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Objective: To date no clinical trials have evaluated the role of dietary patterns on the incidence of microvascular diabetes complications. We hypothesized that a nutritional intervention based on the Mediterranean diet (MedDiet) would have greater protective effect on diabetic retinopathy and nephropathy than a low-fat control diet., Research Design and Methods: This was a post hoc analysis of a cohort of patients with type 2 diabetes participating in the PREvención con DIeta MEDiterránea (PREDIMED) study, a multicenter randomized nutritional intervention trial conducted in a population at high cardiovascular risk. Individuals with type 2 diabetes who were free of microvascular complications at enrollment (n = 3,614, aged 55-80 years) were randomly assigned to one of three dietary interventions: MedDiet supplemented with extravirgin olive oil (MedDiet+EVOO), MedDiet supplemented with mixed nuts (MedDiet+Nuts), or a low-fat control diet. Two independent outcomes were considered: new onset of diabetic retinopathy and nephropathy. Hazard ratios (HRs) were calculated using multivariable-adjusted Cox regression., Results: During a median follow-up of 6.0 years, we identified 74 new cases of retinopathy and 168 of nephropathy. Compared with the control diet, multivariable-adjusted HRs for diabetic retinopathy were 0.56 (95% CI 0.32-0.97) for the MedDiet+EVOO and 0.63 (0.35-1.11) for the MedDiet+Nuts. No between-group differences were found for nephropathy. When the yearly updated information on adherence to the MedDiet was considered, the HR for retinopathy in the highest versus the lowest quintile was 0.34 (0.13-0.89; P = 0.001 for trend). No significant associations were found for nephropathy., Conclusions: A MedDiet enriched with EVOO may protect against diabetic retinopathy but not diabetic nephropathy., (© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.)

Objective: An association between dietary acid load and cardiovascular disease risk has been reported in epidemiologic studies; however, there are no reports to our knowledge of this association in patients with diabetic nephropathy (DN). Therefore, the aim of this study was to examine the association between dietary acid load, based on potential renal acid load (PRAL) and protein:potassium ratio (Pro:K) scores, and cardiovascular disease risk factors in individuals with DN., Methods: In this cross-sectional study, we randomly enrolled 547 patients with DN. Dietary intake was assessed using a validated food frequency questionnaire. Biochemical and anthropometric measures were assessed using standard methods., Results: Participants had a mean age of 66.8 y and body mass index of 24 kg/m(2). After controlling for potential confounders, participants in the low PRAL group had lower hemoglobin (Hb)A1c (5.7% ± 0.5% versus 7.8% ± 0.5%; P = 0.01), triacylglycerols (246.9 ± 2.3 mg/dL versus 257.4 ± 2.3 mg/dL; P = 0.006), systolic blood pressure (103.6 ± 0.7 mm Hg versus 106.1 ± 0.7 mm Hg; P = 0.03), and lower creatinine and fasting blood sugar compared with the high PRAL group. Pro:K was positively related to HbA1c (5.8% ± 0.5% versus 7.6% ± 0.5%; P = 0.03), but inversely associated with low-density lipoprotein and waist circumference., Conclusions: We found that both PRAL and Pro:K were positively related to HbA1c in the setting of DN, whereas other biochemical and kidney-related markers varied with PRAL and Pro:K status. Future studies are warranted to clarify the clinical outcomes of dietary acid load in older populations as well as in patients with chronic kidney disease., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Diabetic nephropathy (DN) is a common microvascular complication of diabetes mellitus (DM) that worsens its morbidity and mortality. There is evidence that camel milk (CM) improves the glycemic control in DM but its effect on the renal complications especially the DN remains unclear. Thus the current study aimed to characterize the effects of CM treatment on streptozotocin (STZ)-induced DN. Using STZ-induced diabetes, we investigated the effect of CM treatment on kidney function, proteinuria, renal Smad1, collagen type IV (Col4), blood glucose, insulin resistance (IR), lipid peroxidation, the antioxidant superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH). In addition renal morphology was also examined. The current results showed that rats with untreated diabetes exhibited marked hyperglycemia, IR, high serum urea and creatinine levels, excessive proteinuria, increased renal Smad1 and Col4, glomerular expansion, and extracellular matrix deposition. There was also increased lipid peroxidation products, decreased antioxidant enzyme activity and GSH levels. Camel milk treatment decreased blood glucose, IR, and lipid peroxidation. Superoxide dismutase and CAT expression, CAT activity, and GSH levels were increased. The renoprotective effects of CM were demonstrated by the decreased serum urea and creatinine, proteinuria, Smad1, Col4, and preserved normal tubulo-glomerular morphology. In conclusion, beside its hypoglycemic action, CM attenuates the early changes of DN, decreased renal Smad1 and Col4. This could be attributed to a primary action on the glomerular mesangial cells, or secondarily to the hypoglycemic and antioxidant effects of CM. The protective effects of CM against DN support its use as an adjuvant anti-diabetes therapy., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

TGF-β 1 has been recognized as a key mediator in DN. This study aimed to observe the effects of low-protein diets supplemented with ketoacid on mRNA and protein expression of TGF-β and TβRI and t TβRII receptors in the renal tissue of diabetic rats. A diabetes model was established in 72 male SD rats. They were then equally randomized to three groups: NPD group, LPD group, and LPD + KA group. Additional 24 male SD rats receiving normal protein diets were used as the control. Eight rats from each group were sacrificed at weeks 4, 8, and 12 after treatment, from which SCr, BUN, serum albumin, and 24 h urinary protein excretion were collected. The expressions of TGF-β 1, TβRI, and TβRII in LPD and LPD + KA groups were significantly lower than those in NPD group and lower in LPD + KA group than those in LPD group. Low-protein diets supplemented with ketoacid have been demonstrated to provide a protective effect on the renal function as represented by reduced SCr, BUN, and urinary protein excretion, probably through downregulating the gene expression of TGF-β 1 and its receptors in LPD + KA group.

Non-enzymatic protein glycation and resultant accumulation of advanced glycation endproducts (AGE) are implicated in the pathogenesis of diabetic complications including diabetic nephropathy (DN). It is considered that antiglycating agents offer protection against AGE mediated pathologies including DN. Earlier we characterized procyanidin-B2 (PCB2) as the active component from cinnamon (Cinnamomum zeylanicum) that inhibits AGE formation in vitro. In this study, we have investigated the potential of PCB2-enriched fraction of cinnamon to prevent in vivo accumulation of AGE and to ameliorate renal changes in diabetic rats. Streptozotocin-induced diabetic rats were fed with either 3% cinnamon or 0.002% PCB2-fraction in diet for 12weeks. Biochemical analysis of blood and urine was performed at the end of experiment. Evaluation of glomerular markers that serve as indicators of renal function was done by immunohistochemistry, immunoblotting and qRT-PCR. Supplementation of diabetic rats with cinnamon and PCB2-fraction prevented glycation mediated RBC-IgG cross-links and HbA1c accumulation in diabetes rats. Cinnamon and PCB2-fraction also inhibited the accumulation of N-carboxy methyl lysine (CML), a prominent AGE in diabetic kidney. Interestingly, cinnamon and its PCB2-fraction prevented the AGE mediated loss of expression of glomerular podocyte proteins; nephrin and podocin. Inhibition of AGE by cinnamon and PCB2-fraction ameliorated the diabetes mediated renal malfunction in rats as evidenced by reduced urinary albumin and creatinine. In conclusion, PCB2 from cinnamon inhibited AGE accumulation in diabetic rat kidney and ameliorated AGE mediated pathogenesis of DN., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

The prevention and treatment of chronic kidney disease (CKD) in diabetes through diet and lifestyle have been a topic of much interest over the years. Consideration of the type and amount of carbohydrate, protein and fat is required for optimal blood glucose control, for clinical outcomes related to renal function and for consideration of risk reduction for cardiovascular disease. Controversy has existed regarding the clinical significance of a protein-controlled diet, not to mention the ideal recommended intake in view of the benefits and risks. Furthermore, the level of CKD with which to implement dietary changes should also be considered. This review seeks to provide guidance and clarity concerning the nutritional management of CKD in diabetes., (Copyright © 2014 Canadian Diabetes Association. Published by Elsevier Inc. All rights reserved.)

Background: Suboptimal vitamin D status is highly prevalent in Northern communities, particularly in those patients with chronic diseases such as diabetes and chronic renal disease. Emerging literature suggests that adherence to daily vitamin D supplementation may be an important factor influencing vitamin D status and overall bone health, but compliance with therapies for bone health is a major challenge. It is unknown what level of vitamin D supplementation will ameliorate or improve suboptimal vitamin D status in patients with diabetic nephropathy or contribute to improved bone health, particularly for those living in northern climates., Methods/design: The study purpose was to examine two different strategies of vitamin D3 supplementation; daily dosing of 2000 IU per day verses monthly dosing of 40,000 IU per month on markers of vitamin D status, bone health and to examine whether adherence, quality of life and patient satisfaction with the supplementation strategy differs between the two vitamin D strategies in adults diagnosed with diabetic nephropathy., Discussion: The need for RCTs assessing higher doses of vitamin D3 supplementation at varying frequencies of administration and its impact on bone health in adults with diabetes and chronic kidney disease are needed., Trial Registration: ClinicalTrials.gov NCT01476501.

Human epidemiological and animal studies have shown the beneficial effect of zinc supplementation on mitigating diabetic nephropathy. However, the mechanism by which zinc protects the kidney from diabetes remains unknown. Here we demonstrate the therapeutic effects of zinc on diabetes-induced renal pathological and functional changes. These abnormalities were found in both transgenic OVE26 and Akt2-KO diabetic mouse models, accompanied by significant changes in glucose-metabolism-related regulators. The changes included significantly decreased phosphorylation of Akt and GSK-3β, increased phosphorylation of renal glycogen synthase, decreased expression of hexokinase II and PGC-1α, and increased expression of the Akt negative regulators PTEN, PTP1B, and TRB3. All of these were significantly prevented by zinc treatment for 3 months. Furthermore, zinc-stimulated changes in glucose metabolism mediated by Akt were actually found to be metallothionein dependent, but not Akt2 dependent. These results suggest that the therapeutic effects of zinc in diabetic nephropathy are mediated, in part, by the preservation of glucose-metabolism-related pathways via the prevention of diabetes-induced upregulation of Akt negative regulators. Given that zinc deficiency is very common in diabetics, this finding implies that regularly monitoring zinc levels in diabetic patients, as well as supplementing if low, is important in mitigating the development of diabetic nephropathy., (© 2013 Elsevier Inc. All rights reserved.)

The objective of the present study was to investigate the effects of β-conglycinin and soya isoflavones on diabetic nephropathy (DN). DN was induced by an intravenous injection of streptozotocin (25 mg/kg) in spontaneously hypertensive rats. DN rats were divided into a non-diabetic group (C, control group) and three DN groups (D, DN with control diet; B, DN+control diet with one-eighth of casein replaced by β-conglycinin as the protein source; and I, DN+control diet with 0·01 % soya isoflavones). After a 4-week experimental period, we found that fasting blood sugar and plasma and kidney advanced glycation end product levels and 24 h urinary protein excretion of the B group were significantly lower than those of the D group and insulin sensitivity and nephrin expression of the B group were significantly higher than those of the D group. In addition, systolic blood pressure, angiotensin-converting enzyme activity, angiotensin II level and plasma TAG level of the B group were significantly lower than those of the D group, whereas only the levels of plasma TAG and thiobarbituric acid-reactive substances of the I group were lower than those of the D group. In conclusion, β-conglycinin may be beneficial for retarding DN progression and this effect cannot be completely explained by its isoflavone content.

Diabetic nephropathy is the leading cause of progressive kidney disease, leading to end-stage renal disease and renal replacement therapy. Angiotensin-converting enzyme inhibitors and/or angiotensin receptor blockers have been considered effective at slowing the progression of kidney function deterioration. However, these drugs cannot sufficiently halt the progression of nephropathy to the extent that is required. A low-protein diet (LPD) is believed to be a nutritional intervention that may slow kidney disease progression. In fact, preclinical animal experiments have demonstrated excellent renoprotective effects of an LPD. However, in human clinical trials, analyses of the effects of protein restriction on diabetic nephropathy have not yet revealed consistently positive outcomes of this nutritional intervention. In this review, we analyze the potential renoprotective effects of an LPD on diabetic nephropathy and summarize the outcomes of clinical trials that have systematically investigated the efficacy of an LPD in diabetic nephropathy. In addition, we discuss some potential approaches associated with nutritional interventions to combat progressive kidney disease.

The effect of rice protein (RP) on diabetic nephropathy in non-obese, spontaneous type 2 diabetic Goto-Kakizaki (GK) rats was investigated.GK rats at 7 weeks of age were fed 20% RP or casein (C) in standard or high-sucrose diets for 10 weeks. Plasma total cholesterol,TAG, alkaline phosphatase (ALP), adiponectin, creatinine and urinary albumin excretion (UAE) were measured and renal histology was evaluated. Compared with C, RP lowered plasma TAG and improved plasma adiponectin levels in GK rats fed the standard diet (P<0·05), and also lowered total cholesterol and ALP in high-sucrose-fed GK rats (P<0·05). RP markedly suppressed the sharp increase in UAE when GK rats were fed high-sucrose diets (P<0·05), and prevented glomerular mesangial matrix expansion in the deep renal cortex near the corticomedullary junction (P<0·05). These results strongly indicate that dietary RP can ameliorate the progression of diabetic nephropathy at an early stage compared with C.

Diabetic nephropathy is one of the secondary complications of diabetes mellitus that is marked by changes in extracellular matrix components leading to end-stage renal failure. Diet plays an important role in managing diabetes. In the present study, the effect of Coccinia indica consumption on diabetes-mediated kidney damage was determined. Both control and diabetic rats were fed with AIN-76 diet supplemented with C. indica fruits and leaves individually at 10% and 5%, respectively, for a period of 2 months. Various parameters, such as fasting blood glucose, urine sugar, albumin excretion, kidney index, and glomerular filtration rate, were ameliorated to various extents by the supplementation of C. indica in the diet. Additionally, diabetic rats fed with diet supplemented with C. indica fruits or leaves showed improvement in glucose tolerance compared to control diabetic rats. They also exhibited beneficial effects on key antioxidant enzymes of the kidney. Furthermore, an increase in laminin and fibronectin as a result of diabetes was alleviated in C. indica-fed rats. These results indicate that the consumption of C. indica is beneficial in partially containing diabetes-mediated deleterious effects on the kidney.

Purpose: Dietary protein content is related clinically to the development of diabetic nephropathy. Here, we investigated how dietary protein content (12-24 % energy) within the range used by humans affected renal manifestations including the expressions of genes involved in the renin-angiotensin (RA) system in control and diabetic mice. Moreover, we examined the effects of dietary protein content on HbA1c and urinary glucose., Methods: Control (CT) and leptin receptor-deficient obese (db) mice, 5 weeks old, were fed the diets below. Under ad libitum conditions, mice were fed 12, 18, and 24 % energy from protein (L-, M-, and H-diets) for 8 weeks. Under pair-feeding conditions, db mice were supplied H-diet (db-Hp) to the equivalent energy to that consumed by db-L mice. Renal manifestations and values related to glucose and insulin were examined biochemically and pathologically., Results: Under ad libitum conditions, db mice consumed food and water dose dependently of the dietary protein content, although they were consumed similarly by CT mice. CT-L mice showed lower urinary albumin and kidney weight, in association with lower mRNA levels of angiotensinogen and renin, than CT-H mice. Under pair-feeding conditions, db-L mice showed a lower ratio of kidney/body weight, HbA1(C), and urinary glucose, and a higher β-cell distribution rate in the pancreas than db-Hp mice., Conclusions: Low-protein intake in the range used by humans may relieve renal manifestations through the suppressed expression of genes in the renal RA system of CT mice. On the other hand, in db mice, low-protein intake improved hyperglycemia and the renal manifestations of diabetes.

Background: In an effort to slow the deterioration of renal function, several authors have recommended in the diabetic stage renal disease with moderate renal impairment decreased protein intake to 0.7 or 0.3 g / kg / day associated with energy intake of at least 30 to 35 kcal / kg / day. However, in clinical practice this proved difficult to achieve without exposing patients to the risk of under nutrition., Aim: To evaluate the effects of a protein restricted diet on the development of diabetic nephropathy and the nutritional status of diabetic patients with renal impairment at the stage of moderate renal impairment compared with those of a group of diabetics with the same characteristics put under basal diabetic diet., Methods: Prospective study of 57 diabetic patients in moderate stage renal disease of middle age (32 ± 0.6 years) followed at the National Institute of Nutrition of Tunis in 2010. Our patients were separated into two groups (group A comprising 30 patients, put on diabetic diet basal and group B comprising 27 patients used in protein-deficient diet: 0.6 to 0.7 g / kg /d). We followed the evolution of certain parameters: glomerular filtration rate (GFR), serum albumin, albuminuria, nutritional risk index (NRI) and we analyzed dietary intake at D0, D90 and D180., Results: Renal function in patients in group B improved as demonstrated by the trend towards higher GFR. It increased from day 0 to day 90 and at day 180. In parallel, there was a beneficial effect on albuminuria which was reduced from 380 ± 56 mg/24h on day 0, to 322 ± 50mg/24h at day J90 and 302 ± 16 mg/24h at day 180. In group A, the opposite phenomena occurred. The patients in Group B have also reduced their overall caloric intake to less than 1800 kcal / day making sure that the balance of their diet quality could no longer be assured the result has a tendency to under nutrition noted more frequently in the latter group (NRI0 = 97.90%, NRI 90= 90.10% , NRI180=90,0%). In the literature these results were found by several studies., Conclusion: The protein-deficient diet (0.6 to 0.7 g/ kg /d) must be integrated into the overall care of diabetic renal insufficiency with moderate renal impairment but requires rigorous repeated dietary interviews and customized to avoid malnutrition can result.

The maintenance of normal metabolism and body defenses depends on the balance between cellular antioxidant and anti-inflammatory factors. This balance can be disrupted by agents/mechanisms in the extracellular milieu that induce excess reactive oxygen species (ROS) and inflammation. Cytopathic advanced glycation endproducts, present in ever increasing amounts in the modern diet, are one of the major environmental factors that cause excess ROS and/or inflammation at all ages and induce complications in aging, such as chronic kidney disease (CKD) and type 2 diabetes. Increased ROS and/or inflammation are present in both aging and CKD, and are associated with reduced cellular defenses against ROS and/or inflammation. Affected individuals have reduced defenses against further stress and are predisposed to organ failure, now a well-known phenomenon in aging. Thus, new methods are urgently needed to safely reduce ROS and/or inflammation in the aging type 2 diabetes patient with CKD. Studies of both normal aging and diabetic patients with kidney disease underline the fact that increased ROS and/or inflammation can be managed in these conditions by economical, safe, and effective interventions that reduce the uptake of advanced glycation endproducts by either modifying preparation of food or an oral drug. This communication reviews these data and adds new information on the efficacy of a drug, sevelamer carbonate, required to reduce ROS and/or inflammation in the aging type 2 diabetes patient complicated by CKD. If larger and longer studies confirm the hypothesis that one or both of these interventions reduce progression of CKD, it could represent a new paradigm in the management of complications in the type 2 diabetes patient with CKD.

Dietary sodium restriction has been shown to enhance the short-term response of blood pressure and albuminuria to angiotensin receptor blockers (ARBs). Whether this also enhances the long-term renal and cardiovascular protective effects of ARBs is unknown. Here we conducted a post-hoc analysis of the RENAAL and IDNT trials to test this in patients with type 2 diabetic nephropathy randomized to ARB or non-renin-angiotensin-aldosterone system (non-RAASi)-based antihypertensive therapy. Treatment effects on renal and cardiovascular outcomes were compared in subgroups based on dietary sodium intake during treatment, measured as the 24-h urinary sodium/creatinine ratio of 1177 patients with available 24-h urinary sodium measurements. ARB compared to non-RAASi-based therapy produced the greatest long-term effects on renal and cardiovascular events in the lowest tertile of sodium intake. Compared to non-RAASi, the trend in risk for renal events was significantly reduced by 43%, not changed, or increased by 37% for each tertile of increased sodium intake, respectively. The trend for cardiovascular events was significantly reduced by 37%, increased by 2% and 25%, respectively. Thus, treatment effects of ARB compared with non-RAASi-based therapy on renal and cardiovascular outcomes were greater in patients with type 2 diabetic nephropathy with lower than higher dietary sodium intake. This underscores the avoidance of excessive sodium intake, particularly in type 2 diabetic patients receiving ARB therapy.

Objectives: The long term effects of a low protein diet (LPD) on depressive symptoms and the quality of life in elderly Type 2 diabetic are unclear., Methods: 38 elderly Type 2 diabetic patients with CRD (Stage 3 - 4) were enrolled in the study. After 4 weeks on a normal protein diet regimen (NPD) providing 1.0 g/kg per day, all participants were assigned for 30 months, randomly, to a LPD (0.7 g/kg per day), either 7 days a week (LPD 7/7) or 6 days a week (LPD 6/7). Mini mental state examination (MMSE), activities daily living (ADL), cumulative illness severity (CIRS-IS), geriatric depression scale (GDS-15) and short-form healthy survey (SF- 36) were evaluated every 3 months., Results: Before the LPD regimen creatinine clearance (CrCl), MMSE, ADL, CIRS-IS, GDS-15 and SF-36 were similar in both LPD 7/7 and LPD 6/7 groups. After 30 months, the mean GDS- 15 increased significantly more in LPD 7/7 group than in LPD 6/7 group (p < 0.05). Both mean SF-36 MCS and SF-36 PCS were decreased significantly more in LPD 7/7 group than in LPD 6/7 group (p < 0.05). After 30 months, the decline in CrCl observed was similar in LPD 7/7 and LPD 6/7 groups (2.77 ± 0.3 and 2.84 ± 0.3 ml/min/year, respectively)., Conclusion: In elderly Type 2 diabetic patients, long term effects of LPD 6/7 regimen in comparison to LPD 7/7 are associated with a similar decline in CrCl, but with decreased depressive symptoms and a better quality of life.

Interactions between sodium intake, the renin-angiotensin system, and renal and cardiovascular outcomes are incompletely understood. The analysis by Lambers Heerspink et al. shows that angiotensin receptor blockade improves diabetic nephropathy and cardiovascular disease more when dietary sodium intake is low, and suggests possible harm when sodium intake is high. These findings highlight dietary salt as a modifiable cardiovascular and renal risk factor and emphasize the need for detailed mechanistic studies.

Objective: To investigate if a-keto/amino acid supplemented low protein diet can slow down the progression of diabetic nephrophathy in comparison with non-supplemented diabetes diet., Methods: A prospective, randomized, controlled clinical study was conducted. Twenty three cases of type 2 diabetic nephropathy in IV stage were randomly divided into alpha-keto/amino acid supplemented diet group (trial group) and conventional diabetes diet group (control group), The treatment duration was 52 weeks. 24 h urine protein was measured at 0, 12, 20, 36 and 52 weeks. Before and after the 52 weeks treatment, all the patients received the measurement of glomerular filtration rate (GFR), blood glucose, blood lipids, inflammatory markers, as well as nutritional status., Results: After the treatment for 20, 36, 52 weeks, mean 24 h urine protein decreased significantly in trial groups (P < 0.05), and 24 h urine protein in trial group were significantly decreased (P < 0.05) compared with control group in 20 weeks after treatment. Either in trial group or in control group, GFR remained relatively stable during the observation period. Nutrition status, inflammatory markers, and serum calcium, phosphorus levels between the two groups were no significantly difference. The adverse events experienced by the patients in trial group were similar and consistent with the patients underlying renal diseases., Conclusion: Alpha-keto/amino acid can reduce proteinuria more effectively, while improve renal function and nutritional status in diabetic nephropathy patients with well-toleration.

Diabetes mellitus is one of the major causes of chronic kidney disease and end-stage renal disease. Diet and lifestyle modification are vital components of optimal treatment for both conditions. This paper will address appropriate and often diverse treatment for each individual, understanding that advising changes which positively impact both conditions is a major challenge for health care professionals working within either speciality. It will also highlight where overlap can be contradictory rather than complementary, and offers practical guidance to support patients in making the necessary lifestyle changes to have maximal positive impact upon both conditions and their overall health., (© 2012 European Dialysis and Transplant Nurses Association/European Renal Care Association.)

Akita mice have type 1 diabetes mellitus caused by a spontaneous point mutation in the Ins2 gene which leads to misfolding of insulin, resulting in pancreatic β-cell failure. Akita mice develop pronounced and sustained hyperglycemia, high levels of albuminuria, and consistent histopathological changes, suggesting that these mice may be suitable as an experimental platform for modeling diabetic nephropathy. One key feature of diabetic kidney disease in Akita mice is that the severity of renal injury is significantly influenced by genetic background. In this chapter, we describe the Akita model and present some of the experimental studies utilizing Akita mice as a model of type 1 diabetes. For example, deficiency in bradykinin receptors, endothelial nitric oxide synthase, or angiotensin-converting enzyme 2 leads to development of functionally and structurally more advanced diabetic nephropathy in these mice, while ketogenic diet has been shown to reverse kidney injury associated with diabetes. This chapter also describes the application of 24-h urine collections from mice for careful measurement of urinary albumin excretion.

Objective: The implications of celiac disease (CD) in adult patients with type 1 diabetes are unknown, with respect to diabetes-related outcomes including glycemic control, lipids, microvascular complications, quality of life, and the effect of a gluten-free diet (GFD). We identified CD in adults with type 1 diabetes and investigated the effect of a GFD on diabetes-related complications., Research Design and Methods: This was a case-control study conducted at a U.K. teaching hospital. Patients with type 1 diabetes aged >16 years (n = 1,000) were assessed for CD. HbA(1c), lipid profile, quality of life, retinopathy stage, nephropathy stage, and degree of neuropathy before and after 1 year on a GFD were assessed., Results: The prevalence of CD was 33 per 1,000 subjects (3.3% [95% CI 2.3-4.6]). At diagnosis of CD, adult type 1 diabetic patients had worse glycemic control (8.2 vs. 7.5%, P = 0.05), lower total cholesterol (4.1 vs. 4.9, P = 0.014), lower HDL cholesterol (1.1 vs. 1.6, P = 0.017), and a higher prevalence of retinopathy (58.3 vs. 25%, P = 0.02), nephropathy (41.6 vs. 4.2%, P = 0.009), and peripheral neuropathy (41.6 vs. 16.6%, P = 0.11). There was no difference in quality of life (P > 0.1). After 1 year on a GFD, only the lipid profile improved overall, but in adherent individuals HbA(1c) and markers for nephropathy improved., Conclusions: Adults with undetected CD and type 1 diabetes have worse glycemic control and a higher prevalence of retinopathy and nephropathy. Treatment with a GFD for 1 year is safe in adults with type 1 diabetes and does not have a negative impact on the quality of life.

Intensive insulin therapy and protein restriction delay the development of nephropathy in a variety of conditions, but few interventions are known to reverse nephropathy. Having recently observed that the ketone 3-beta-hydroxybutyric acid (3-OHB) reduces molecular responses to glucose, we hypothesized that a ketogenic diet, which produces prolonged elevation of 3-OHB, may reverse pathological processes caused by diabetes. To address this hypothesis, we assessed if prolonged maintenance on a ketogenic diet would reverse nephropathy produced by diabetes. In mouse models for both Type 1 (Akita) and Type 2 (db/db) diabetes, diabetic nephropathy (as indicated by albuminuria) was allowed to develop, then half the mice were switched to a ketogenic diet. After 8 weeks on the diet, mice were sacrificed to assess gene expression and histology. Diabetic nephropathy, as indicated by albumin/creatinine ratios as well as expression of stress-induced genes, was completely reversed by 2 months maintenance on a ketogenic diet. However, histological evidence of nephropathy was only partly reversed. These studies demonstrate that diabetic nephropathy can be reversed by a relatively simple dietary intervention. Whether reduced glucose metabolism mediates the protective effects of the ketogenic diet remains to be determined.

The complex metabolic, vascular and inflammatory perturbations that characterize diabetes mellitus often lead to progressive albuminuria, renal injury and dysfunction (diabetic nephropathy [DN]), and diabetes is the leading cause of end-stage renal disease in the US and Europe. Diet has an important role in cardiometabolic disorders and its potential influence on DN is of interest. Fatty acids are a major source of energy, but in excess, fatty acids (particularly saturated fatty acids) can induce lipotoxicity. Omega-3 polyunsaturated fatty acids (PUFAs) confer protection against cardiovascular disease-the major cause of death in patients with DN-by virtue of their antihyperlipidemic, antihypertensive, anti-inflammatory and other properties. Omega-6 PUFAs are also cardioprotective. However, a significant proportion of adults consume insufficient quantities of these essential nutrients. This Review describes the role of omega-3 and omega-6 PUFAs in nutrition and metabolism, with a focus on experimental, epidemiologic and clinical studies that have investigated their renoprotective effect in patients with diabetes. Results from a number of studies suggest, but do not firmly establish, that long-chain omega-3 PUFAs (found in fish oil) reduce albuminuria in the setting of DN. Intake of omega-6 fatty acids is associated with reduced albuminuria in experimental settings and in epidemiologic studies of DN. Although PUFAs do not seem to attenuate glomerular dysfunction, insufficient evidence exists to rule out such an effect. We feel that further research is needed into the potential of PUFA consumption and supplementation in DN.

Aim: Despite the beneficial effects of dietary restriction (DR) on lifespan, age-related diseases, including diabetes and cardiovascular diseases, its effects on type 2 diabetic nephropathy remain unknown. This study examined the renoprotective effects of DR in Wistar fatty (fa/fa) rats (WFRs)., Methods: WFRs were treated with DR (40% restriction) for 24 weeks. Urinary albumin excretion, creatinine clearance, renal histologies, acetylated-NF-κB (p65), Sirt1 protein expression, and p62/Sqstm 1 accumulation in the renal cortex, as well as electron microscopic observation of mitochondrial morphology and autophagosomes in proximal tubular cells were estimated., Results: DR ameliorated renal abnormalities including inflammation in WFRs. The decrease in Sirt1 levels, increase in acetylated-NF-κB, and impaired autophagy in WFRs were improved by DR., Conclusions: DR exerted anti-inflammatory effects and improved the dysregulation of autophagy through the restoration of Sirt1 in the kidneys of WFRs, which resulted in the amelioration of renal injuries in type 2 diabetes., (Copyright © 2011 Munehiro Kitada et al.)

Diabetic nephropathy is now the most common cause of end-stage renal failure in many countries of the world. Despite increasing implementation of preventive treatment, the chance that an individual diabetic patient will reach end-stage renal failure has been increasing rather than decreasing during recent decades. Current dietary habits in The Netherlands and the rest of the Western world are slowly shifting from relatively alkalinizing (e.g., potatoes and vegetables) toward more acidifying (e.g., rice and meat). Moreover, immigrants who consumed traditional diets in their homelands, usually adapt to Western dietary habits. This phenomenon of diet acculturation could, for instance, be involved in the up to 40 times higher chance of development of end-stage renal failure in association with diabetes in South-Asian immigrants compared with whites, in Western countries. High ingestion of nonvolatile acids with food increases susceptibility for progression to end-stage renal failure. These high dietary acid loads lead to compensatory increases in renal acid excretion and ammoniagenesis. The price paid for maintenance of acid-base homeostasis is renal tubulointerstitial injury, with subsequent decline in renal function and induction of hypertension. The tendency for metabolic acidosis that results from the changing dietary habits could be corrected by a shift toward more alkalinizing food. We hypothesize that promoting such a shift can prevent the epidemic of end-stage renal failure in diabetes.

Objectives: Late-life depression is one of the main health problems among elderly diabetic subjects. In addition, depression is a common psychopathological condition among renal failure patients and most of these patients follow a low protein diet regimen (LPD). However, the effects of LPD on depressive symptoms are unclear., Design: In the present study, the effects of LPD regimen on depressive symptoms in elderly type 2 diabetic subjects with renal failure were investigated., Participants: Fifty-two young-old type 2 diabetic patients with renal failure were enrolled in the study. All participants after normal protein diet regimen providing 1.2g/kg per d were instructed to consume either a LPD providing 0.8 g/kg per d, 7 d a wk (LPD 7/7), or a LPD providing 0.8 g/kg per d 6 d a wk (LPD 6/7) randomly., Results: Mean 15-item Geriatric Depression Scale (GDS-15) (2.0±0.6) and Beck Depression Inventory (BDI) (4.1±1.0), during normal protein diet regimen, significantly increased to (6.7±1.6) and (12.2±1.4), respectively, after LPD 7/7 (P<0.05 versus normal protein diet). However, after LPD 6/7, mean GDS-15 and BDI significantly decreased to (4.4±1.5) and (6.7±1.6), respectively (P<0.05 versus LPD 7/7)., Conclusion: LPD 6/7 regimen significantly decreased depressive symptoms in young-old type 2 diabetic patients., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Background: There is strong evidence that our current consumption of salt is a major factor for increased blood pressure (BP) and a modest reduction in salt intake lowers BP whether BP levels are normal or raised. Tight control of BP in diabetics lowers the risk of strokes, heart attacks and heart failure and slows the progression of diabetic kidney disease (DKD). Currently there is no consensus in restricting salt intake in diabetic patients., Objectives: To evaluate the effect of altered salt intake on BP and markers of cardiovascular disease and DKD., Search Strategy: In January 2010, we searched the Cochrane Renal Group's Specialised Register, CENTRAL (in The Cochrane Library), MEDLINE (from 1966) and EMBASE (from 1980) to identify appropriate articles., Selection Criteria: We included all randomised controlled trials of salt reduction in individuals with type 1 and type 2 diabetes., Data Collection and Analysis: Two authors independently assessed studies and resolved differences by discussion with a third independent author. We calculated mean effect sizes using both the fixed-effect and random-effects models., Main Results: Thirteen studies (254 individuals) met our inclusion criteria. These included 75 individuals with type 1 diabetes and 158 individuals with type 2 diabetes. The median reduction in urinary sodium was 203 mmol/24 h (11.9 g/day) in type 1 diabetes and 125 mmol/24 h (7.3 g/day) in type 2 diabetes. The median duration of salt restriction was one week in both type 1 and type 2 diabetes. BP was reduced in both type 1 and type 2 diabetes. In type 1 diabetes (56 individuals), salt restriction reduced BP by -7.11/-3.13 mm Hg (systolic/diastolic); 95% CI: systolic BP (SBP) -9.13 to -5.10; diastolic BP (DBP) -4.28 to -1.98). In type 2 diabetes (56 individuals), salt restriction reduced BP by -6.90/-2.87 mm Hg (95% CI: SBP -9.84 to -3.95; DBP -4.39 to -1.35). There was a greater reduction in BP in normotensive patients, possibly due to a larger decrease in salt intake in this group., Authors' Conclusions: Although the studies are not extensive, this meta-analysis shows a large fall in BP with salt restriction, similar to that of single drug therapy. All diabetics should consider reducing salt intake at least to less than 5-6 g/day in keeping with current recommendations for the general population and may consider lowering salt intake to lower levels, although further studies are needed.

Objective: To investigate the association between dietary n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFAs) and the degree and development of albuminuria in type 1 diabetes., Research Design and Methods: We analyzed longitudinal data from 1,436 participants in the Diabetes Control and Complications Trial. We defined the average intake of eicosapentaenoic and docosahexaenoic acid from diet histories. Urinary albumin excretion rates (UAERs) were measured over 24 h; incident albuminuria was considered the first occurrence of an UAER >40 mg/24 h sustained for >or=1 year in normoalbuminuric individuals. RESULTS In a mean follow-up of 6.5 years, we observed a lower mean UAER (difference 22.7 mg/24 h [95% CI 1.6-43.8)]) in the top versus the bottom third of dietary n-3 LC-PUFAs, but we found no association with incident albuminuria., Conclusions: Dietary n-3 LC-PUFAs appear inversely associated with the degree but not with the incidence of albuminuria in type 1 diabetes. These findings require further investigation in prospective studies.

Objective: Adipokines play an important role in metabolic regulations. Obesity, diabetes, and renal disturbances affect adipokine profile by influencing their complex effects on metabolism. Our objective was to assess the effect of low-energy diet intervention on serum adiponectin, leptin, and resistin levels in diabetic nephropathy., Methods: Seventeen subjects with diabetes type 2 and nephropathy participated in the study. After estimation of individual resting metabolic rates by indirect calorimetry, diets introducing 20% energy deficit were applied. At baseline and after 2 months of dieting, the following parameters were measured: body composition by dual x-ray spectrometry and serum adiponectin (Adp), leptin (Lep), resistin (Res), insulin, urea, creatinine, glucose, glycosylated hemoglobin, C-reactive protein, and tumor necrosis factor-alpha concentrations. Homeostatic model assessment (HOMA) was used to quantify insulin resistance., Results: Total energy, protein, and fat intakes diminished significantly with intentional dieting. Significant decreases in total body fat mass (FM) and its percentage in body mass (FM%) and trunk and gynoid fat mass, as well as in serum resistin and tumor necrosis factor-alpha levels, were also observed. Responses of adipokines to dietary treatment varied individually. Generally, they were affected by FM. Alterations in Lep concentrations correlated negatively with baseline FM, FM%, and android and gynoid fat mass and positively with changes in intake of protein, carbohydrates, and total energy of the consumed diet. Changes in Adp were inversely related to FM after therapy. Alterations in Res concentrations correlated positively with android fat mass before therapy and initial Lep levels. Adiponectin was inversely related to HOMA index before and after treatment., Conclusions: Low-energy diet applied in diabetic nephropathy may decrease serum resistin levels and inflammation. In addition, responses of all adipokines to dieting appear to be affected by body fat mass, especially android fat mass., (Copyright 2010 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Hyperlipidemia is a risk factor for development and progression of diabetic nephropathy. However, it is not known if reduction of hyperlipidemia is protective against progression of disease. The goal of this study was to determine if reduction of hypercholesterolemia could limit progression of diabetic nephropathy. Diabetic and nondiabetic LDL receptor deficient (LDLR(-/-)) mice were fed diets containing either no cholesterol (0%) or high cholesterol (0.12%) for 36 weeks. One group each of diabetic and nondiabetic mice were fed the high-cholesterol diet for 26 weeks then changed to the 0% cholesterol diet for the last 10 weeks. Consumption of the high-cholesterol diet exacerbated the development of diabetic nephropathy with elevations in urine albumin excretion, glomerular and renal hypertrophy, and mesangial matrix expansion. Increased glomerular lipid and apolipoprotein B accumulation was found in diabetic mice that consumed the 0.12% cholesterol diet compared with other groups. However, diabetic mice that changed from the high-cholesterol diet to the 0% cholesterol diet for the last 10 weeks had lower urine albumin excretion and mesangial matrix expansion compared with mice that consumed the 0.12% cholesterol diet throughout. This suggests that hyperlipidemia causes continuous renal injury, and that lowering cholesterol levels by dietary means can improve renal function in diabetic LDLR(-/-) mice.

Increased collaboration between the vascular specialities is clearly leading to increased understanding of the interrelationships between the different disease states and how each impacts and influences the other. This advantage will be reflected in improved patient care if the practical outputs of this growing knowledge are carefully implemented at service level. This article outlines how the aspects of diet and lifestyle associated with vascular-related disease complement, contrast and in some cases contradict each other. It gives information and guidelines as to how the expertise of dietitians working in the different specialist areas might usefully be shared to be of maximum advantage to all patients.

Aim: To estimate the prevalence of chronic kidney disease (CKD) among diabetes patients in New Zealand, using estimated Glomerular filtration rate (eGFR); to measure the agreement between the Modification of Diet in Renal Disease (MDRD) and Cockcroft-Gault (CG) equations in identifying CKD among Europeans and Māori; to review the metabolic control and treatment in patients with evidence of CKD., Method: Diabetes patients were identified though general practice records of diagnosis codes, diabetes annual reviews, prescriptions and laboratory results. The MDRD and CG equations were used to calculate the eGFR. Agreement between the two equations was expressed using Kappa statistics and was tested using McNemar's chi-square test. Logistic regression model was used to identify the predictors of CKD (eGFR<60 ml/min/1.73m2)., Results: Overall prevalence of CKD among diabetes patients was 19.5% (MDRD) and 23.5% (CG). Maori were significantly more likely to have CKD [Odds-ratio 1.8(1.2-2.8)]. There were significant differences between the MDRD and the CG equations in identifying patients with CKD. While CG equation identifies more European of both genders, more Māori females were identified by MDRD., Conclusion: Patients with decreased eGFR who do not have proteinuria or microalbuminuria might benefit from more intensive management of blood pressure. MDRD equation may be overestimating CKD among Māori females. Each ethnic subpopulation may need to be validated separately, and by gender.

The aim of this study was to clarify the factors influencing the dietary behavior of patients with diabetic nephropathy. One hundred twenty-two patients with type 2 diabetes were recruited from the outpatients of Okayama University Hospital in Okayama, Japan. We performed a cross-sectional study using a questionnaire including 206 items among 18 categories as follows: background factors, coping behavior (coping scale), degree of uncertainty in illness (uncertainty scale), and dietary behavior. The data were analyzed by correlation analysis, t-test, one-way analysis of variance, Pearson correlation analysis, and multiple regression analysis. We found that those patients with microalbuminuria alone tended to recognize more mild about their kidney status than those with macroalbuminuria and chronic renal failure. We also found that common factors influencing the dietary behavior of diabetic patients with and without nephropathy are as follows: 1. coping with the problem (beta = 0.342, p < 0.01); 2. anxiety about prognosis (beta = -0.344, p < 0.01); 3. sex (beta = -0.234, p < 0.05); 4. uncertainty regarding treatment (beta = 0.377, p < 0.01); 5. negative coping (beta = -0.354, p< 0.01); and 6. employment status (beta = 0.367, p < 0.01). Coping and uncertainty in illness had a significant relation to positive support and lack of support. To maintain appropriate dietary behavior in diabetic patients, medical staff need to determine what the social supports are important for the patient, and also to ensure good communication among healthcare personnel as well as positive support for patients and families.

Aims/hypothesis: There is currently insufficient evidence to recommend a low-protein diet for type 2 diabetic patients with diabetic nephropathy. We assessed whether a low-protein diet could prevent the progression of diabetic nephropathy., Methods: This was a multi-site parallel randomised controlled trial for prevention of diabetic nephropathy progression among 112 Japanese type 2 diabetic patients with overt nephropathy. It was conducted in Japan from 1 December 1997 to 30 April 2006. The participants were randomly assigned using a central computer-generated schedule to either low-protein diet (0.8 g kg(-1) day(-1)) and normal-protein diet (1.2 g kg(-1) day(-1)), and were followed for 5 years. The participants and investigators were not blinded to the assignment. The primary outcomes were the annual change in estimated GFR and creatinine clearance, the incidence of doubling of serum creatinine and the time to doubling of baseline serum creatinine., Results: The study was completed by 47 (84%) of 56 participants in the low-protein diet group and 41 (73%) of 56 participants in the normal-diet group. During the study period, the difference in mean annual change in estimated GFR between the low-protein diet and the normal-protein diet groups was -0.3 ml min(-1) 1.73 m(-2) (95% CI -3.9, 4.4; p = 0.93). The difference in mean annual change in creatinine clearance between the low-protein diet and the normal-protein diet groups was -0.006 ml s(-1) 1.73 m(-2) (95% CI -0.089, 0.112; p = 0.80). A doubling of serum creatinine was reached in 16 patients of the low-protein group (34.0%), compared with 15 in the normal-protein group (36.6%), the difference between groups being -2.6% (95% CI -22.6, 17.5; p = 0.80). The time to doubling of serum creatinine was similar in both groups (p = 0.66)., Conclusions/interpretation: It is extremely difficult to get patients to follow a long-term low-protein diet. Although in the low-protein group overall protein intake was slightly (but not significantly) lower, it did not confer renoprotection., Clinical Trial Registration: ClinicalTrials.gov NCT00448526., Funding: Research grant from the Ministry of Health, Labour and Welfare of Japan.

Diabetic nephropathy is originally microvascular in nature and is widely considered an important complication of diabetes. The present study was carried out to determine the efficacy of camel milk in controlling diabetic nephropathy. Twenty-four type-1 diabetic patients were randomly recruited from the outpatient diabetic clinic in PBM Hospital, Bikaner, India. All subjects gave their written consent before participation in the study. Patients with any acute metabolic complications were not included in the study. Eligible patients entered a run-in period of 1 month in which they were oriented to achieve the best possible glycemic control through standardized diet, standardized exercise regimen and insulin administration. During this period frequent monitoring of blood sugar was performed to maintain euglycemia. At the end of the run-in period, a base line evaluation was performed, then these patients were given camel milk in addition with usual care for six months. Urine microalbumin and blood sugar was measured twice a week before breakfast and dinner. There was a significant improvement in the microalbuminuria (119.48 +/- 1.68 to 22.52 +/- 2.68; p < 0.001) after receiving camel milk for 6 months. A significant reduction in the mean dose of insulin for obtaining glycemic control was achieved (41.61 +/- 3.08 to 28.32 +/- 2.66; p < 0.01). This study was performed to observe the role of camel milk in controlling microalbuminuria levels in type-1 diabetic patients. It was observed that after adding camel milk to the usual regimen an improvement in microalbuminuria was reached (119.48 +/- 1.68 to 22.52 +/- 2.68; p < 0.001). This may be due to good glycemic control or to the direct effect of camel milk. The mechanism behind this effect is still unknown.

The aim of the present study was to review the possible role of dietary lipids in diabetic nephropathy (DN), taking into account associated abnormalities of serum lipids and interaction of dietary and genetic aspects. Dietary lipids may have an important role in the development and progression of DN. The fat diet composition has been associated with DN, particularly with microalbuminuria, serum lipids abnormalities, and endothelial function. However, the beneficial effect of fat intake modification for these patients is not fully established, especially regarding hard outcomes, such as DN incidence and progression, kidney failure, and death. Moreover, genetic factors may influence the response of serum lipids to fat intake. The identification of specific genetic polymorphisms associated with this interaction could allow adoption of individual nutritional strategies in DN.

Background: A low-protein diet (LPD) has been proposed for many years to delay the progression of diabetic nephropathy. However, the efficacy of an LPD with respect to renal outcome is disputed., Objective: We aimed to determine the effect of an LPD on renal function in patients with type 1 or 2 diabetic renal diseases by using a meta-analysis of randomized controlled trials., Design: Medline, EMBASE, and the Cochrane Central Register of Controlled Trials were searched. Eight studies met the inclusion criteria for our meta-analysis: a duration of >6 mo, use of a randomized control group, availability of outcome data for changes in glomerular filtration rate (GFR) or creatinine clearance rate (CCR), and albuminuria or proteinuria in patients with type 1 or 2 diabetic nephropathy. Data were combined by means of a fixed-effects model. Weighted mean differences (WMD) were calculated for the change in GFR or CCR, glycated hemoglobin (HbA(1c)), and serum albumin between the LPD and control groups. A random-effects model was also used to calculate the standardized mean difference for the change in urinary albumin excretion or proteinuria., Results: Overall, a change in WMD for GFR or CCR was not significantly associated with an LPD, but a decrease in WMD for HbA(1c) was significant in the LPD group (P = 0.005). Although the benefit of LPD therapy on proteinuria was significant (P = 0.003), great heterogeneity was observed. In a subgroup analysis, LPD resulted in lower serum albumin concentrations., Conclusion: LPD was not associated with a significant improvement of renal function in patients with either types 1 or 2 diabetic nephropathy.

Aims/hypothesis: Estimation of GFR (eGFR) is recommended for the assessment of kidney function in all patients with diabetes. We studied performance of the traditional '186' Modification of Diet in Renal Disease (MDRD) equation, and the 2005 revised '175' MDRD equation in patients with type 2 diabetes., Methods: Two hundred and ninety-three mainly normoalbuminuric (267/293) patients were recruited. Patients were classified as having mild renal impairment (group 1, GFR <90 ml min(-1) 1.73 m(-2)) or normal renal function (group 2, GFR >or=90 ml min(-1) 1.73 m(-2)). eGFR was calculated by the traditional 186 MDRD equation using traditional creatinine values and the revised 175 MDRD equation using isotope dilution mass spectrometry-standardised creatinine values. Isotopic GFR was measured by the four-sample plasma clearance of (51)Cr-EDTA., Results: For patients in group 1, mean +/- SD isotopic (51)Cr-EDTA GFR (iGFR) was 83.8 +/- 4.3 ml min(-1) 1.73 m(-2), and eGFR was 73.2 +/- 11.9 and 75.8 +/- 13.7 ml min(-1) 1.73 m(-2) using the 186 and 175 MDRD equations, respectively. Method bias was -10.6 with the 186 MDRD and -7.9 ml min(-1) 1.73 m(-2) (p < 0.05) with the 175 MDRD equation. In group 2, iGFR was 119.4 +/- 20.2 ml min(-1) 1.73 m(-2), and eGFR was 92.3 +/- 18.6 and 97.5 +/- 21.6 ml min(-1) 1.73 m(-2) using the 186 and 175 MDRD equations, respectively. Method bias was -27.1 with the 186 MDRD equation and -21.9 ml min(-1) 1.73 m(-2) (p < 0.05) with the 175 MDRD equation., Conclusions/interpretation: In patients newly diagnosed with type 2 diabetes, the revised 175 MDRD equation was less biased than the traditional 186 MDRD equation. Despite a continued tendency to underestimate isotopically measured GFR, use of standardised creatinine values is a positive step towards improved estimation of GFR.

Diabetic nephropathy is one of the principal causes of chronic renal failure. The disease prevailingly develops in men. The incidence of diabetic nephropathy doubled from 1991 to 2001. There are different traditional dietary guidelines for the different states of diabetic nephropathy, as well as pharmacotherapy options, and, last but not least, also modern ways of application of nutritional pharmacology. Organ specific nutritional substrates - amino acids, polyunsaturated fatty acids and other components of nutrition with pharmacological effects have become indispensable in modern care for diabetic patients.