Metabolic Syndrome
Jahangir Moini, Matthew Adams, Anthony LoGalbo in Complications of Diabetes Mellitus, 2022
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.
A
Anton Sebastian in A Dictionary of the History of Medicine, 2018
Albuminuria Albumin present in the urine. White clouds in the urine were noted by Hippocrates (460–377 BC). Albumin in the urine was shown by boiling and the addition of acetic acid by Fredericus Dekkers (1648–1720) of Leiden in 1694. Dominic Cotugno (1736–1822) of Vienna rediscovered it in the urine by a similar method in 1764 and the term albuminuria was introduced by Martin Solon of Paris in 1838. English physician John Blackall (1771–1860) demonstrated it in cases of dropsy in 1813.The relationship between albuminuria and renal disease was established by Richard Bright (1789–1858) in 1827. Its occurrence in fevers was described by Martin Solon in 1838 and named febrile albuminuria by Carl Gerhardt (1833–1902) of Germany in 1868.The presence of albumin in the urine of mothers with puerperal convulsions or eclampsia was observed by John Charles Lever (1811–1858), a lecturer in midwifery at Guy’s Hospital in London in 1843. The presence of massive albuminuria in subarachnoid hemorrhage was noted by French pathologist and microbiologist, Georges Fernand Isidore Widal (1862–1929) in 1903. See benign albuminuria.
Practice Paper 8: Answers
Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar in Get ahead! Medicine, 2016
Microalbuminuria is defined by the presence of 20–300 mg/L albumin in the urine on two separate occasions or a urine albumin:creatinine ratio >2.5 mg/mmol in males and >3.5 in females. It should be noted that these concentrations of albumin are too low to be identified on urine dipstick and require a specific analysis. Microalbuminuria is an important predictor of renal and cardiovascular disease in diabetes. If it is identified and treated appropriately, the natural progression to persistent albuminuria, diabetic nephropathy and renal failure can be prevented. Treatment involves strict glycaemic and blood pressure control, with the use of ACE inhibitors or angiotensin II receptor antagonists in all patients, including those who are normotensive.
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].
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].
Extending the ambit of SGLT2 inhibitors beyond diabetes: a review of clinical and preclinical studies on non-diabetic kidney disease
Published in Expert Review of Clinical Pharmacology, 2021
Saurabh Nayak, Vinay Rathore, Joyita Bharati, Kamal Kant Sahu
Significant albuminuria reduction has been noted among diabetic subjects both in preclinical as well as clinical studies. The Evaluation of the Effects of Canagliflozin on Renal and Cardiovascular Outcomes in Participants with Diabetic Nephropathy (CREDENCE) trial has been instrumental in making SGLT2i a quantum leap in retarding CKD progression [6]. Exploratory analysis of the study has linked long-term kidney outcomes to early albuminuria reduction [16]. Alteration in glomerular hemodynamics has been attributed to albuminuria reduction caused by SGLT2i. While albuminuria reduction follows a decline in GFR during the initial weeks of therapy, sustained albuminuria reduction up to 2 years has been documented to be associated with improvement in long-term GFR [17]. In a post hoc analysis of stage 3 CKD patients treated with Dapagliflozin, albuminuria reduction was maintained even after adjustment for change in GFR, blood pressure, HbA1c, and uric acid reduction were made [18]. These findings suggest that perhaps renal hemodynamics alterations only partly explain sustained albuminuria reduction with SGLT2i. In that case, what underlying mechanisms ensure the continued benefits of these agents is yet to be known.
Related Knowledge Centers
- Diabetes
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- Kidney
- Blood Protein
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