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Stimulated drinking could induce decreases in microalbuminuria of diabetic patients
Submit responseDear Sir,
I was interested to read the recent article by Rudy Bilous and colleagues (1) in the Journal entitled “Effect of Candesartan on Microalbuminuria and Albumin Excretion Rate in Diabetes: Three Randomized Trials” the authors present the results of an angiotensin receptor specific blocker on microalbuminuria in type 1 and type 2 diabetic patients. The studies were carried out in mainly normotensive patients candesartan did not appear to prevent micoralbuminuria. There are many substances available to inhibit the renin-angiotensin system and although they all work they do not appear to be as effective as would have been thought given the results from the animal trials that went into the development of these drugs. This is certainly the case with candesartan where early studies in various animal models of renal dysfunction showed that it reduced proteinuria and albuminuria (2). But perhaps the problem does not lie entirely with the drugs themselves but with the behaviour of the patient to the drugs !
In a recent letter concerning the use of antagonists of the renin angiotensin system and obesity it was suggested that the increased drinking observed with use of an inhibitor of the angiotensin converting enzyme was responsible for the decreased weight in the obese animals studied (3). Furthermore, in several studies in mice and rats concerned with either inhibition or “knock-out” of the renin-angiotensin system the animals drink twice, if not more, water than in the control situation (see 3). An increase in fluid intake has been demonstrated to decrease urine albumin concentration in diabetic patients (4). This would imply perhaps two things, one: is that the renin-angiotensin system has an important role in diabetes (5), and two: that diabetic patients do not increase their liquid consumption as much as animals do.
This is supported in part by the fact that angiotensin levels are high in many modern clinical conditions yet this hormone is released principally in response to hypovolaemia under normal physiological conditions. Thus, as has been suggested before, not drinking a sufficient volume of fluids per day could lead to chronic mild hypovolaemia and with time this could lead to the development, maintenance and/or aggravation of diabetes.
It would be of interest to suggest that fluid, especially water, consumption be monitored, if not encouraged, in studies of human diabetes and the use of drugs in the manipulation of the renin-angiotensin system.
References
1. Bilous R, Chaturvedi N, Sjølie AK, Fuller J, Klein R, Orchard T, Porta M, Parving HH. Effect of Candesartan on Microalbuminuria and Albumin Excretion Rate in Diabetes: Three Randomized Trials. Ann Intern Med. 2009 May 18. [Epub ahead of print]
2. Gohlke P, Jürgensen T, von Kügelgen S, Unger T. Candesartan cilexetil: development and preclinical studies. Drugs Today (Barc). 1999; 35 (2): 105-115.
3. Thornton SN, Even PC, van Dijk G. Hydration increases cell metabolism. Int J Obes (Lond). 2009; 33 (3): 385.
4. Ravikovich E, Messersmith T, Mick G, McCormick K. Effect of oral fluid intake on urinary albumin excretion in diabetes mellitus. J Diabetes Complications. 2002; 16 (4): 310-312.
5. Thornton SN. Angiotensin, the hypovolaemia hormone, aggravates hypertension, obesity, diabetes and cancer. J Intern Med. 2009; 265 (5): 616-617.
Conflict of Interest:
None declared