A low-carbohydrate diet may prevent end-stage renal failure in type 2 diabetes.

A low-carbohydrate diet may prevent end-stage renal failure in type 2
diabetes. A case report
Jørgen Vesti Nielsen1 , Per Westerlund1 and Per Bygren2
1Dept. of Medicine, Blekingesjukhuset, Karlshamn, Sweden
2Formerly Department of Nephrology, University Hospital, Lund, Sweden

Nutrition & Metabolism 2006, 3:23 doi:10.1186/1743-7075-3-23

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An obese patient with type 2 diabetes whose diet was changed from the
recommended high-carbohydrate, low-fat type to a low-carbohydrate diet
showed a significant reduction in bodyweight, improved glycemic
control and a reversal of a six year long decline of renal function.
The reversal of the renal function was likely caused by both improved
glycemic control and elimination of the patient's obesity.

Insulin treatment in type 2 diabetes patients usually leads to weight
increase which may cause further injury to the kidney. Although other
unknown metabolic mechanisms cannot be excluded, it is likely that the
obesity caused by the combination of high-carbohydrate diet and
insulin in this case contributed to the patient's deteriorating kidney
function. In such patients, where control of bodyweight and
hyperglycemia is vital, a trial with a low-carbohydrate diet may be
appropriate to avoid the risk of adding obesity-associated renal
failure to already failing kidneys.


In Sweden the number of patients with type 2 diabetes accompanied by
end-stage renal failure has increased by 80 % since 1991 [1]. Control
of blood glucose is crucial because of the proven link between HbA1c
and the rate of decline of the kidney function in diabetic nephropathy
[2]. Metabolic control in such patients is, however, difficult because
the recommended low-fat diet with its high content of carbohydrates
usually leads to a vicious cycle: hyperglycemia caused by the high-
carbohydrate diet necessitates the use of insulin; efforts to
normalise the blood glucose with insulin leads to increase of appetite
and bodyweight [3]; the rise of bodyweight exposes the patient to the
risk of obesity-associated renal failure [4]. A low-carbohydrate diet,
however, is a potent antihyperglycemic remedy and may at the same time
lead to weight loss [5,6].

We report here a significant reduction in body weight, improved
glycemic control and reversal of a six year long decline of renal
function in a patient with type 2 diabetes, whose diet we changed from
the usually recommended high-carbohydrate, low-fat type to the

Case report

The patient is a 60-year old man who was diagnosed with type 2
diabetes in 1989 and had a family history of overweight and diabetes.
Retinopathy was diagnosed in the mid-90s. The patient had been treated
several times with focal laser photocoagulation. In 2003 he developed
proliferative retinopathy and was treated with photocoagulation. In
addition to glimepiride and the ACE-inhibitor quinapril, medication
included metoprolol, furosemide, simvastatin and aspirin. In 1995–
1997, his blood pressure (BP) was on average 125/90 mm Hg. Over the
same period, the patient's bodyweight varied between 89 kg and 85 kg.
Traditional dietary counselling for weight loss usually resulted in a
short-term loss of a few kg, but the bodyweight soon increased again.

In July 1997 albuminuria was noted with a urine concentration of 116
mg/l. That year the patient's average body mass index (BMI) was 29.4
kg/m2 and the average bodyweight was 87.0 kg.

Insulin treatment was started four months later resulting in a
temporary improvement of HbA1c but an increase in bodyweight. One year
later, his BMI was 32.5 kg/m2 and his weight was 94 kg. The insulin
dose was lowered in order to avoid further increase in bodyweight. In
the years 1998–1999, following the weight increase and despite
improved glycemic control, his BP increased to an average 145/90 mm
Hg. Likewise, urine albumin increased as seen in the Figure. In 2000,
despite a still reasonable glycemic control but following further
weight increase, the albuminuria reached an average of more than 2000
mg/l and the BP was 160/90 mm Hg. Both were controlled by exchanging
quinapril for the angiotensin II receptor antagonist candesartan, and
by adding amlopidine. The BP has since been stable, averaging 130/76
(± 10/7) mm Hg, but the decline of renal function continued. The
Figure shows the albuminuria record and the increase in HbA1c, serum
creatinine and body weight with increasing insulin dosage.

In January 2004 his diet was changed radically by reducing dietary
carbohydrates to 80–90 g per day, consisting only of vegetables and
small amounts of hard bread (crisp bread). Potatoes, bread, pasta,
rice and cereals were excluded, and the caloric requirements were
covered by protein and fat. To ease the transition the patient was
supplied with a number of meal recipes suggesting a caloric
restriction to about 1800 calories per day. The per cent proportions
of carbohydrates, fat and protein in the recipes were 20 : 50: 30.

Less than two weeks later the patient discontinued his insulin
treatment and 6 months later his bodyweight had decreased by 19 kg.
HbA1c had dropped to 6.5 % after 3 months, and the steady rise of his
serum creatinine stopped. The creatinine has since – for two-and-a-
half years – been stable as seen in the figure. When insulin was
discontinued rosiglitazone was prescribed. In the Table measured
parameters are shown before the dietary change, and now. As of late
2005 there was no sign of proliferative disease in the patient's


As early as two years after the appearance of albuminuria, the patient
had increased creatinine and urine albumin and higher BP. This
happened despite a significantly improved glycemic control, although
following an increase of bodyweight. A change of medication did affect
BP and albuminuria but not the decline in kidney function. Only after
a weight loss of 19 kg and an HbA1c reduction from a mean of about 8.5
% to 6.5 % was the steady decline of the kidney function reversed.

Diabetic nephropathy normally progresses to end-stage renal failure
irrespective of the treatment. Only a complete 24 hour normoglycemia,
as seen after pancreas transplants, can give the patient a chance to
preserve the remaining kidney function.

In the Diabetes Control and Complication Trial (DCCT) a reduction of
HbA1c from 9 % to 7 % (DCCT) led to a 40–50 % reduction in the number
of patients whose kidney function deteriorated [2]. The reduction of
HbA1c cannot by itself explain the change of the rate of decline. Also
the HbA1c is far from normal. This level of hyperglycemia would not be
able to produce a reversal to a completely preserved kidney function.
Moreover, an almost normalised HbA1c in the years following the
commencement of insulin treatment had no effect on the decline then.

Obesity and renal failure

Obesity is a strong risk factor for renal failure especially in
patients with diabetes and hypertension [4]. Even lean persons with
central body fat distribution are at risk of having a lower rate of
glomerular filtration [7]. An obesity-related glomerulopathy has been
described [8]. The etiology may be ascribed to the fact that adipose
tissue is a source of hormones including angiotensinogen, renin and
leptin that may well influence renal function and BP [9,10]. Numerous
inflammatory mediators such as TNFα, IL-6, resistin and others [11]
are also secreted from fatty tissue. These contribute to chronic
inflammation, general atherosclerosis and probably insulin resistance.

Beneficial effect of weight loss in proteinuric nephropathy has been
shown in a controlled study [12]. A weight reduction of about 25 kg in
an overweight diabetes patient after gastric by-pass lowered the
proteinuria by 84 % and after further weight loss led to normalisation
of a slightly elevated creatinine [13]. Finally, two case reports have
described the partially resolving and stabilisation of dialysis-
requiring renal failure after weight loss following bariatric surgery

The common adverse effect of insulin treatment, the increase in
bodyweight, may have contributed to the deterioration of the patient's
kidney function in the years before the dietary change. Some degree of
insulin sensitivity in the adipocytes is necessary for weight
increase. During the first couple of years, with relatively modest
insulin doses, the patient had a reasonable glycemic control while he
increased in weight, which points at some degree of insulin
sensitivity. By the year 2000, body weight may have exceeded an
individual threshold for the accumulation of visceral fat after which
insulin resistance increased [16 ] necessitating more insulin.

It may be assumed that improved glycemic control as well as weight
loss contributed to stabilization of the patient's kidney function.
The actual mechanisms behind the course of the patient's kidney
disease are not known, however, and it cannot be excluded that other
metabolic changes have contributed to the improvement of the renal
function independently of weight loss. Even though other unknown
metabolic pathways and mechanisms may have been involved, it is still
unlikely that this patient would have avoided dialysis if his diet had
not been changed. This is suggestive of a causal relationship between
the diet and the course of the patient's kidney disease.

Low-carbohydrate diet and weight loss

Low plasma insulin is a prerequisite for maximally stimulating the
hormone-sensitive lipase that is responsible for lipolysis in fatty
tissue. It therefore makes sense for an obese diabetes patient to
reduce the high intake of carbohydrates. In this way the blood glucose
is reduced and the patient is able to diminish or discontinue insulin.
In addition, a low-carbohydrate diet with ad libitum food intake has
been shown to be superior to the traditional calorie-restricted, low-
fat, high-carbohydrate diet for weight loss in five randomised
controlled studies [17-21]. The primary effect is caused by a lowering
of appetite and a caloric intake reduced to the appropriate level for
the patient's height [22].

The protein content of a diet may be a concern, but the actual size of
the effect of protein restriction is modest [23,24]. It is also a
misconception that a low-carbohydrate diet automatically is high in
protein. This misconception may be a barrier for the use of a low-
carbohydrate diet which is a highly effective tool in the management
of type 2 diabetes. Such a diet can be modified so it suits the
patient's needs i.e. the energy from carbohydrates can be replaced by
energy from dietary fat and not necessarily from protein. The patient
here was given a number of meal recipes at start. The aim was to give
him the means to learn how to use this new dietary tool, which in
essence leads to a completely different mind-set regarding diet. He
was then recommended to consume about 70–90 g low-starch carbohydrates
per day and to eat more fat. The patient is today still keeping the
carbohydrates at the recommended level. He eats more fat and probably
about 80–90 g of protein per day.

A motivating factor, in addition to being able to see that the kidney
function has stabilized, was probably the increased feeling of well-
being that followed very soon after the dietary change. Within 1–2
weeks of the dietary change – before any significant weight reduction
had occurred – poor sleep and chronic fatigue was exchanged for a
sound sleep pattern and increased vitality. This effect soon allowed
the patient to again involve himself wholly in the running of his
company. The reversal of the tiredness seen with chronic hyperglycemia
may have been the cause. It may be that reversal of carbohydrate-
induced memory impairment in type 2 diabetes played a role in
restoring the patient's alertness and self-confidence [25 ].


The present case report shows that a low-carbohydrate, high-fat diet
improves glycemic control, reduces body weight and may prevent the
development of end-stage renal failure in an overweight patient with
type-2 diabetes. Furthermore, it raises the concern that the obesity
caused by the combination of a high-carbohydrate diet and insulin may
have contributed to the patient's failing kidney function.

Competing interests

The author(s) declare that they have no competing interests.