I would need more detail to comment meaningfully, but the post is intriguing. Acutely, blood glucose has little effect on the kidneys, although if blood glucose is high an osmotic diuresis will be seen. Chronically, all of the complications of diabetes may of course follow. However, the impact on SGLT2 expression has recently come into focus because of the availability of SGLT2 inhibitors. GLUT2 and SGLT2 are upregulated by chronic hyperglycaemia increasing not only glucose but also sodium reabsorption. The clinical consequences of this sodium reabsorption are not clear but I would suggest worthy of investigation?

Considering the other side of this coin, chronic kidney disease (CKD) has a number of effects on glucose homeostasis. Although a number of statements have been made and often repeated, in clinical practice I find the effects of progressive CKD unpredictable. CKD is undoubtedly associated with increased insulin resistance. However, insulin is cleared by the kidney and so with progressive CKD insulin clearance falls increasing the plasma insulin concentration. Furthermore, the kidneys account for approximately 20% of total gluconeogenesis. So this drive to hyperglycaemia may be lost as the kidneys fail. Perhaps, given these multiple factors, it is not surprising that the relationship between kidney function and glycaemic control is complicated in both non-diabetic and diabetic individuals.

Not sure if this is of interest: just a few random thoughts!

Hi Dr. Wagh, Dr. Smith gave a very nice answer to your question, which I agree. My humble answers would be it depends. Please read two papers we published in this area in animal models to see whether they may answer your question (Clin Sci (Lond). 2008 May;114(9):591-601; and Current Hypertension Report, 15(5):522-30, 2013). The widely accepted dogma would be of course that high blood glucose is clinically relevant to kidney function and that hyperglycemia will cause kidney injury eventually. However, in one study we just fed mice with 2% glucose continuously for 4 weeks (even longer for 4 months). What disappointed us are that high glucose administration alone for 4 weeks did not elevate fasting blood glucose levels, impair glucose tolerance, or induce renal injury. By contrast, if we induced hyperglucagonemia by infusing glucagon for 4 weeks, it would elevate fasting blood glucose levels, impair glucose tolerance, or induce early renal injury phenotypes. The experience suggests that we should have an open mind to the possibility that insulin or hyperglycemia alone may not be adequate to explain whether high blood glucose is clinically relevant to kidney injury. To induce kidney injury, other factors are certainly involved. Just a thought.

A few thoughts in response to the above. I am not surprised that the physiological mechanisms preventing hyperglycaemia 'coped' with feeding 2% glucose maintaining normal blood glucose in the time frame quoted. However, glucagon infusion will impact directly and significantly on this basic physiology, elevating glucose. Diabetic nephropathy progresses over months and years with the first changes being glomerular hyper perfusion with an increase in glomerular filtration rate (kidney function). The clinical correlate of this glomerular hypertension/hyperperfusion is albuminuria. I agree it is always good to be sceptical, but feel that the clinical evidence for improved glycaemic control preventing progression to microalbuminuria (but not progression once nephropathy is established) is secure arguing that hyperglycaemia is the injurious agent? Whether some people are more susceptible to this insult than others is a moot point. I believe there to be significant differences, with some people protected to a remarkable degree. But this is personal opinion.

Occasional blood sugar may not have an automatic repercussion in the renal function. As a long standing issue, it is well known that high blood sugar correlates with nephropathy. We have known this for many years, but it was "evidence base" proven with the Diabetes Control and Complications Trial (DCCT) in type 1 diabetes and followed by other trials.

If you are interested in having mean BG and kidney function, it is more accurate to use Hemoglobin A1c that gives you a real average of the blood sugars in the past 3 months or fructosamine that covers for 15-30 days.

The blood sugar values will vary according to the time of the day. So, it is better to have the same time for your average BG.

You should also take in account what Dr. Smith and Dr Zhuo said in their interesting comments.