018 ESC/ESH Guidelines for the Management of Arterial Hypertension
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Bryan Williams, Giuseppe Mancia, Wilko Spiering, Enrico Agabiti Rosei, Michel Azizi, Michel Burnier, Denis L. Clement, Antonio Coca, Giovanni de Simone, Anna F. Dominiczak, Thomas Kahan, Felix Mahfoud, Josep Redon, Luis M. Ruilope, Alberto Zanchetti, Mary Kerins, Sverre E. Kjeldsen, Reinhold Kreutz, Stéphane Laurent, Gregory Y.H. Lip, Richard McManus, Krzysztof Narkiewicz, Frank Ruschitzka, Roland E. Schmieder, Evgeny Shlyakhto, Konstantinos P. Tsioufis, Victor Aboyans, Ileana Desormais
Reduction of albuminuria has also been considered as a therapeutic target. Analyses of data from RCTs have reported that changes in urinary albumin excretion are predictors of renal and cardiovascular events [186,486]. However, there are also studies in which treatment that was less effective at reducing albuminuria was more effective at reducing cardiovascular events [175] and vice versa [176,291]. Thus, whether reducing albuminuria per se is a proxy for CVD prevention remains unresolved.
Cardiorenal benefits of finerenone: protecting kidney and heart
Published in Annals of Medicine, 2023
José R. González-Juanatey, Jose Luis Górriz, Alberto Ortiz, Alfonso Valle, Maria Jose Soler, Lorenzo Facila
Individuals with T2D and CKD are at high risk of progressing to end-stage kidney disease, and even more so of developing CV complications, including atherosclerotic coronary artery disease and HF, or of dying prematurely, especially if there is prior CV disease [3–5]. In this sense, the presence of diabetes and CKD is common in persons with ischemic heart disease and those with HF [56–58]. On the other hand, it is important to note that the presence of albuminuria itself increases the risk of renal complications, CV, and death in the general population and in individuals with T2D [7]. For this reason, it is essential to determine albuminuria in persons with CKD and/or T2D, a population that is frequent in cardiology consultations, to better stratify CV risk and optimize CV protective treatment [8,56–58].
Albuminuria as a predictor of mortality in type II diabetic patients after living-donor liver transplantation
Published in Annals of Medicine, 2022
Ahmed Abdallah Salman, Mohamed Abdalla Salman, Mostafa Said, Hesham Elkassar, Mohammad El Sherbiny, Ahmed Youssef, Mohammed Elbaz, Ahmed M. Elmeligui, Mohamed Badr Hassan, Mahmoud Gouda Omar, Hussien Samir, Mohamed Abdelkader Morad, Hossam El-Din Shaaban, Mohamed Youssef, Ahmed Moustafa, Mohamed Sabry Tourky, Ahmed Elewa, Sadaf Khalid, Khaled Monazea, Mohamed Shawkat
The present study has some limitations. The retrospective nature of the study was the main limitation of the present study. However, the relatively large number of the study sample and the reasonably acceptable follow-up period are points of strength that can support the findings. Another limitation was the heterogenous causes of liver disease that indicated LT. However, to our knowledge, only a few studies addressed the impact of urinary albumin excretion in diabetic patients, especially after LDLT. Therefore, this article adds momentum to the literature regarding this unique topic. Furthermore, it is sensible to say that this work may point to nongraft potential contributing factors that may affect prognosis after LT and may provide novel horizons in terms of this aspect. This can make it an attractive goal for therapeutic approaches to focus on detecting albuminuria to improve the outcome after LT. Most importantly, given the statistical results, the study underlines that urinary albumin excretion has a substantial impact on mortality after LT.
Impact of SGLT2 inhibitors on the kidney in people with type 2 diabetes and severely increased albuminuria
Published in Expert Review of Clinical Pharmacology, 2022
Nasir Shah, Vlado Perkovic, Sradha Kotwal
The earliest easily detectable clinical marker of DKD is the presence of moderately increased albuminuria (defined as a urinary albumin excretion of between 30 and 300 mg/day). Albumin excretion above 300 mg/day is defined as severely increased albuminuria. The risk of moderately elevated albuminuria increases with the duration of diabetes. Typically, in patients with type 2 diabetes mellitus, severely increased albuminuria is associated with progressive decline in renal function measured via the glomerular filtration rate. The risk of renal function decline has a linear or log-linear relation to all levels of albumin excretion, with increased levels associated with a faster decline in renal function. Moderately increased albuminuria is also a marker for increased cardiovascular risk and the development of microvascular disease in patients with diabetes, thus contributing to their already elevated risk of cardiovascular events. Reduction in albuminuria has been associated with slowing the progression of renal function decline. Change in albuminuria is a widely used surrogate end point for the progression of chronic kidney disease, especially in patients with high baseline albuminuria with a meta-analysis suggesting that for each 30% reduction in albuminuria, the risk of ESKD decreased by 23.7%. This was shown to be irrespective of the medication type used to reduce albuminuria; therefore, postulating that any reductions in albuminuria are beneficial and that any class of medication that reduces albuminuria is likely to have kidney protective effects [53,54].