Medical management of nephropathy in type I diabetes mellitus: current recommendations.

1995 ◽  
Vol 6 (6) ◽  
pp. 1523-1529
Author(s):  
J A Breyer

Diabetic nephropathy is the single most common cause of end-stage renal disease in the United States. Recently, several major therapeutic interventions have been developed and demonstrated to slow or halt the progression of renal failure in patients with diabetes and diabetic kidney disease. The Diabetes Control and Complications Trial demonstrated that microalbuminuria developed in fewer patients in the intensive blood sugar control group than in the conventional therapy group. Similarly, the risk of developing proteinuria was reduced by intensive blood sugar control. Multiple studies have demonstrated that in patients with insulin-dependent diabetes and proteinuria, lowering the systemic blood pressure slows the rate of decline in renal function and improves patients' survival. In the recently completed trial of ACE inhibition in diabetic nephropathy, ACE inhibitors were specifically shown to decrease dramatically the risk of doubling of serum creatinine or reaching a combined outcome of end-stage renal disease or death. In studies in small numbers of patients with insulin-dependent diabetes and established diabetic nephropathy, dietary protein restriction has also been demonstrated to slow the rate of decline of renal function. New potential interventions currently undergoing study include the use of aldose reductase inhibitors, the use of drugs that prevent the formation of advanced glycosylation end-products, and the use of angiotensin II receptor antagonists. Thus, several established benefits have recently been demonstrated to help prevent the development of or slow the progression of diabetic nephropathy, including blood pressure control, blood sugar control, and treatment with ACE inhibitors. Dietary protein restriction may also be of benefit. Multiple new interventions are undergoing clinical trials currently.

2016 ◽  
Vol 21 (4) ◽  
pp. 344-352 ◽  
Author(s):  
Yusuke Sata ◽  
Markus P. Schlaich

Sympathetic activation is a hallmark of chronic and end-stage renal disease and adversely affects cardiovascular prognosis. Hypertension is present in the vast majority of these patients and plays a key role in the progressive deterioration of renal function and the high rate of cardiovascular events in this patient cohort. Augmentation of renin release, tubular sodium reabsorption, and renal vascular resistance are direct consequences of efferent renal sympathetic nerve stimulation and the major components of neural regulation of renal function. Renal afferent nerve activity directly influences sympathetic outflow to the kidneys and other highly innervated organs involved in blood pressure control via hypothalamic integration. Renal denervation of the kidney has been shown to reduce blood pressure in many experimental models of hypertension. Targeting the renal nerves directly may therefore be specifically useful in patients with chronic and end-stage renal disease. In this review, we will discuss the potential role of catheter-based renal denervation in patients with impaired kidney function and also reflect on the potential impact on other cardiovascular conditions commonly associated with chronic kidney disease such as heart failure and arrhythmias.


2019 ◽  
Vol 8 (5) ◽  
pp. 755 ◽  
Author(s):  
Mee Kyoung Kim ◽  
Kyungdo Han ◽  
Hun-Sung Kim ◽  
Yong-Moon Park ◽  
Hyuk-Sang Kwon ◽  
...  

Aim: Metabolic parameters, such as blood pressure, glucose, lipid levels, and body weight, can interact with each other, and this clustering of metabolic risk factors is related to the progression to end-stage renal disease (ESRD). The effect of variability in metabolic parameters on the risk of ESRD has not been studied previously. Methods: Using nationally representative data from the Korean National Health Insurance System, 8,199,135 participants who had undergone three or more health examinations between 2005 and 2012 were included in this analysis. Intraindividual variability in systolic blood pressure (SBP), fasting blood glucose (FBG), total cholesterol (TC), and body mass index (BMI) was assessed by examining the coefficient of variation, variability independent of the mean, and average real variability. High variability was defined as the highest quartile of variability and low variability was defined as the lower three quartiles of variability. Results: Over a median (5–95%) of 7.1 (6.5–7.5) years of follow-up after the variability assessment period, 13,600 (1.7/1000 person-years) participants developed ESRD. For each metabolic parameter, an incrementally higher risk of ESRD was observed for higher variability quartiles compared with the lowest quartile. The risk of ESRD was 46% higher in the highest quartile of SBP variability, 47% higher in the highest quartile of FBG variability, 56% higher in the highest quartile of BMI variability, and 108% higher in the highest quartile of TC variability. Compared with the group with low variability for all four parameters, the group with high variability for all four parameters had a significantly higher risk for incident ESRD (hazard ratio (HR) 4.12; 95% CI 3.72–4.57). Conclusions: Variability in each metabolic parameter was an independent predictor of the development of ESRD among the general population. There was a composite effect of the variability in additional metabolic parameters on the risk of ESRD.


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