Photomicrography of nodular glomerulosclerosis in Kimmelstein-Wilson syndrome. Source: CDC
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Diabetic nephropathy

Diabetic nephropathy (nephropatia diabetica), also known as Kimmelstiel-Wilson syndrome and intercapillary glomerulonephritis, is a progressive kidney disease caused by angiopathy of capillaries in the kidney glomeruli. It is characterized by nodular glomerulosclerosis. It is due to longstanding diabetes mellitus, and is a prime cause for dialysis in many Western countries. more...

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The syndromed was discovered by British physician Clifford Wilson (1906-1997) and Germany-born American physician Paul Kimmelstiel (1900-1970) and was published for the first time in 1936.


The syndrome can be seen in patients with chronic diabetes (15 years or more after onset), so patients are usually of older age (between 50 and 70 years old). The disease is progressive and may cause death two or three years after the initial lesions. and is more frequent in women. Diabetic nephropathy is the most common cause of chronic kidney failure and end-stage kidney disease in the United States. People with both type 1 and type 2 diabetes are at risk. The risk is higher if blood-glucose levels are poorly controlled. However, once nephropathy develops, the greatest rate of progression is seen in patients with poor control of their blood pressure.


The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus. At this stage, the kidney may start allowing more albumin (plasma protein) than normal in the urine (albuminuria), and this can be detected by sensitive medical tests for albumin. This stage is called "microabuminuria". It can appear 5 to 10 years before other symptoms develop. As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed by nodular glomerulosclerosis. Now the amounts of albumin being excreted in the urine increases, and may be detected by ordinary urinalysis techniques. At this stage, a kidney biopsy clearly shows diabetic nephropathy.

Signs and symptoms

Kidney failure provoked by glomerulosclerosis lead to fluid filtration deficits and other disorders of kidney function. There is an increase in blood pressure (hypertension) and of fluid retention in the body (edema). Other complications may be arteriosclerosis of the renal artery and proteinuria (nephrotic syndrome).

Throughout its early course, diabetic nephropathy has no symptoms. They develop in late stages and may be a result of excretion of high amounts of protein in the urine or due to renal failure:

  • edema: swelling, usually around the eyes in the mornings; later, general body swelling may result, such as swelling of the legs
  • foamy appearance or excessive frothing of the urine
  • unintentional weight gain (from fluid accumulation)
  • anorexia (poor appetite)
  • nausea and vomiting
  • malaise (general ill feeling)
  • fatigue
  • headache
  • frequent hiccups
  • generalized itching

The first laboratory abnormality is a positive microalbuminuria test. Most often, the diagnosis is suspected when a routine urinalysis of a person with diabetes shows too much protein in the urine (proteinuria). The urinalysis may also show glucose in the urine, especially if blood glucose is poorly controlled. Serum creatinine and BUN may increase as kidney damage progresses.


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ARBs vs ACE inhibitors for preventing diabetic nephropathy
From Journal of Family Practice, 5/1/05 by Vanessa Greenwood

To the Editor:

A POEM in the February 2005 issue ("ARB no better than ACE inhibitor for prevention of nephropathy progression," J Fam Pract 2005; 54:108-109) discussed the head-to-head randomized double-blind trial from the New England Journal of Medicine by Barnett and colleagues, "Angiotensin-receptor blockade versus converting-enzyme inhibition in type 2 diabetes and nephropathy." (1) This POEM would be better titled "ARB as good as ACE inhibitor" because the study was a non-inferiority trial, designed to prove that the angiotensin receptor blocker (ARB) was "non-inferior" to the angiotensin-converting enzyme (ACE) inhibitor in preventing the progression of diabetic nephropathy. In the age of biases with drug company--sponsored research protocols, we must also be mindful of the language used in reporting results back to the target audience.

Currently, non-inferiority trials are much less common than standard randomized clinical trials (RCTs) for a number of reasons. First, non-inferiority trials are held to more stringent standards than RCTs. The non-inferiority trial is powered to have a 95% chance of detecting a predetermined maximum acceptable difference between the treatment arms that is "clinically insignificant," thus changing the null hypothesis to state that there is a significant difference between the 2 treatments.

Second, these trials must be conducted in a very meticulous manner, since any factor that would be important for generality in an RCT, including a broad range of ages, severity, ethnicities, comorbid conditions, would increase the "noise" in a non-inferiority trial, and subsequently increase the likelihood that the trial would find no difference between the 2 treatments.

Third, due to the number and range of medications already available, new medications are increasingly being developed for indications in which a placebo control group would be unethical, thus necessitating head-to-head comparisons. Examples include comparing 2 selective serotonin reuptake inhibitors in patients with suicidal ideation, or comparing 2 anticoagulants in preventing stroke in atrial fibrillation. (2)

As newer treatments become available, clinicians will want to know 1) is it better than what they are using now, and 2) if not, is it as good as what they are using now ("non-inferior") and preferable for some other reason. (3) Using an alternative treatment rather than the standard treatment may be justified if it is proven that the alternative is more advantageous with respect to availability, safety, or cost. In this study, the ARB is shown to be non-inferior to the ACE inhibitor in preventing diabetic nephropathy. The reader must now decide if this "as good as" drug is worth using in their patient population.

Vanessa Greenwood, MD, Combined Resident Family Medicine/Psychiatry, University of California at San Diego Medical Center

Dr Mark Ebell responds:

The author makes a good point, and I thank her for her attention to detail. I agree with her point that the drugs are equivalent from the perspective of efficacy.

Many physicians, perhaps the majority, behave as if they believed that ARBs are preferred to ACE inhibitors.

However, ARBs are not safer; are not better tolerated (except by those patients with a cough caused by ACE inhibitors); are not simpler to take; and are certainly not cheaper. I would argue that since ARBs are similarly effective but much more expensive, not only are they no better than ACE inhibitors, they are actually worse.

The point of POEMs is not only to convey the results of research accurately, but to evaluate its relevance and validity, and put it into context. I feel that my version of the statement does this better than the suggested alternative.

Mark H. Ebell, MD, MS, InfoPoems, Inc


(1.) Barnett AH, Bain SC, Bouter P, et al. Angiotensin-receptor blockade versus converting-enzyme inhibition in type 2 diabetes and nephropathy. N Engl J Med 2004; 351:1952-1961.

(2.) Stroke prevention with the oral direct thrombin inhibitor ximelagatran compared with warfarin in patients with non-valvular atrial fibrillation (SPORTIF Ill): randomized controlled trial. Lancet 2003; 362:1691-1698.

(3.) Sackett DL. Superiority trials, non-inferiority trials, and prisoners of the 2-sided null hypothesis. Evidence Based Med 2004; 9:38-39.

COPYRIGHT 2005 Dowden Health Media, Inc.
COPYRIGHT 2005 Gale Group

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