|Year : 2016 | Volume
| Issue : 3 | Page : 65-72
Diabetic kidney disease: difference in the prevalence and risk factors worldwide
Osama Gheith MD, PhD 1, Nashwa Othman2, Naryanan Nampoory3, Medhat A Halimb3, Torki Al-Otaibi3
1 Nephrology Department, Hamed Al-Essa Organ Transplant Center, Kuwait; Transplantation and Dialysis Unit, Urology and Nephrology Center, Mansoura University, Mansoura, Egypt
2 Education Department, Dasman Diabetes Institute, Kuwait; Community Department, Faculty of Nursing, Mansoura University, Mansoura, Egypt
3 Nephrology Department, Hamed Al-Essa Organ Transplant Center, Kuwait
|Date of Submission||01-Sep-2015|
|Date of Acceptance||25-Sep-2015|
|Date of Web Publication||2-Jan-2017|
Internal Medicine and Nephrology Department, Urology and Nephrology Center, Mansoura University, Mansoura, 35511, Egypt
Source of Support: None, Conflict of Interest: None
Diabetic nephropathy, which is defined as elevated urine albumin excretion or reduced glomerular filtration rate or both, is a serious complication that occurs in 20–40% of all diabetic patients. In this review, we try to highlight the prevalence of diabetic nephropathy, which is not an uncommon complication of diabetes all over the world. The prevalence of diabetes worldwide has extended epidemic magnitudes and is expected to affect more than 350 million people by the year 2035. There is marked racial/ethnic difference besides international difference in the epidemiology of diabetic nephropathy, which could be attributed to the differences in economic viability and governmental infrastructures. Approximately one-third of diabetic patients showed microalbuminuria after 15 years of disease duration and less than half develop real nephropathy. Diabetic nephropathy is more frequent in African-Americans, Asian-Americans, and Native Americans. Progressive kidney disease is more frequent in Caucasian patients with type 1 than in those with type 2 diabetes mellitus (DM), although its overall prevalence in the diabetic population is higher in patients with type 2 DM because this type of DM is more prevalent. Hyperglycemia is a well-known risk factor for diabetic kidney disease, in addition to other risk factors such as male sex, obesity, hypertension, chronic inflammation, resistance to insulin, hypovitaminosis D, dyslipidemia, and some genetic loci and polymorphisms in specific genes. Diabetic nephropathy is not an uncommon complication of diabetes (type 1 and 2) all over the world and in geriatric population. Management of its modifiable risk factors might help in reducing its incidence in the nearby future.
Keywords: diabetic kidney disease, outcome, risk factors
|How to cite this article:|
Gheith O, Othman N, Nampoory N, Halimb MA, Al-Otaibi T. Diabetic kidney disease: difference in the prevalence and risk factors worldwide. J Egypt Soc Nephrol Transplant 2016;16:65-72
|How to cite this URL:|
Gheith O, Othman N, Nampoory N, Halimb MA, Al-Otaibi T. Diabetic kidney disease: difference in the prevalence and risk factors worldwide. J Egypt Soc Nephrol Transplant [serial online] 2016 [cited 2017 Dec 17];16:65-72. Available from: http://www.jesnt.eg.net/text.asp?2016/16/3/65/197379
| Introduction|| |
Diabetic kidney disease (DKD) is a complication that occurs in 20–40% of all diabetic patients. In the Western world, diabetic nephropathy is the primary single cause of end-stage kidney disease (ESKD) . Both type 1 and type 2 diabetes can lead to nephropathy, but, in type 2 diabetes, a smaller proportion of patients progress to ESKD. Because of the higher prevalence of type 2 diabetes, these patients represent more than half of diabetic patients on dialysis . The incidence of diabetic nephropathy as a cause of ESKD is increasing each year . For clinical care and epidemiological studies, DKD is characterized by raised urine albumin excretion or reduced glomerular filtration rate (GFR), or both .
The prevalence of diabetes around the world has reached epidemic proportions. Although diabetes is already estimated to affect more than 8% of the global population (nearly more than 350 million people), this is predictable to grow to over 550 million people by the year 2035 . It has been estimated that more than 40% of people with diabetes will develop chronic kidney disease , including a significant number who will develop ESKD requiring renal replacement therapies (dialysis and or transplantation).
Diabetic nephropathy is uncommon if diabetes is less than one decade’s duration. The highest incidence rates of 3% per year are on average seen 10–20 years after diabetes onset, after which the rate of nephropathy tapers off. It is worthy of mention that a diabetic patient for 20–25 years without clinical signs of DKD has low chances of developing such complication (only 1% per year) . There is marked racial/ethnic and international difference in the epidemiology of DKD ,. Native Americans, Hispanics, and African-Americans have a much greater risk of developing ESKD compared with non-Hispanic whites with type 2 diabetes . On the basis of 2002 US data, diabetes is the cause of renal disease in 44–45% of incident ESKD cases, making the US having one of the highest incidences worldwide . Internationally, there is considerable variability among countries, with percentages fluctuating from 9% in Russia to 49% in Malaysia. This discrepancy could be attributed to the differences in economic viability and governmental infrastructures .
Stages of diabetic nephropathy
Diabetic nephropathy is a chronic complication of both type 1 diabetes mellitus (DM) (β-cell damage and absolute lack of insulin) and type 2 DM (insulin resistance and/or decreased secretion of insulin) . There are five stages in the development of diabetic nephropathy. Stage I: GFR is either normal or increased, and lasts around 5 years from the onset of the diabetes. The size of the kidneys is increased by nearly 20% and renal plasma flow is increased by 10–15%, but without albuminuria or hypertension. Stage II: It starts more or less 2 years after the onset of the disease, with thickening of the basement membrane and mesangial proliferation with normalization of GFR but without clinical signs of the disease. Many patients continue in this stage for life. However, stage III represents the first clinically detectable sign of glomerular damage and microalbuminuria (albumin 30–300 mg/day). It usually occurs 5–10 years after the onset of the disease with or without hypertension. Approximately 40% of patients reach this stage. Stage IV is the stage of chronic kidney disease with irreversible proteinuria (>300 mg/day), decreased GFR below 60 ml/min/1.73 m2, and sustained hypertension. Stage V is defined when ESKD with GFR less than 15 ml/min/1.73 m2 is detected. Nearly 50% of patients will need renal replacement therapy in the form of peritoneal dialysis, hemodialysis, or kidney transplantation . In the early stages of diabetic nephropathy, nephromegaly and changed Doppler indicators may be the early morphological signs of renal damage; however, proteinuria and GFR are the best indicators of the degree of the damage .
The predictive value of microalbuminuria for the progression of kidney damage in patients with type 1 or 2 DM was confirmed in the early 1980s . Almost 20–30% of the patients progress to microalbuminuria after 15 years of disease duration and less than half develop real nephropathy . The European Diabetes (EURODIAB) Prospective Complications Study Group  and 18-year Danish study  reported an overall occurrence of microalbuminuria (after 7.3 years) in patients with type 1 and 2 DM of 12.6 and 33%, respectively. Conferring to the United Kingdom Prospective Diabetes Study (UKPDS), the incidence of microalbuminuria in patients with type 2 DM in Great Britain is 2% per year and the prevalence is 25% 10 years after the diagnosis . Proteinuria develops more frequently in patients with type 1 diabetes (15–40%), usually after 15–20 years of DM duration , but in patients with type 2 DM the prevalence varies between 5 and 20% .
Risk factors for kidney disease in type 1 diabetes
Hyperglycemia is a well-known risk factor for DKD and it recognized that intensive glucose control reduces the risk for DKD . Specifically, during the Diabetes Control and Complications Study (DCCT), near normalization of blood sugar decreased the risks for incident microalbuminuria and macroalbuminuria by 39% [95% confidence interval (CI) 21–52%] and 54% (95% CI 29–74%), respectively, compared with conventional therapy. Even with long-term follow-up in observational Epidemiology of Diabetes Interventions and Complications (EDIC) study, formerly assigned patients to DCCT intensive therapy study continued to experience lower rates of incident microalbuminuria and macroalbuminuria with risk reductions of 45% (95% CI 26–59%) and 61% (95% CI 41–74%), respectively . Beneficial effects of intensive therapy on the worsening of GFR have become evident during long-term combined DCCT/EDIC follow-up, with a risk reduction of 50% (95% CI 18–69%). Other risk factors for DKD in diabetic patients include male sex, obesity, hypertension, inflammation, resistance to insulin, hypovitaminosis D, and dyslipidemia ,,. Moreover, a hereditary component to DKD has long been recognized as some genetic loci, and polymorphisms in specific genes have been associated with DKD.
Diabetic kidney disease in type 1 diabetes
During the last century, landmark studies of type 1 diabetes considered the natural history of DKD as a progressive increase in urine albumin excretion followed by GFR loss and the development of ESKD. Microalbuminuria was defined as albumin excretion rate (AER) 30–299 mg/24 h ‘incipient nephropathy’, progressed steadily to macroalbuminuria with AER of at least 300 mg/24 h ‘diabetic nephropathy’. Microalbuminuric patients are commonly noted to have higher GFR ‘hyperfiltration’, whereas macroalbuminuric patients showed rapid GFR loss leading steadily to ESKD. Frequent exceptions had been observed. Specifically, albuminuria has been observed to revert, whereas GFR loss has been observed without albuminuria and is not always progressive. Therefore, albuminuria and impaired GFR are not necessarily complementary, overlapping manifestations of DKD .
Incidence of kidney disease in type 1 diabetes
Nearly half of patients with type 1 DM develop DKD over the course of their lifetime. However, albuminuria and reduced GFR both are infrequent during the first 10 years after type 1 diabetes diagnosis . In more recent studies, the lifetime increasing incidence of macroalbuminuria has been defined as 15–25%, and the cumulative incidence of microalbuminuria has been reported as 25–40% . In early studies, up to 35% of participants developed ESKD. In Finland and in the Pittsburgh Epidemiology of Diabetes Cohort (Pittsburgh, Pennsylvania, USA), the long-term cumulative incidence of ESKD has dropped to less than 10%, although the rate of ESKD has remained higher in the Joslin type 1 diabetes cohort (Boston, Massachusetts, USA) .
Progression of kidney disease in type 1 diabetes
The progression of DKD in type 1 diabetes is unpredictable. In the Joslin type 1 diabetes cohort, 29% of participants with microalbuminuria showed reduced GFR within 12 years’ average follow-up. EURODIAB type 1 diabetes study reported that 14% of microalbuminuric patients developed macroalbuminuria above 7.3 years’ follow-up. Steno type 1 diabetes cohort showed that 34% of participants with microalbuminuria went on to develop macroalbuminuria over 7.5 years’ average follow-up . In the DCCT/EDIC cohort, participants who had incident microalbuminuria, the 10-year cumulative incidence of macroalbuminuria was 28% .
In the DCCT/EDIC cohort, patients with macroalbuminuria lost GFR at a mean rate of 5.7% per year, and the 10-year cumulative incidence of impaired GFR was 32%. However, in patients with microalbuminuria, the mean rate of estimated GFR loss was 1.2% per year, and the 10-year cumulative incidence of diminished GFR was 15%. Interestingly, in the Joslin type 1 diabetes cohort, ‘early renal function decline’ developed in nearly one-third of microalbuminuric participants and also occurred occasionally in persistent normoalbuminuric participants with AER less than 30 mg/24 h. Such findings suggest that albuminuria and GFR loss are interrelated but are not essentially indicative of a single, homogenous underlying disease process .
Regression of kidney disease in type 1 diabetes
Microalbuminuria commonly regresses to normoalbuminuria as reported in the Joslin type 1 diabetes cohort. They showed that 58% of patients with persistent microalbuminuria regressed to persistent normoalbuminuria over the next 6 years, frequently without inhibitors of the renin–angiotensin–aldosterone system (RAAS) . Similar results were observed in the DCCT/EDIC ,. Therefore, better control of diabetes, hypertension, and lipids were associated with a greater likelihood of microalbuminuria regression. Of DCCT/EDIC participants who developed macroalbuminuria, 52% regressed to sustained microalbuminuria or normoalbuminuria within 10 years, but many were managed with RAAS inhibitors . Moreover, regression of macroalbuminuria was associated with an 89% lower risk of progressing to reduced GFR. In the same direction, longitudinal studies of pancreas transplantation demonstrate that the pathological lesions of diabetic glomerulopathy can regress with euglycemia .
Kidney disease in type 2 diabetes
The incidence of DKD and rates of DKD progression are less clear in type 2 compared with type 1 diabetes, mainly due to the highly variable age of onset, complexity of defining the exact time of diabetes onset, and the relative scarcity of long-term type 2 diabetes cohorts. Therefore, two of the best characterized type 2 diabetes cohorts are the UKPDS and the Pima Indian population. The UKPDS enrolled more than 5000 participants with new-onset type 2 diabetes, and, after a median of 15 years of follow-up, they found that microalbuminuria (defined as persistent urine albumin concentration ≥50 mg/l) occurred in 38% of participants and reduced GFR (defined as persistent estimated creatinine clearance ≤60 ml/min/1.73 m2) occurred in 29% of participants . Among Pima Indians, for whom the onset and duration of diabetes are more precisely determined due to systematic diabetes screening, the cumulative incidence of heavy proteinuria (≥1 g per gram creatinine) was 50% at 20 years’ duration, before the widespread use of RAAS inhibitors. The high rate of proteinuria in the Pima population has remained stable over time, although the incidence of ESKD has declined .
In most type 2 diabetic patients, the prevalence of DKD at any point in time is ∼30–50%. Among US adults with diabetes (>90% type 2), the prevalence of DKD was ∼35% overall, ranging from nearly 25% in patients younger than 65 years to nearly 50% in patients older than 65 years . At younger ages, microalbuminuria predominates, whereas in older age reduced GFR is increasingly prevalent among cases with DKD. This finding could be attributed to the trend in using medications that reduce albuminuria, such as glucose-lowering medications and RAAS inhibitors.
However, the phenotype of reduced GFR with normoalbuminuria has been increasingly recognized in type 2 diabetes. In population-based studies of diabetes in the USA and Australia, 36–55% of individuals with reduced GFR did not have concurrent microalbuminuria or macroalbuminuria. Frequently, nonalbuminuric reduced GFR was observed in the absence of diabetic retinopathy, suggesting underlying processes other than diabetic glomerulopathy. In the UKPDS, female sex, increased age, and insulin resistance were risk factors for reduced GFR but not microalbuminuria, whereas male sex, adiposity, hyperglycemia, and dyslipidemia were risk factors for microalbuminuria but not reduced GFR . Higher blood pressure was a risk factor for both reduced GFR and microalbuminuria.
Progression of kidney disease in type 2 diabetes
The progression and regression of established DKD is highly variable in type 2 diabetes. In the UKPDS, evolution from microalbuminuria to macroalbuminuria occurred at a rate of 2.8% per year, and change from macroalbuminuria to elevated plasma creatinine or ESKD occurred at a rate of 2.3% per year . Similar to what happened with type 1 diabetes; loss of GFR can occur at any level of urine albumin excretion but tends to be more rapid with greater urine albumin excretion. At diagnosis of type 2 diabetes, 7.3% of patients had microalbuminuria or worse rising to 17.3% after 5 years, 24.9% after 10, and 28.0% after 15 years .
Health consequences of diabetic kidney disease
The high mortality risk observed among people with both types 1 and 2 diabetes is largely confined to those with evidence of DKD, because it is associated with a number of interrelated cardiovascular diseases, including microangiopathies and macroangiopathies.
Diabetic kidney disease in different countries
Diabetic nephropathy is more frequent in African-Americans, Asian-Americans, and Native Americans . Progressive kidney disease is more frequent in Caucasians patients with type 1 than in those with type 2 DM, although its overall prevalence in the diabetic population is higher in patients with type 2 DM because this type of DM is more prevalent . The occurrence of diabetic nephropathy in Pima Indians is very interesting, indeed. Craig et al.  reported that around 50% of Pima Indians with type 2 DM developed nephropathy after 20 years of the disease, and 15% of them were already in the terminal stage of kidney failure. In the USA, the occurrence of diabetic nephropathy in patients beginning kidney replacement therapy doubled in the late 90s . Fortunately, the trend has been decreasing, most likely due to the better prevention and earlier diagnosis and treatment of DM .
In the USA, 25.6 million adults (11.3%) aged 20 years and older had diabetes in 2011, with the prevalence increasing in older age groups (26.9% of people aged ≥65 years). However, nearly 3% of newly diagnosed patients with type 2 DM have overt nephropathy. Among people with diabetes, the prevalence of DKD remained stable . Approximately 44% of new patients entering dialysis in the USA are diabetic. Early diagnosis of diabetes and early intervention are critical in preventing the normal progression to renal failure seen in many type 1 and a significant percentage of type 2 diabetic patients. The prevalence of diabetes is higher in certain racial and ethnic groups, affecting ∼13% of African-Americans, 9.5% of Hispanics, and 15% of Native Americans, primarily with type 2 diabetes ,. Nearly 20–30% of all diabetic patients will develop evidence of nephropathy, although a higher percentage of type 1 patients progress to ESKD.
Epidemiologic differences occur among European countries, mainly Germany. The proportion of patients admitted for renal replacement therapy is higher than that reported from the USA. In Heidelberg (southwest of Germany), nearly 60% of patients admitted for renal replacement therapy in 1995 had diabetes, with the majority (90%) of type 2 DM. An increase in ESKD secondary to type 2 DM has been noted even in countries known to have low incidences of type 2 DM, such as Denmark and Australia. The exact incidence and prevalence from Asia are not readily available .
Pavkov et al.  reported that diabetic nephropathy affects male and female sex equally, and it rarely developed before 10 years’ duration of type 1 DM. The role of age in the development of DKD is unclear despite that the mean age of patients who reach ESKD is about 60 years and the incidence of DKD is higher among elderly individuals who have had type 2 diabetes for a longer generation. In Pima Indians with type 2 diabetes, the earlier the onset of diabetes, the higher the risk for progression to ESKD. The incidence and severity of diabetic nephropathy is 3-fold to 6-fold higher in blacks than in whites. Similarly, diabetic nephropathy is more common among Mexican-Americans and Pima Indians with type 2 DM. This suggests that socioeconomic factors, such as diet, poor control of hyperglycemia, hypertension, and obesity, have a primary role in the development of diabetic nephropathy. Familial clustering may be one of the important factors in these populations.
Bhalla et al.  reported that, in patients with type 2 diabetes, racial/ethnic minorities were more likely to have proteinuric DKD and less likely to have nonproteinuric DKD.
Diabetic nephropathy has become an important clinical and public health challenge as reported by de Boer et al. , who estimated the disease burden in the US adult population aged 20 years or older using data from the National Healthand Nutrition Examination Survey.
Parving et al.  reported the prevalence of microalbuminuria/macroalbuminuria in a cross-sectional study among 32 208 type 2 diabetes patients’ from 33 countries to be 38.8 and 9.8%, respectively. Asian and Hispanic patients had the highest prevalence of microalbuminuria (43.2 and 43.8%) and macroalbuminuria (12.3 and 10.3%), whereas Caucasians had the lowest microalbuminuria (33.3%) and macroalbuminuria (7.6%). Twenty-two percent of patients had compromised renal function (GFR<60 ml/min/1.73 m2). Unnikrishnan et al.  reported that the prevalence of overt nephropathy and microalbuminuria was 2.2 and 26.9%, respectively, among urban Asian Indians with type 2 diabetes. Among 8897 Japanese type 2 diabetic patients from 29 medical clinics or general/university-affiliated hospitals from different areas, the prevalence of microalbuminuria and decreased GFR (<60 ml/min/1.73 m2) was 31.6 and 10.5%, respectively .
In the US population, the Pathways Study-across-sectional analysis among 2969 primary care diabetic patients of a large local health maintenance organization observed the racial/ethnic differences in early diabetic nephropathy despite comparable access to diabetes care. Among nonhypertensive patients, microalbuminuria was two-fold greater (odds ratio 2.01; 95% CI 1.14–3.53) and macroalbuminuria was three-fold greater (odds ratio 3.17; 95% CI 1.09–9.26) for Asians as compared with whites. Among hypertensive patients, adjusted odds of microalbuminuria were greater for Hispanics (odds ratio 3.82; 95% CI 1.16–12.57) than for whites, whereas adjusted odds of macroalbuminuria were three-fold greater for blacks (odds ratio 3.32; 95% CI 1.26–8.76) than for whites .
What is new is the recent unreasonable rise in the prevalence of metabolic syndrome  and of type 2 diabetes  worldwide, which is extremely pronounced in Asian countries , especially in India ‘diabetes capital of the world’ ,,,. Indian diabetic patients have a propensity to have insulin resistance, higher waist circumference despite lower BMI as well as lower adiponectin, and higher inflammatory markers . The prevalence of overt diabetes is particularly high in Indian elderly , in addition to prediabetes and overt diabetes in the young ,, and consequently diabetic nephropathy, especially in the rural populations of India ,,,,. The estimated overall incidence rate of chronic kidney disease and ESKD in India is currently 800 and 150–200 per million population, respectively .
Of great interest is the fact that the risks for impaired fasting glucose and impaired glucose tolerance are markedly higher in citizens of a South-East Asian origin compared with the local populations of European origin . Furthermore, the prevalence of any type of chronic kidney disease and its rate of progression, but specifically also of diabetic nephropathy, is significantly higher in citizens of Asian origin, as observed both in the UK  and in Canada  presumably the result of different genetics and/or lifestyle and lack of awareness of kidney complications of diabetes .
As many as six Arabic-speaking countries have the highest prevalences of type II diabetes: these countries are Kuwait, Lebanon, Qatar, Saudi Arabia, Bahrain, and UAE. Rapid economic growth brings with it great opportunities for improvements in infrastructure (e.g. healthcare and education); it also carries with it the burden of greater reliance on mechanization, a proliferation of Western-style fast food, access to cheap migrant labor, and as elsewhere, greater opportunities for sedentary lifestyles, especially in the young .
In a cross-sectional study from Egypt, 42% of diabetic patients had nephropathy ; in Jordan, 33% of diabetic patients at a national diabetes center had nephropathy  and at a diabetic clinic in Libya 25% of patients had nephropathy .
Geriatrics and diabetic nephropathy
The increased prevalence of diabetic nephropathy also derives directly from the growth in the prevalence of diabetic nephropathy among individuals aged 65 years and older. Individuals older than 65 years are unduly affected by diabetes and related end-stage renal disease. According to data from the National Health and Nutrition Examination Survey, diabetes prevalence was 26.9% among people aged 65 years and above ,. The prevalence of diabetic nephropathy was increased from 7.1% in 1988–1994 to 8.6% in 1999–2004 and 10.7% in 2005–2008 among individuals aged 65 years and older ,. Recent data also revealed that the adjusted point prevalence rates per million population of reported diabetes-related ESKD for individuals aged 60–69 and 70 years and above were 410.3 and 475.7 in whites and 1439.9 and 1471.5 in Africans ,.One of the challenges of managing the elderly with diabetic nephropathy is that they may develop more complications, especially heart, eye, and peripheral vascular diseases. In its 2011 National Diabetes Fact Sheet, the Centers for Disease Control (CDC) reported that, in 2004, heart disease and prior stroke were, respectively, noted on 68 and 16% of diabetes-related death certificates among people aged 65 years or older . Moreover, the CDC indicated that, in 2005, 27% of adults with diabetes who were 75 years or older reported some degree of visual impairment compared with 15% of diabetic patients who were between 18 and 44 years of age . Individuals aged 65 years or older account for 55% of diabetic patients who had nontraumatic lower extremity amputations . Caring for elderly patients with diabetic renal disease imposes a huge financial burden on governments and family members. For example, the American Diabetes Association indicated that the total estimated cost of diabetes in 2007 was $174 billion, including $58 billion to treat diabetes-related chronic complications .
Diabetic nephropathy in the elderly is mainly due to type 2 diabetes and its distribution is uneven among racial groups. American-Indians, African-Americans, and Mexican-Americans have a greater incidence compared with Caucasians by as much as three to one depending on the minority cohort selected for comparison .
Nearly all studies demonstrating beneficial effects of metabolic and blood pressure controls on DKD have been performed in young to middle-aged cohorts. Importantly, the management of DKD in older people is frequently based on extrapolations of data gathered in selected and motivated younger people. Moreover, people older than 70 years have been virtually excluded in trials supporting major US practice guidelines for the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in chronic kidney disease. In managing diabetes and diabetic nephropathy in the elderly, clinicians should keep in mind several key points: (a) elderly diabetic patients constitute a diverse group expressing various clinical and functional situations. (b) The American Geriatric Society Panel on Improving Care for Elders with Diabetes recommends that treatment of elderly patients with diabetes focus on specific problems and priorities . (c) The American Geriatric Society has also introduced the concept of time horizon for the benefits of certain treatments. Glycemic control may take as long as 8 years to have positive results on microvascular complications. Benefits of good blood pressure and lipid control may not be noticeable before 2 or 3 years . (d) Many elderly patients with diabetes are fragile and are also at a greater risk of developing several common geriatric syndromes, such as depression, cognitive impairment, urinary incontinence, injurious falls, and persistent pain. The Assessing Care of Vulnerable Elders (ACOVE) project defines a frail elderly patient as a vulnerable person who is older than 65 years and is at an increased risk for death or functional decline within 2 years . (e) In consequence, renoprotection in a geriatric population should be tailored according to patients’ autonomy, degree of frailty, life expectancy, comorbidity index, and the stage of diabetic nephropathy. (f) Elderly diabetic patients may be susceptible to nephrotoxic agents such as radiocontrast; specific caution should be taken in preventing and monitoring radiocontrast-induced nephropathy.
| Conclusion|| |
Diabetic nephropathy is not an uncommon complication of diabetes (type 1 and 2) all over the world and in geriatric population. Management of its modifiable risk factors might help in reducing its incidence in the near future.
Authors’ contribution: Osama Gheith: conception, design, drafting the article, critical revising of important intellectual content, final approval of manuscript; Nashwa Othman: share in conception, design, drafting the article, critical revising of important intellectual content, and final approval of manuscript; Naryanan Nampoory: share in critical revising of important intellectual content, final approval of manuscript; Medhat A. Halim: share in critical revising of important intellectual content, final approval of manuscript; Torki Al-Otaibi: share in critical revising of important intellectual content, final approval of manuscript.
Ethical considerations: Ethical issues (including plagiarism, data fabrication, double publication) have been completely observed by the authors.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Rabkin R. Diabetic nephropathy. Clin Cornerstone 2003; 5:1–11.
American Diabetes Association. Nephropathy in diabetes. Diabetes Care 2004; 27(Suppl 1):S79–S83.
De Boer IH, Rue TC, Hall YN, Heagerty PJ, Weiss NS, Himmelfarb J. Temporal trends in the prevalence of diabetic kidney disease in the United States. JAMA 2011; 305:2532–2539.
Andersen AR, Christiansen JS, Andersen JK, Kreiner S, Deckert T. Diabetic nephropathy in type 1 (insulin-dependent) diabetes: an epidemiological study. Diabetologia 1983; 25:496–501.
American Diabetes Association. Standards of medical care in diabetes. Diabetes Care 2014; 37(Suppl 1):S14–S80.
De Boer IH. Kidney disease and related findings in the diabetes control and complications trial/epidemiology of diabetes interventions and complications study. Diabetes Care 2014; 37:24–30.
de Boer IH, Afkarian M, Rue TC, Cleary PA, Lachin JM, Molitch ME et al.
Renal outcomes in patients with type 1 diabetes and macroalbuminuria. J Am Soc Nephrol 2014; 25:2342–2350. doi: 10.1681/ASN.2013091004. Epub 2014 Jun 12.
US Renal. Data System. USRDS Annual Data Report: Atlas of end-stage renal disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2004.
Vrhovac B, Jakšić B, Reiner Ž, Vucelić B. Internamedicina. Zagreb: NakladaLjevak; 2008. 1258–1259
Mogensen CE. Microalbuminuria, blood pressure and diabetic renal disease: origin and development of ideas. Diabetologia 1999; 42:263–285.
Buchan IE. ArcusQuickStat biomedical version. Cambridge: Addison Wesley Longman Ltd; 1997.
Viberti GC, Hill RD, Jarrett RJ, Argyropoulos A, Mahmud U, Keen H. Microalbuminuria as a predictor of clinical nephropathy in insulin-dependent diabetes mellitus. Lancet 1982; 1:1430–1432.
Mogensen CE. Microalbuminuria predicts clinical proteinuria and early mortality in maturity-onset diabetes. New Eng J Med 1984; 310:356–360.
Orchard TJ, Dorman JS, Maser RE, Becker DJ, Drash AL, Ellis D et al.
Prevalence of complications in IDDM by sex and duration. Pittsburgh Epidemiology of Diabetes Complications Study II. Diabetes 1990; 39:1116–1124.
Chaturvedi N, Bandinelli S, Mangili R, Penno G, Rottiers RE, Fuller JH. Microalbuminuria in type 1 diabetes: rates, risk factors and glycemic threshold. Kidney Int 2001; 60:219–227.
Hovind P, Tarnow L, Rossing P, Jensen BR, Graae M, Torp I et al.
Predictors of the development of microalbuminuria and macroalbuminuria in patients with type 1 diabetes: inception cohort study. Br Med J 2004; 328:1105–1108.
De Boer IH, Sun W, Gao X et al.
DCCT/EDIC research group. Effect of intensive diabetes treatment on albuminuria in type 1 diabetes: long-term follow-up of the Diabetes Control and Complications Trial and Epidemiology of Diabetes Interventions and Complications study. Lancet Diabetes Endocrinol 2014; 2:793–800. doi: 10.1016/S2213-8587(14)70155-X. Epub 2014 Jul 17.
Hovind P, Tarnow L, Rossing P, Jensen BR, Graae M, Torp I et al.
Predictors for the development of microalbuminuria and macroalbuminuria in patients with type 1 diabetes: inception cohort study. BMJ 2004; 328:1105. Epub 2004 Apr 19.
Krolewski AS, Warram JH, Christlieb AR, Busick EJ, Kahn CR. The changing natural history of nephropathy in type I diabetes. Am J Med 1985; 78:785–794.
Fioretto P, Steffes MW, Sutherland DE, Goetz FC, Mauer M. Reversal of lesions of diabetic nephropathy after pancreas transplantation. New Engl J Med 1998; 339:69–75.
Retnakaran R, Cull CA, Thorne KI, Adler AI, Holman RR. Risk factors for renal dysfunction in type 2 diabetes: UK prospective diabetes study 74. Diabetes 2006; 55:1832–1839.
Pavkov ME, Knowler WC, Bennett PH, Looker HC, Krakoff J, Nelson RG. Increasing incidence of proteinuria and declining incidence of end-stage renal disease in diabetic Pima Indians. Kidney Int 2006; 70:1840–1846.
Adler AI, Stevens RJ, Manley SE, Bilous RW, Cull CA, Holman RR. Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney Int 2003; 63:225–232.
Unnikrishnan RI, Rema M, Pradeepa R, Deepa M, Shanthirani CS, Deepa R, Mohan V. Prevalence and risk factors of diabetic nephropathy in an urban South Indian population: the Chennai Urban Rural Epidemiology Study (CURES 45). Diabetes Care 2007; 30:2019–2024. Epub 2007 May 8.
Young BA, Maynard C, Boyko EJ. Racial differences in diabetic nephropathy, cardiovascular disease, and mortality in a national population of veterans. Diabetes Care 2003; 26:2392–2399.
Cowie CC, Port FK, Wolfe RA, Savage PJ, Moll PP, Hawthorne VM. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. NEJM 1989; 321:1074–1079.
Craig KJ, Donovan K, Munnery M, Owens DR, Williams JD, Phillips AO. Identification and management of diabetic nephropathy in the diabetes clinic. Diabetes Care 2003; 26:1806–1811.
Caramori ML, Kim Y, Huang C, Fish AJ, Rich SS, Miller ME et al.
Cellular basis of diabetic nephropathy 1. Study design and renal structural-functional relationships in patients with long-standing type 1 diabetes. Diabetes 2002; 51:506–513.
United States Renal Data System. Incidence of reported end-stage renal disease. Available at: United States Renal Data System Incidence of reported end-stage renal disease. Available at: http://www.usrds.org/2008/ref/A_Incidence_08.pdf
. [Accessed 10 March 2009]
Pavkov ME, Bennett PH, Knowler WC, Krakoff J, Sievers ML, Nelson RG. Effect of youth-onset type 2 diabetes mellitus on incidence of end-stage renal disease and mortality in young and middle-aged Pima Indians. JAMA 2006; 296:421–426.
Bhalla V, Zhao B, Azar KM, Wang EJ, Choi S, Wong EC et al.
Racial/ethnic differences in the prevalence of proteinuric and nonproteinuric diabetic kidney disease. Diabetes Care 2013; 36:1215–1221.
Parving HH, Lewis JB, Ravid M, Remuzzi G, Hunsicker LG; DEMAND investigators. Prevalence and risk factors for microalbuminuria in a referred cohort of type II diabetic patients: a global perspective. Kidney Int 2006; 69:2057–2063.
Unnikrishnan R, Rema M, Pradeepa R et al.
Prevalence and risk factors of diabetic nephropathy in an urban South Indian population: the Chennai Urban Rural Epidemiology Study (CURES 45). Diabetes Care 2007; 30:2019–2024.
Yokoyama H, Sone H, Oishi M, Kawai K, Fukumoto Y, Kobayashi MJapan Diabetes Clinical Data Management Study Group. Prevalence of albuminuria and renal insufficiency and associated clinical factors in type 2 diabetes: the Japan Diabetes Clinical Data Management study (JDDM15). Nephrol Dial Transplant 2009; 24:1212–1219.
Young BA, Katon WJ, Von Korff M, Simon GE, Lin EHB, Ciechanowski PS et al.
Racial and ethnic differences in microalbuminuria prevalence in a diabetes population: the Pathways Study. J Am Soc Nephrol 2005; 16:219–228.
Kaur P, Radhakrishnan E, Rao SR, Sankarasubbaiyan S, Rao TV, Gupte MD. The metabolic syndrome and associated risk factors in an urban industrial male population in South India. JAssoc Physicians India 2010; 58:363–371.
Zimmet P, Alberti KG, Shaw J. Global and societal implications of the diabetes epidemic. Nature 2001; 414:782–787.
Ramachandran A, Ma RC, Snehalatha C. Diabetes in Asia. Lancet 2010; 375:408–418.
Yoon KH, Lee JH, Kim JW, Cho JH, Choi YH, Ko SH et al.
Epidemic obesity and type 2 diabetes in Asia. Lancet 2006; 368:1681–1688.
Sridhar GR, Putcha V, Lakshmi G. Time trends in the prevalence of diabetes mellitus: ten year analysis from southern India (1994-2004) on 19,072 subjects with diabetes. J Assoc Physicians India 2010; 58:290–294.
Mohan V, Sandeep S, Deepa R, Shah B, Varghese C. Epidemiology of type 2 diabetes: Indian scenario. Indian J Med Res 2007; 125:217–230.
Ravikumar P, Bhansali A, Walia R, Shanmugasundar G, Ravikiran M. Alterations in HbA(1c) with advancing age in subjects with normal glucose tolerance: Chandigarh Urban Diabetes Study Group. Diabet Med 2011; 28:590–594.
Deepa M, Pradeepa R, Rema M, Mohan A, Deepa R, Shanthirani S et al.
The Chennai Urban Rural Epidemiology Study (CURES) − study design and methodology (urban component) (CURES-I). J Assoc Physicians India 2003; 51:863–870.
Abdul FB. Type 2 diabetes and rural India. Lancet 2007; 369:273–274.
Gupta SK, Singh Z, Purty AJ, Kar M, Vedapriya D, Mahajan P et al.
Diabetes prevalence and its risk factors in rural area of Tamil Nadu. Indian J Community Med 2010; 35:396–399.
Jonas JB, Panda-Jonas S, Nangia V, Joshi PP, Matin A. Diabetes mellitus in rural India. Epidemiology 2010; 21:754–755.
Pradeepa R, Anjana RM, Unnikrishnan R, Ganesan A, Mohan V, Rema M. Risk factors for microvascular complications of diabetes among South Indian subjects with type 2 diabetes − the Chennai Urban Rural Epidemiology Study (CURES) Eye Study-5. Diabetes Technol Ther 2010; 12:755–761.
Agarwal SK, Srivastava RK. Chronic kidney disease in India: challenges and solutions. Nephron Clin Pract 2009; 111:c197–c203.
Gray LJ, Tringham JR, Davies MJ, Webb DR, Jarvis J, Skinner TC et al.
Screening for type 2 diabetes in a multiethnic setting using known risk factors to identify those at high risk: a cross-sectional study. Vasc Health Risk Manag 2010; 6:837–842.
Lightstone L, Rees AJ, Tomson C, Walls J, Winearls CG, Feehally J et al.
High incidence of end-stage renal disease in Indo-Asians in the UK. QJM 1995; 88:191–195.
Barbour SJ, Er L, Djurdjev O, Karim M, Levin A. Differences in progression of CKD and mortality amongst Caucasian, Oriental Asian and South Asian CKD patients. Nephrol Dial Transplant 2010; 25:3663–3672.
Wilkinson E, Randhawa G, Farrington K, Greenwood R, Feehally J, Choi P, Lightstone L. Lack of awareness of kidney complications despite familiarity with diabetes: a multi-ethnic qualitative study. J Ren Care 2011; 37:2–11.
Badran M, Laher I. Type II diabetes mellitus in Arabic-speaking countries. Int J Endocrinol 2012; 2012:902873. doi: 10.1155/2012/902873. Epub 2012 Jul 18.
Herman WH, Aubert RE, Engelgau MM, Thompson TJ, Ali MA, Sous ES et al.
Diabetes mellitus in Egypt: glycaemic control and microvascular and neuropathic complications. Diab Med 1998; 15:1045–1051.
Jbour AS, Jarrah NS, Radaideh AM, Shegem NS, Bader IM, Batieha AM et al.
Prevalence and predictors of diabetic foot syndrome in type 2 diabetes mellitus in Jordan. Saudi Med J 2003; 24:761–764.
Kadiki OA, Roaed RM. Epidemiological and clinical patterns of diabetes mellitus in Benghazi, Libyan Arab Jamahiriya. East Mediterr Health J 1999; 5:6–13.
Centers for Disease Control and Prevention. National diabetes factsheet: national estimates and general information on diabetes and prediabetes in the United States, 2014. US Department of Health and Human Services. Atlanta, GA: Centers for Disease Control and Prevention; 2014.
McDonald M, Hertz RP, Unger AN, Lustik MB. Prevalence, awareness, and management of hypertension, dyslipidemia, and diabetes among United States adults aged 65 and older. J Gerontol A Biol Sci Med Sci 2009; 64:256–263. doi: 10.1093/gerona/gln016. Epub 2009 Jan 30.
Coresh J, Selvin E, Stevens LA, Manzi J, Kusek JW, Eggers P et al.
Prevalence of chronic kidney disease in the United States. JAMA 2007; 298:2038–2047.
US Renal Data System. USRDS 2012 Annual Data Report: Atlas of chronic kidney disease and end-stage renal disease in the Unit ed States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. 2012.
Unit ed States Renal Data System. USRDS 2008 annual data report. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2008.
Sugarman JR, Reiber GE, Baumgardner G, Prela CM, Lowery J. Use of the therapeutic footwear benefit among diabetic medicare beneficiaries in three states, 1995. Diabetes Care 1998; 21:777–781.
American Diabetes Association. Economic costs of diabetes in the U.S. in American Diabetes Association. Economic costs of diabetes in the U.S. in 2007. Diabetes Care 2008; 31:596–615.
Brown AF, Mangione CM, Saliba D, Sarkisian CA. California Healthcare Foundation/American Geriatrics Society Panel on Improving Care for Elders with Diabetes. Guidelines for improving the care of the older person with diabetes mellitus. J Am Geriatr Soc 2003; 51(Suppl 5):S265–S280.
Wenger NS, Shekelle PG, Roth CP, The ACOVE Investigators. Introduction to the assessing care of vulnerable elders − 3 quality indicator measurement set. J Am Geriatr Soc 2007; 55(Suppl 2):S247–S252.