Time to abandon microalbuminuria?

Abstract

The term microalbuminuria--a urinary albumin excretion (UAE) between 20 and 200 microg/min--has been introduced to identify subjects at increased risk of renal and cardiovascular disease. However, the relationship between albuminuria and risk is not restricted to the microalbuminuric range and extends to as low as 2-5 microg/min. On the contrary, the increase of UAE above 200 microg/min (macroalbuminuria) heralds the onset of proteinuria (urinary protein excretion above 0.5 g/24 h) and progressive renal and cardiovascular disease. Albuminuria is a component of the metabolic syndrome and may represent a marker of the increased risk of renal and cardiovascular disease associated with insulin resistance and endothelial dysfunction. Proteinuria is a sign of established kidney damage and plays a direct pathogenic role in the progression of renal and cardiovascular disease. Albuminuria reflects functional and potentially reversible abnormalities initiated by glomerular hyperfiltration, proteinuria, a size-selective dysfunction of the glomerular barrier normally associated with glomerular filtration rate (GFR) decline that may result in end-stage renal disease. Thus, the limit of 200 microg/min segregates patients with albuminuria or proteinuria who are at quite different risk. Among subjects with albuminuria, however, there is a continuous relationship between albumin excretion and risk and no lower bound between normal albuminuria and microalbuminuria can be identified that segregates subjects at different risk. Thus, the terms microalbuminuria and macroalbuminuria could be replaced by the concepts of albuminuria- and proteinuria-associated diseases. Future studies are needed to identify levels of albuminuria below which therapy is no longer beneficial.

Effects of Manidipine and Delapril in Hypertensive Patients With Type 2 Diabetes Mellitus

“…Several factors might be involved, including kidney hypoperfusion secondary to concomitant vascular disease, structural changes related to chronic hyperglycemia or accelerated tissue ageing, chronic inflammation, oxidative stress, or insulin resistance. 22,23 These mechanisms were not appreciably affected by study drugs, because GFR decline was virtually identical among treatment arms with or without considering baseline GFR values. These findings were in harmony with those of the Renin-Angiotensin System Study, showing no effect of ACE inhibitor therapy compared with placebo on GFR, albuminuria, and glomerular structural changes in normotensive type 1 diabetic patients with normal UAE at inclusion.…”

“…These findings were in harmony with those of the Renin-Angiotensin System Study, showing no effect of ACE inhibitor therapy compared with placebo on GFR, albuminuria, and glomerular structural changes in normotensive type 1 diabetic patients with normal UAE at inclusion. 24 Altogether, these data highlight the need for early intervention with novel treatments targeting potential mediators of accelerated renal dysfunction other than overt proteinuria 23,25 to slow or prevent GFR decline already at the stage of normoalbuminuria or microalbuminuria. Actually, in subjects with overt proteinuric nephropathies, angiotensin inhibitors slow renal disease progression more effectively than other antihypertensive agents.…”

Very low-grade albuminuria reflects susceptibility to chronic kidney disease in combination with cardiovascular risk factors

“…Recently, microalbuminuria has been identified as an indicator of insulin resistance and of increased renal and cardiovascular risks (also known as cardio-renal syndrome) associated with metabolic syndrome. 16,17 Insulin resistance has been reported to increase the risk of CKD. 18,19 Chen et al 18,19 determined that metabolic syndrome 19 and insulin resistance estimated by a homeostasis model assessment 18 were associated with an increased CKD risk in participants in the NHANES III study.…”

Renal resistive index and low-grade inflammation in patients with essential hypertension

“…3 Increased urinary albumin excretion (UAE), namely either micro-or macroalbuminuria, is a well-established marker of hypertensive renal target-organ damage (TOD), mainly characterized by glomerular vasculature involvement. 4 An increase in both hsCRP and UAE occurs in a large proportion of nondiabetic essential hypertensive patients, 5 and a strict direct association between high hsCRP levels and increased UAE were found. 6,7 The ultrasound measurement of the renal resistive index (RRI) has been proposed in adjunct to UAE to assess the severity of renal TOD in hypertension.…”