scholarly journals Early Recognition and Treatment of Diabetic Kidney Disease

2014 ◽  
Vol 26 (1) ◽  
pp. 56-62
Author(s):  
Sheikh Salahuddin Ahmed ◽  
Md Abu Saleh Mohammad Rizwan ◽  
Md Abdul Mahid Khan ◽  
Tarafdar Runa Laila ◽  
Md Abdul Hafez
Keyword(s):  
Risk Factor ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Early Stage ◽  
Kidney Damage ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Lipid Lowering ◽  
Diabetic Kidney ◽  
Cardiovascular Morbidity And Mortality

Diabetic kidney disease (DKD) is a progressive condition and is an important cause of end stage renal disease (ESRD) as well as a risk factor for cardiovascular morbidity and mortality. This paper reviews various evidence based clinical guidelines, scientific papers and research studies on early detection and treatment of DKD. Microalbuminuria describes the urinary excretion of small amounts of albumin which identifies the early stage of DKD. In addition to an earliest marker of kidney damage, microalbuminuria is an established high risk factor for cardiovascular morbidity and mortality. Patients with microalbuminuria who progress to macroalbuminuria are likely to progress to ESRD. However effective treatment in the early stage of DKD reduces the risk and slows the progression of kidney damage. There is general agreement that people with diabetes should be screened regularly to detect early markers of kidney damage. People with diabetes and microalbuminuria should be treated with a multifactorial intervention approach to retard the progression of DKD. Studies have clearly demonstrated that the use of angiotensin converting enzyme inhibitors or angiotensin 2 receptor blockers with improved glycemic control, hypertension control, lipid lowering, aspirin use, smoking cessation, exercise programs and dietary intervention reduced the development of overt nephropathy and ESRD. DOI: http://dx.doi.org/10.3329/medtoday.v26i1.21317 Medicine Today 2014 Vol.26(1): 56-62

scholarly journals Proteinuria in Chronic Kidney Disease and its Management

2013 ◽  
Vol 25 (1) ◽  
pp. 36-41 ◽  
Author(s):  
SS Ahmed ◽  
TR Laila ◽  
HA Begum ◽  
M Moniruzzaman
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Early Stage ◽  
Kidney Damage ◽  
Similar Degree ◽  
Converting Enzyme Inhibitors ◽  
Diabetic Kidney ◽  
Early Stages ◽  
Cardiovascular Morbidity And Mortality

Proteinuria is a marker of kidney damage and an important risk factor for progression of chronic kidney disease as well as cardiovascular morbidity and mortality. Albumin is the principal component of proteinuria in glomerular disease. The presence of persistent albumin in the urine is a clear sign of glomerular abnormality. Microalbuminuria describes the urinary excretion of small amounts of albumin which identifies the very early stage of diabetic kidney disease. The albumin creatinine ratio is the preferred method of detecting microalbuminuria. There is strong evidence that treatment in the early stages of chronic kidney disease reduces progression of kidney damage. The levels of proteinuria in both diabetic and non-diabetic kidney disease at which management should be addressed have been reviewed. This article also reviews the interventions recommended for early stages of chronic kidney disease to reduce the risk of progression to end stage kidney failure. Angiotensin converting enzyme inhibitors and angiotensin 2 receptor blockers are more effective in reducing proteinuria and retarding the progression of kidney disease in comparison to other therapies which lower systemic blood pressure to a similar degree. DOI: http://dx.doi.org/10.3329/medtoday.v25i1.16070 Medicine Today 2013 Vol.25(1): 36-41

scholarly journals A renaissance in the treatment of diabetic kidney disease, hypertension in chronic kidney disease, and beyond

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Jordana Yahr ◽  
Juan Calle ◽  
Jonathan J. Taliercio
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Primary Care Physicians ◽  
Diabetic Kidney Disease ◽  
Morbidity And Mortality ◽  
Diabetic Kidney ◽  
Cardiovascular Morbidity And Mortality ◽  
Management Of Complications ◽  
Progression Of Disease

Abstract Chronic kidney disease (CKD) affects approximately 15% of the US population and is associated with significant cardiovascular morbidity and mortality. The two leading causes of end stage kidney disease are hypertension and diabetes mellitus, both of which are modifiable risk factors. The cornerstones of CKD care include early detection, management of associated risk factors, modification of cardiovascular disease risk, slowing progression of disease, and management of complications including anemia, acid base disturbance, and mineral and bone disorders. For the last 20 years, renin-angiotensin system inhibitors were the mainstay treatment for proteinuric diabetic and nondiabetic kidney disease. Recently, new therapies such as sodium-glucose linked transporter 2 inhibitors, have emerged as powerful tools in the treatment of CKD with indications in both diabetic and nondiabetic kidney disease. In this article, we define CKD staging, review new hypertension and diabetic guidelines for CKD patients, and discuss major trials for new potential therapies in CKD, particularly diabetic kidney disease. We will provide practical guidance for primary care physicians to diagnose CKD and implement these agents early in the disease course to prevent the progression of disease and reduce the morbidity and mortality of this vulnerable population.

scholarly journals Non-Albumin Proteinuria (NAP) as a Complementary Marker for Diabetic Kidney Disease (DKD)

Life ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 224
Author(s):  
Jaehyun Bae ◽  
Young Jun Won ◽  
Byung-Wan Lee
Keyword(s):  
Kidney Disease ◽  
Filtration Rate ◽  
Diabetic Kidney Disease ◽  
Estimated Glomerular Filtration Rate ◽  
Early Stage ◽  
Screening Tools ◽  
Tubular Injury ◽  
Current Standard ◽  
Diabetic Kidney ◽  
Wide Range

Diabetic kidney disease (DKD) is one of the most common forms of chronic kidney disease. Its pathogenic mechanism is complex, and it can affect entire structures of the kidney. However, conventional approaches to early stage DKD have focused on changes to the glomerulus. Current standard screening tools for DKD, albuminuria, and estimated glomerular filtration rate are insufficient to reflect early tubular injury. Therefore, many tubular biomarkers have been suggested. Non-albumin proteinuria (NAP) contains a wide range of tubular biomarkers and is convenient to measure. We reviewed the clinical meanings of NAP and its significance as a marker for early stage DKD.

scholarly journals Effects of Dapagliflozin on Circulating Markers of Phosphate Homeostasis

2018 ◽  
Vol 14 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Maarten A. de Jong ◽  
Sergei I. Petrykiv ◽  
Gozewijn D. Laverman ◽  
Antonius E. van Herwaarden ◽  
Dick de Zeeuw ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Early Stage ◽  
Glycosylated Hemoglobin ◽  
Fibroblast Growth Factor 23 ◽  
Serum Phosphate ◽  
Phosphate Homeostasis ◽  
Double Blind ◽  
Diabetic Kidney ◽  
Albumin Excretion

Background and objectivesThe sodium glucose cotransporter 2 (SGLT-2) inhibitor dapagliflozin is a novel drug for the treatment of diabetes mellitus. Recent studies suggest that SGLT-2 inhibitors affect phosphate homeostasis, but their effects on phosphate-regulating hormones in patients with diabetic kidney disease are still unclear.Design, setting, participants, & measurementsWe performed a post-hoc analysis of a double-blind, randomized, crossover trial in patients with type 2 diabetes with early-stage diabetic kidney disease on stable renin–angiotensin–aldosterone system blockade, with an albumin-to-creatinine ratio between 100 and 3500 mg/g, eGFR≥45 ml/min per 1.73 m2, and glycosylated hemoglobin≥7.2% and <11.4%. Patients were randomized to dapagliflozin 10 mg/d or placebo during consecutive 6-week study periods, separated by a 6-week wash-out. We investigated effects on circulating phosphate, calcium, parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), 25-hydroxyvitamin D (25[OH]D), and 1,25-dihydroxyvitamin D (1,25[OH]2D) levels.ResultsThirty-one patients (age 62 years; 23% female) were analyzed. Compared with placebo, dapagliflozin increased serum phosphate by 9% (95% confidence interval, 4% to 15%; P=0.002), PTH increased by 16% (3% to 30%; P=0.01), FGF23 increased by 19% (0.3% to 42%; P=0.05), and serum 1,25(OH)2D decreased by −12% (−25% to 4%; P=0.12). Calcium and 25(OH)D were unaffected. We found no correlation between changes in markers of phosphate homeostasis and changes in eGFR or 24-hour albumin excretion during dapagliflozin treatment.ConclusionsDapagliflozin increases serum phosphate, plasma PTH, and FGF23. This effect was independent of concomitant changes in eGFR or 24-hour albumin excretion.

scholarly journals Sulodexide Protects Renal Tubular Epithelial Cells from Oxidative Stress-Induced Injury via Upregulating Klotho Expression at an Early Stage of Diabetic Kidney Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Yu Ning Liu ◽  
Jingwei Zhou ◽  
Tingting Li ◽  
Jing Wu ◽  
Shu Hua Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Epithelial Cells ◽  
Diabetic Kidney Disease ◽  
Early Stage ◽  
Collaborative Study ◽  
Oxidative Activity ◽  
Dependent Manner ◽  
Diabetic Kidney ◽  
Collaborative Study Group

The hypoalbuminuric effect of sulodexide (SDX) on diabetic kidney disease (DKD) was suggested by some clinical trials but was denied by the Collaborative Study Group. In this study, the diabetic rats were treated with SDX either from week 0 to 24 or from week 13 to 24. We found that 24-week treatment significantly decreased the urinary protein and HAVCR1 excretion, inhibited the interstitial expansion, and downregulated the renal cell apoptosis and interstitial fibrosis. Renoprotection was also associated with a reduction in renocortical/urinary oxidative activity and the normalization of renal klotho expression. However, all of these actions were not observed when SDX was administered only at the late stage of diabetic nephropathy (from week 13 to 24). In vitro, advanced glycation end products (AGEs) dose-dependently enhanced the oxidative activity but lowered the klotho expression in cultured proximal tubule epithelial cells (PTECs). Also, H2O2 could downregulate the expression of klotho in a dose-dependent manner. However, overexpression of klotho reduced the HAVCR1 production and the cellular apoptosis level induced by AGEs or H2O2. Our study suggests that SDX may prevent the progression of DKD at the early stage by upregulating renal klotho expression, which inhibits the tubulointerstitial injury induced by oxidative stress.

scholarly journals MMP-10 is Increased in Early Stage Diabetic Kidney Disease and can be Reduced by Renin-Angiotensin System Blockade

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
José María Mora-Gutiérrez ◽  
José Antonio Rodríguez ◽  
María A. Fernández-Seara ◽  
Josune Orbe ◽  
Francisco Javier Escalada ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Diabetic Kidney Disease ◽  
Early Stage ◽  
Renin Angiotensin System ◽  
Diabetic Patients ◽  
Diabetic Mice ◽  
Angiotensin System ◽  
Diabetic Kidney ◽  
Renin Angiotensin

AbstractMatrix metalloproteinases have been implicated in diabetic microvascular complications. However, little is known about the pathophysiological links between MMP-10 and the renin-angiotensin system (RAS) in diabetic kidney disease (DKD). We tested the hypothesis that MMP-10 may be up-regulated in early stage DKD, and could be down-regulated by angiotensin II receptor blockade (telmisartan). Serum MMP-10 and TIMP-1 levels were measured in 268 type 2 diabetic subjects and 111 controls. Furthermore, histological and molecular analyses were performed to evaluate the renal expression of Mmp10 and Timp1 in a murine model of early type 2 DKD (db/db) after telmisartan treatment. MMP-10 (473 ± 274 pg/ml vs. 332 ± 151; p = 0.02) and TIMP-1 (573 ± 296 ng/ml vs. 375 ± 317; p < 0.001) levels were significantly increased in diabetic patients as compared to controls. An early increase in MMP-10 and TIMP-1 was observed and a further progressive elevation was found as DKD progressed to end-stage renal disease. Diabetic mice had 4-fold greater glomerular Mmp10 expression and significant albuminuria compared to wild-type, which was prevented by telmisartan. MMP-10 and TIMP-1 are increased from the early stages of type 2 diabetes. Prevention of MMP-10 upregulation observed in diabetic mice could be another protective mechanism of RAS blockade in DKD.

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