REVIEW ON THE IMPACT OF DIABETES ON KIDNEY DISEASEHTML Full Text
REVIEW ON THE IMPACT OF DIABETES ON KIDNEY DISEASE
Yasir Ansari *, Akhilesh Patel, Kulbhushan Haldeniya, Rajesh Sharma, Mohd Haneef, Sourabh Kosey and Ramesh Kumar
Department of Pharmacy Practice, NIMS Institute of Pharmacy, NIMS University, Jaipur, Rajasthan, India.
ABSTRACT: Diabetic kidney disease (DKD) is the main reason for end-stage renal disease on a global scale. About 40% of developing diabetic kidney disease, which is the most common cause of chronic kidney diseases worldwide. Although ESRD may be the most complication of diabetics, as a result of their physical health and any co-morbidities they may have, such as obesity, hypertension, dyslipidemia, intrarenal vascular disease, renal ischemia, or age-related nephron loss, One-third of people with type 1 diabetes and at least half of people with type 2 diabetes will eventually develop renal dysfunction. CKD is present and is severe. Glomerular hyperfiltration, falling GFR, and finally, ESRD are parts of the diabetic kidney disease natural history. Diabetes-related complications can lead to diabetic kidney disease. Disturbances in glucose metabolism, hypertension, dyslipidemia, develop kidney disease. Controlling blood sugar levels, blood pressure, and renin-angiotensin-aldosterone system blockage are all part of intensive therapy for diabetic patients; For diabetic kidney damage to be postponed or prevented, glycemic management is crucial. Several glucose-lowering drugs are on the market, but only a small percentage of them can be used safely in chronic kidney disease. The risk of kidney failure and cardiovascular events is significantly increased by diabetic renal disease, which has a significant global disease burden. There is still with current treatments. In order to find treatments that can halt the progression and lower risks, it is crucial to better understand the molecular pathways behind diabetic kidney disease. Which is subsequently accompanied by various metabolic, hemodynamic and inflammatory markers.
Keywords: Diabetic kidney disease, Renin-angiotensin-aldosterone, End-stage renal disease, chronic kidney disease, Renin-angiotensin-aldosterone system
INTRODUCTION: Low estimated glomerular filtration rate (eGFR), albumin, or both are chronic kidney disease (CKD) symptoms 1. Chronic kidney disease (CKD) and kidney failure are most frequently caused by diabetes mellitus, which is an epidemic that is getting worse. About 20–40% of people with diabetes develop diabetic nephropathy 2.
Chronic kidney disease (CKD) is the most expensive of diabetes' long-term consequences and has the most negative effects on daily living. Individuals with CKD are more likely to experience negative health outcomes, such as frailty, a lower end-stage renal disease (ESRD), early mortality, and increasing end-organ damage at various sites.
Indeed, persons who have CKD are most affected by the increased mortality linked to both type 1 and type 2 diabetes. Individuals with CKD are more likely to experience. Negative health outcomes, such as frailty, lower end-stage renal disease (ESRD), early mortality, and increasing end-organ damage at various sites. Indeed, persons who have CKD are most affected by the increased mortality linked to both type 1 and type 2 diabetes 3. Due mostly to the rise in type 2 diabetes, the incidence and prevalence of diabetes mellitus have considerably increased globally. This rise in the number of persons getting diabetes has had a significant effect. Explain how diabetic kidney disease develops (DKD) 4. In 1552 BC, the link between diabetes and kidney disease in people was first identified 5.
DKD's rising incidence is mirrored by diabetes's sharply rising prevalence over the world 6. Adult diabetes prevalence increased in the United States, rising from 9.8% in the 1988–1994 era to 12.3% in the 2011–2012 decade 7.
The estimated global prevalence of diabetes in 2015 was 415 million; by 2040, it is expected to rise to 642 million, with a disproportionate increase in low- to middle-income nations 8 at each stage, it's critical to create cost-effective strategies 9: prevention of obesity 10 screening for diabetes and its prevention in a population at risk 11.
Once diabetes manifests, glycemic control 12 controlling blood pressure (BP) after the onset of hypertension 13 Inhibition or blocking of the rennin-angiotensin-aldosterone system (RAAS) in people with diabetic CKD 14. Control of other cardiovascular (CV) risk factors, such as controlling cholesterol levels in low-density lipoprotein (LDL-C) 15.
The worldwide obesity pandemic is what is causing the prevalence of diabetes to rise. In general, between 1980 and 2000, the predominance of In the United States, adult obesity increased dramatically, rising from 15% to 31%. By 2013–2014, 35% of men and 40% of women were overweight on an adjusted basis 16.
A large but unappreciated burden of sickness is diabetes-related renal damage. DKD-related deaths have become more frequent by 94% between 1990 and 2012. This sharp increase is one of the greatest ever recorded for reported chronic conditions. Notably, the majority of the elevated risk of mortality from all causes and cardiovascular disease (CVD) in people with diabetes is linked to the occurrence of DKD 17.
The Glomerular Filtration Rate does not Necessarily Fall in DKD Patients with Albuminuria: The most common clinical signs of DKD are albuminuria, which eventually develops into macroalbuminuria or overt proteinuria, microscopic hematuria, which only occurs in a limited percentage of patients, and a delayed improvement in renal function. DKD is traditionally divided into five stages.
Preclinical stages 1 and 2 are distinguished by an increase in GFR, normoalbuminuric (stage 1) or intermittent microalbuminuria (MA; stage 2), and normal blood pressure. Stage 3 is the beginning of the clinical stage, and it is distinguished and characterized by chronic MA, mild hypertension, and a stable or mildly declining GFR.
Macroalbuminuria, hypertension, and greater GFR reduction characterize stage 4 as compared to earlier stages. the latter stage of renal illness is stage 5. Recent epidemiological studies, however, especially for those with type 2 diabetes mellitus, evidence suggests that not all DKD patients fall into the aforementioned categories (DM). Not all people have proteinuria. Prior to the decrease of renal function associated with diabetes, in contrast to the traditional development of DKD outlined above 18. 20.
In some patients, the change from MA to overt proteinuria may not take place until DKD progresses to ESRD. Perkins and others 21. report an early decline in the majority of patients with just MA experience GFR. Additionally, nonproteinuric DKD a reduction in GFR without albuminuria is becoming a more well-known condition, particularly in type 2 diabetes 22, 26.
Renal insufficiency develops in persons with type 2 diabetes even when there is no albuminuria or retinopathy. Population-based research from Western nations found that over half of the people with a loss in kidney function either never developed proteinuria in type 2 diabetes or had no prior history of it 27.
A reduced correlation between nonproteinuric DKD and diabetic retinopathy was discovered than proteinuria DKD 28. All of the findings point to the normoalbuminuric pathway for the progression of DKD. Fig. 1 depicts a high-level overview of DKD. Table 1 Increased blood pressure, sustained reduction in glomerular filtration rate (GFR), increased cardiovascular events and cardiovascular event-associated mortality.
TABLE 1: DEFINITION OF THE ALBUMINURIA IN DIABETIC KIDNEY DISEASED
|Normoalbuminuria||Daily urine albumin amount: <30 mg|
|Moderately increased albuminuria (Microalbuminuria)||Daily urine albumin amount: 30 mg–300 mg or Ratio of urine albumin over urine creatinine: 30–300|
|Severely increased albuminuria (Macroalbuminuria)||Daily urine albumin amount: >300 mg or The ratio of urine albumin over urine creatinine: >300|
FIG. 1: DKD OVERVIEW. DKD STANDS FOR DIABETIC KIDNEY DISEASE; ACEI STANDS FOR ANGIOTENSIN-CONVERTING ENZYME INHIBITOR; ARB STANDS FOR ANGIOTENSIN II RECEPTOR BLOCKER; SGLT2 STANDS FOR SODIUM-GLUCOSE COTRANSPORTER 2; EGFR STANDS FOR ESTIMATED GLOMERULAR FILTRATION RATE; AND BP STANDS FOR BLOOD PRESSURE
Identification of DKD Patients at High Risk: DKD is a chronic, progressive disease that takes time to develop. In type 1 diabetes, the median period from the onset of overt proteinuria to the development of ESRD was 7 years. In the 1970s 29 and it is now 14 years 30. At 30 years, the incidence of ESRD in type I diabetes in Finland is now 7.8% 31. Many studies have found that the renal function of many properly managed individuals is either constant or develops slowly. The speed of the eGFR drop in three recent randomized interventional studies ranged from 0 to 4 mL/min per year 32-34. Acute kidney injury is a major factor that may contribute to the progression of ESRD in diabetic patients (AKI) 35. AKI increases the chance of developing advanced CKD whether it occurs once or repeatedly. In a cohort of 4,082 diabetic patients after that, a significant prospective investigation verified that AKI can predict y bad results. In diabetic patients, such as serum creatinine doubling or ESRD 36.
Increased Albuminuria: Increase excretion of albumin in the urine is a significant risk factor for the emergence and progression of renal disease. In people living with diabetes. It is characterized by increased excretion of albumin/g creatinine in the urine referred to as microalbuminuria (30–300 mg/g) or macroalbuminuria (>300 mg/g) 37.
Hyperglycemia: Hyperglycemia is regarded as one of the most important and independent risk factors for DKD 38. It worsens renal function by altering the antioxidant system, resulting in increased formation of advanced glycation end products. The polyol pathway activation is also thought to be involved in the pathogenesis of DKD 39. Variability in glycated hemoglobin (HbA1c) is linked to the development and progression of nephropathy in both type 1 and type 2 diabetes patients 40. A similar finding was reported by the Italian multicenter study Renal Insufficiency and Cardiovascular Events (RIACE) 41.
Evidence from randomized controlled trials found that intensive glucose control was beneficial in both delaying the onset and preventing the progression of albuminuria in T2DM patients 42 43.
Hypertension: Hypertension is a major risk factor for diabetic nephropathy. A recent meta-analysis found that hypertension is significantly associated with the development of diabetic nephropathy 44. Hypertension is associated with cardiovascular disease in children with CKD 45.
When compared to non-hypertensive patients, hypertensive patients have an odds ratio of 1.67 (95% CI: 13.1-2.14) 46. This was confirmed by a population-based prospective study from China, which found that controlling hypertension can reduce the incidence of end-stage kidney failure by 23% 47.
Dyslipidemia: Dyslipidemia is critical to the development and progression of DKD. The "lipid nephrotoxicity hypothesis" describes the effect of dyslipidemia on renal function impairment 48. Dyslipidemia is characterized in diabetics by a decrease in high-density lipoprotein and an increase in triglycerides, low-density lipoprotein, and very-low-density lipoprotein 49.
Dyslipidemia contributes to the development of DKD by causing podocyte apoptosis, macrophage infiltration, and an increase in extracellular matrix production 50. Hyperglycemia and insulin resistance may aggravate dyslipidemia in DKD patients 51. Epidemiological evidence suggested a positive relationship between dyslipidemia and diabetic nephropathy. An epidemiological study of 581 T2DM patients looked at the relationship between lipoprotein and DKD and discovered a link. Lipoprotein levels were discovered to be directly related to the presence of DKD 52.
Obesity: Obesity and DKD have a strong link, according to the evidence 53. The mechanism by which obesity causes DKD is unknown, but it is assumed that obesity causes glomerular injury, hypertrophy, and proteinuria 54 55. Obesity was identified as a risk factor in the development of nephropathy in a Chinese study of 264 patients with confirmed DKD based on renal biopsy 56. Furthermore, an investigation of the Look AHEAD randomized clinical trial's secondary data suggests that weight loss could be used in conjunction with other treatments to slow the progression of diabetic nephropathy in obese patients 57.
Smoking: Tobacco use is regarded as a separate risk factor in the development and progression of diabetic nephropathy. Smoking has a multifactorial role in the development of diabetic nephropathy, including oxidative stress, hyperlipidemia, deposition of advanced end glycation products, and glomerulosclerosis 58 59. Evidence from a Finnish diabetic nephropathy study of 3613 type 1 DM patients found that smokers had a higher risk of albuminuria and end-stage renal disease than non-smokers 60. The dose of smoking was found to increase the risk of diabetic nephropathy. A recent meta-analysis based on the pooling of nine cohort studies concluded that smokers with T2DM are at an increased risk of developing diabetic nephropathy.61
Pathophysiology of DKD: Hyperglycemia and hyper aminoacidemia, two conditions that encourage glomerular hyperfiltration and hyperperfusion are critical metabolic changes in early diabetes that alter kidney hemodynamics and promote inflammation and fibrosis 62.
Fig. 2 Systemic hypertension and obesity, as well as high transmitted systemic BP and glomerular enlargement, contribute to glomerular hyper-filtration in type 2 diabetes. A common consequence of early diabetes is glomerular hyperfiltration. Overall, 10%–40%, or up to 75%, of type 1 diabetes patients and up to 40% of type 2 diabetes patients exhibit it. Still unidentified are the processes causing diabetes-related glomerular hyperfiltration 63.
One possible explanation is increased sodium-glucose cotransporter 2 activity in the proximal tubules, which results in decreased sodium chloride and other solute delivery to the macula densa at the distal end of the tubule 64, 65. While excessive local angiotensin II production at the efferent arteriole results in vasoconstriction, the tubule glomerular feedback may be reduced, causing the afferent arteriole to expand and increase glomerular perfusion. Hyperfiltration of the glomeruli and high intraglomerular pressure are the overall consequences 66, 67.
Fig. 3 Early diabetes causes significant metabolic alterations, including hyper aminoacidemia, which encourages glomerular hyperfiltration and hyper perfusion, and hyperglycemia, that affect kidney hemodynamics and encourage inflammation and fibrosis. In addition, vasoconstriction is caused by excessive local angiotensin II production at the efferent arteriole. High intraglomerular pressure and glomerular hyperfiltration are the main consequences of hyperfiltration 68.
FIG. 2: THE DEVELOPMENT OF DIABETIC KIDNEY DISEASE INVOLVES A VARIETY OF ROUTES AND NETWORKS. CONNECTIVE TISSUE GROWTH FACTOR (CTGF), AGE (ADVANCED GLYCATION END PRODUCT); JAK-STAT STANDS FOR JANUS KINASE/SIGNAL TRANSDUCER AND ACTIVATOR OF TRANSCRIPTION; PKC STANDS FOR PROTEIN KINASE C; RAAS STANDS FOR THE RENIN-ANGIOTENSINALDOSTERONE SYSTEM; ROS STANDS FOR REACTIVE OXYGEN SPECIES; SAA STANDS FOR SERUM AMYLOID A; AND VASCULAR ENDOTHELIAL GROWTH FACTOR A IS REFERRED TO AS VEGF-A. *JAK/STAT SIGNALLING CAN REMAIN UNAFFECTED (↔)
FIG. 3: THE RENAL HEMODYNAMICS OF NORMAL AND DIABETIC NEPHRONS ARE DIFFERENT
Diagnosis OF DKD: In addition to clinical characteristics including the duration of the patient's diabetes and the existence of diabetic retinopathy, Measurements of eGFR and albuminuria are used to make the clinical diagnosis of DKD.69 DKD is diagnosed clinically by a sustained decline in eGFR < 60 ml/min per 1.73 m2 and/or a persistently high urine albumin-to-creatinine ratio of 30 mg/g 70. Patients with DM1 should start getting screened for DKD every year starting five years after their diagnosis, and patients with DM2 should start getting screened every year at the time of their diagnosis. The occurrence of diabetic retinopathy in patients with albuminuria is a strong indicator of DKD. Urinary albumin-to-creatinine ratio testing is the optimum method for diagnosing albuminuria, and it should be done on a spot sample ideally in the morning 71. The serum creatinine level is used to determine the eGFR. Although the Modification of Diet in Renal Disease equation is more commonly reported by clinical laboratories, the equation developed by the chronic kidney disease-Epidemiologic Prognosis Initiative is more precise, especially when eGFR readings are within the normal or near-normal range 72.
It takes two abnormal measures that are at least three months apart to confirm albuminuria or low eGFR. Other kidney disease reasons should be taken into consideration if symptoms that are not characteristic of DKD are present. Included in the list of unusual characteristics are the development of nephrotic or nephritic syndrome, fast commencement of low eGFR or rapidly dropping eGFR, an abrupt rise in albuminuria, resistant hypertension, symptoms or signs of another systemic disease, and >30% eGFR decline within 2-3 months after beginning a renin-angiotensin system inhibitor 73.
Treatment FOR DKD: For both DM1 and DM2, it is well known that maintaining long-term, intense glycemic control from the beginning of the course of diabetes prevents diabetic complications, including DKD 74, 75. Intensive glucose management, however, has not been demonstrated to lower the risk of DKD development or enhance overall clinical outcomes after the beginning of complications or in long-term diabetes. In this population, aiming for low HbA1C (6%–6.9%) raised the risk of severe hypoglycemia but did not reduce the risk of cardiovascular (CV) or microvascular problems 76 77. In addition, an examination of individuals with DM2 and early-stage CKD revealed that stringent glycemic control was associated with 30% and 40% higher risks for all-cause death and cardiovascular mortality, respectively, than conventional care 78. Long-term research has supported the conclusion that intensive glycemic control carries a high does not lower the risk of CVD or all-cause mortality and increases the risk of hypoglycemia death (8–10 years). Although there was a slight reduction in the incidence of ESRD with strict glycemic control, the actual number of patients was very modest 79. Intensive glycemic management beginning during early diabetes can prevent DKD, according to a stratified analysis, which revealed that the highest effect for preventing ESRD was shown in people without renal disease at the study entrance 80. According to the American Diabetes Association, glycemia objectives should be customized for each patient's age, comorbidities, and expected lifespan. For patients with a shorter course of diabetes, a younger age, no comorbidities, and a longer life expectancy, more demanding objectives, such as HbA1C 6.5% greater, may be reasonable.
Contrarily, individuals with long-standing diabetes, advanced age, micro- and macrovascular problems, and short life expectancy are advised to adhere to less strict HbA1C8% objectives 81. Similar to this, the Kidney Disease Improving Global Outcomes (KDIGO) recommendations and the Kidney Disease Outcomes Quality Initiative of the National Kidney Foundation. Suggest aiming for a goal HbA1c of roughly 7.0% to stop or slow the advancement of diabetes's microvascular adverse effects. However, treating to an HbA1c target of less than 7.0% is not recommended for patients at risk for hypoglycemia, such as those with diabetes and chronic kidney disease 82.
Beginning pharmacologic therapy was recommended by the Eighth Joint National Committee (JNC-8). for hypertension at a systolic blood pressure of fewer than 140 mmHg or a diastolic blood pressure of less than 90 mmHg, with treatment objectives lower than these levels. Initial antihypertensive therapy in the general hypertensive population, including those with diabetes, may consist of a calcium channel blocker, ACE inhibitor, thiazide-type diuretic, or angiotensin receptor blocker (ARB). A thiazide diuretic or calcium channel blocker is advised by the JNC-8. as the first line of treatment for diabetic individuals of color. Regardless of their diabetes condition, people with CKD are advised to maintain the same BP goals. Either an ACE inhibitor or an ARB, either by itself or in conjunction with medication from any of the following groups, should be included in the pharmaceutical regimen for diabetic patients who have high levels of albuminuria 83. Regardless of whether a patient has diabetes, the KDIGO guidelines advise using an ACE or an ARB and keeping their blood pressure at or below 130/80 mmHg 84. There is clear proof that treating patients with macroalbuminuria reduces the development of DKD when combined with an ACE inhibitor or an ARB. By blocking the renin-angiotensin system 85. Combination therapy (the administration of an ACE inhibitor and an ARB simultaneously) does not have any clinical advantages and raises the risk of major side effects, especially hyperkalemia and AKI 86 87. The Systolic BP Intervention Trial results have cast doubt on target blood pressure objectives that have been suggested by the JNC-8's loosened guidelines (SPRINT). 9361 non-diabetic patients with high CV risk and hypertension were involved in the SPRINT study. The systolic blood pressure goals for participants were either intense (120 mmHg) or standard (140 mmHg).
After a median of 3.26 years, the study's early termination was due to a reduction of 25% and 27%, respectively, in the rates of the primary endpoint (myocardial infarction, acute coronary syndrome, stroke, heart failure, or death from CV causes) and all-cause mortality in the intervention group. The group receiving intensive treatment compared to the group receiving the standard regimen. These findings persisted in subgroups that had been previously established based on baseline systolic blood pressure levels, CKD stage, age >75, sex, race, and prior CVD 88, 89.
The risk of nonfatal myocardial infarction, nonfatal stroke, and mortality from any cause was not significantly different when the identical systolic blood pressure objectives were met (120 versus 140 mmHg). A CV cause, or death from any cause, according to 4733 individuals took part in the Diabetes and Action to Control Cardiovascular Risk (ACCORD) Trial. greater risk of cardiovascular events in diabetic people 90. The ACCORD Trial may have been because of the much-reduced rates of CV morbidity and mortality; the study was underpowered to detect between-group differences. Anticipated, which is one reason for this inconsistent finding. However, rigorous BP treatment did not lower the incidence of ESRD, result in a 50% drop in eGFR, or result in a 30% decline in eGFR to a value of less than 60 ml/min per 1.73 m2 in the SPRINT participants who had CKD at study entrance. Additionally, the intensive therapy group saw more hospitalizations or ER visits due to AKI than the conventional regimen group (4.4% versus 2.6%; hazard ratio, 1.71) 91, 92. Similar to this, the ACCORD Trial found evidence that suggests stringent BP control may have a deleterious impact on renal function. Even among participants with normal kidney function at baseline, the proportion of patients with an in the group receiving intense therapy, eGFR of 52 in the group receiving intensive therapy vs. 99 in the group receiving 30 ml/min per 1.73 m2 significantly quadrupled. The control group). control group; P = 0.001) 93.
New Treatments and Methods: There is still a sizable residual risk for DKD despite current methods for managing diabetes and hypertension, including the use of ACE inhibitors and ARB. The discovery of novel drugs that target mechanisms such as glomerular hyperfiltration, inflammation, and fibrosis has been a prominent emphasis. A protein kinase C-inhibitor called ruboxistaurin is one of the treatments that Has shown potential 94. Specifically targeting Janus kinase 1 and Janus kinase 2, baricitinib 95 Anti-inflammatory and antifibrotic drug pentoxifylline 96. A selective endothelin called atrasentan. antagonistic to the receptor 97, 98.
Along with finerenone, a highly specific nonsteroidal mineralocorticoid receptor antagonist 99 Table 2. S. Cr is expressed as milligrams per deciliter. The milligrams per gramme of protein to creatinine ratio is used. In milliliters per minute per 1.73 m2, eGFR is measured. UAE is measured in milligrams daily. In UACR, milligrams per gramme are used. Protein Kinase C, or PKC DM2, type 2 diabetic mellitus; AGE, advance glycation end product; PYR-311, pyridoxamine-311; Pyridoxin (pyridoxamine dihydrochloride) has been shown to be safe and effective in treating subjects with nephropathy brought on by type 2 diabetes in Phase 3 Randomized, Double-Blind, Placebo-Controlled, Multi-Center Study known as PIONEER. Hypertension, or HTN; serum creatinine (SCr); UAE, urinary albumin excretion; JAK1/2, Janus kinases 1/2; Influence of Pentoxifylline on Renal Function as well as Urinary Albumin Excretion in Diabetic Kidney Disease Patients; Reducing Residual Albuminuria using AtRasentan in Subjects with Diabetes and Nephropathy A Phase 2b, Retrospective, Endothelin A, ETA, and the urine albumin-to-creatinine ratio are all used in the randomized, double-blind, placebo-controlled trial known as RADAR/JAPAN. A Randomized, Multicounty, Multicenter, Double-Blind, Comparative, Placebo-Controlled Study to Evaluate the Impact of Atrasentan on Renal Outcomes in Patients With Type 2 Diabetes and Nephropathy; DM1, or type 1 diabetic mellitus; PERL, or Antihypertensive drugs Pilot Study to Prevent GFR Decline: A Multi-Center, Randomized, Double-Blind, Placebo-Controlled Trial (ARTS-DN) was conducted to evaluate the safety
TABLE 2: NOVEL DIABETES-RELATED KIDNEY DISEASE TREATMENT
|Title of the Study||Drug/Intervention Trials||Research Participants||Outcomes|
|Tuttle and others, 2005 (68)||Ruboxistaurin (PKC-inhibitor)||Macralbuminuria (DM2)||albuminuria was reduced, and kidney function was stabilized.|
|Pioneer (81)||PYR-311 (anti-AGE prescription)||DM2, HTN, 1.3 SCr, 3.0 mg/dl, and protein to creatinine ratio of 1200 mg/g||Halted|
|Predian (70)||Pentoxifylline (anti-inflammatory, antifibrotic effect)||DM2, eGFR = 15 to 60 ml/min per 1.73, and UAE > 300 mg/24 h||eGFR reduced 4.3 ml/min per 1.73 m2 quicker in the pentoxifylline group than in the control group, with an average albuminuria difference of 21%.|
|Baricitinib Safety and Efficacy in Participants with Diabetic Kidney Disease: A Clinical Study (69)||JAK1/2 antagonist baricitinib||macroalbuminuria, DM2, with eGFR between 20 to 75 ml/min per 1.73 m||In the highest therapy group, albuminuria decreased by 40% while eGFR was unaffected.|
|Both radar and radar/Japan (71)||Atrasentan (ETA)||DM2, eGFR = 30 of between 75 ml/min/ 1.73 m2, as well as UACR = 300 to 3500 mg/g||Improved albuminuria by 35%|
|SONAR, ongoing (72)||Atrasentan (ETA)||HTN, eGFR=15-90 ml/min for each and every 1.73 m2, with UACR >30 5000 mg/g||Ongoing|
|PERL, ongoing (82)||Allopurinol (xanthine oxidase)||eGFR with DM1 is 40-99 ml/min per 1.73 m2, whereas UAE are 18-5000 mg/d||Ongoing|
|ARTS-DN, 2015 (83)||Finerenone (steroid mineralocorticoid receptorantagonist)||DM2, UACR30 mg/g, with eGFR>30 ml/min with each 1.73 m2||There's no difference in eGFR, but albuminuria declines by 17% to 40% amount of the drug.|
CONCLUSION: A clinical syndrome known as DKD includes persistent albuminuria, a sustained decline in GFR, high blood pressure, an increase in cardiovascular events, and mortality from these events. Compared to individuals without DM, dialysis patients with DM have a greater death rate. Recent research demonstrated that RAAS blockers, blood pressure control, blood glucose and lipid management, and smoking cessation are all effective multifactorial therapies that can dramatically improve the prognosis of individuals with type 2 DM with nephropathy. For the prevention and treatment of DKD, a wide range of novel drugs are being investigated, including SGLT2 inhibitors, GLP-1 analogues, DPP-4 inhibitors, thiazolidinedione, pentoxifylline, vitamin D analogue paricalcitol, pyridoxine, ruboxistaurin, solidified, JAK inhibitors, and nonsteroidal miner corticoid receptor antagonists. To assess the long-term outcomes in DKD patients, additional studies focusing on the renal outcomes, not just changes in albuminuria, are required. One of the main causes of ESRD is DKD, which is also linked to increased cardiovascular morbidity and mortality. genetic and environmental aspects have been proposed as the risk factors that predict who experiences renal damage brought on by hyperglycemia. DKD results from the interaction of the metabolic and hemodynamic processes. Additionally, metabolic pathways in the diabetic kidney are engaged, causing AGE accumulation, PKC activation, the generation of renal polyols, and increased oxidative stress. Different cytokines and growth factors are activated by these aberrations. Mesangial expansion, GBM thickening, and glomerular sclerosis are the three pathways that ultimately result in renal histologic alterations in the glomeruli in diabetic nephropathy. At this time, the cornerstone of pharmacotherapy is the use of ACE inhibitors, ARBs, and glucose-lowering medications to block the RAAS. The most convincing proof of the size of the benefit that can be obtained from the Steno-2 trial is data from that study. putting in place a variety of risk factor reduction-focused strategies. For the prevention and treatment of DKD, more avant-garde methods incorporating pathophysiological mechanisms are required.
ACKNOWLEDGEMENTS: The author would like to express sincere and special thanks to Dr. Kulbhushan Haldeniya, Dr. Rajesh Sharma and Dr. Sourabh Kosey for providing all the guidance and support.
CONFLICTS OF INTEREST: Nil
- Bikbov B, Purcell CA, Levey AS, Smith M, Abdoli A, Abebe M, Adebayo OM, Afarideh M, Agarwal SK, Agudelo-Botero M and Ahmadian E: Global, regional, and national burden of chronic kidney disease, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. The Lancet 2020; 395(10225): 709-33.
- American Diabetes Association. 9. Microvascular complications and foot care. Diabetes Care. 2015 Jan 1;38(Supplement_1): S58-66.
- Group PH, Thomas MC, Moran JL, Waden J, Thorn LM, Mäkinen VP, Rosengård-Bärlund M, Saraheimo M, Hietala K, Heikkilä O and Forsblom C: The presence and severity of chronic kidney disease predicts all-cause mortality in type 1 diabetes. Diabetes 2009; 58(7): 1651-8.
- Orchard TJ, Secrest AM, Miller RG and Costacou T: In the absence of renal disease, 20-year mortality risk in type 1 diabetes is comparable to that of the general population: a report from the Pittsburgh Epidemiology of Diabetes Complications Study. Diabetologia 2010; 53(11): 2312-9.
- Bruno G, Merletti F, Bargero G, Novelli G, Melis D, Soddu A, Perotto M, Pagano G and Cavallo-Perin P: Estimated glomerular filtration rate, albuminuria and mortality in type 2 diabetes: the Casale Monferrato study. Diabetologia 2007; 50(5): 941-8.
- Afkarian M, Katz R, Bansal N, Correa A, Kestenbaum B, Himmelfarb J, De Boer IH and Young B: Diabetes, kidney Diabetic kidney disease: difficulties, advancements, and prospects. Clinical Journal of the American Society of Nephrology Disease, and cardiovascular outcomes in the Jackson Heart Study. Clinical Journal of the American Society of Nephrology 2016; 11(8): 1384-91.
- de Boer IH, Rue TC, Hall YN, Heagerty PJ, Weiss NS and Himmelfarb J: Temporal trends in the prevalence of diabetic kidney disease in the United States. Jama 2011; 305(24): 2532-9.
- Cameron JS: Diabetic nephropathy's discovery: from obscure to prominent. Magazine of Nephrology 2006; 19(10): 75-S87.
- Alicic RZ, Rooney MT and Tuttle KR: 2017; 2032-2045.
- Díaz Bulnes P. Respuesta al estrés de retículo endoplasmático enel daño renal agudo. Regulación epigenética y potenciales dianas terapéuticas.
- Thomas MC, Brownlee M, Susztak K, Sharma K, Jandeleit-Dahm KA, Zoungas S, Rossing P, Groop PH and Cooper ME: Diabetic kidney disease. Nature Reviews Disease primers 2015; 1(1): 1-20.
- Alicic RZ, Rooney MT and Tuttle KR: Diabetic kidney disease: challenges, progress, and possibilities. Clinical journal of the American Society of Nephrology: CJASN 2017; 12(12): 2032.
- Yu SM and Bonventre JV: Acute kidney injury and progression of diabetic kidney disease. Advances in chronic kidney disease 2018; 25(2): 166-80.
- Zimmet P, Alberti KG and Shaw J: Global and societal implications of thediabetes epidemic. Nature 2001; 414: 782–787
- Hemmelgarn BR, Manns BJ, Lloyd A, James MT, Klarenbach S, Quinn RR, Wiebe N and Tonelli M: Alberta Kidney Disease Network. Relation between kidney function, proteinuria, and adverse outcomes. Jama 2010; 303(5): 423-9.
- Astor BC, Matsushita K, Gansevoort RT, Van Der Velde M, Woodward M, Levey AS, De Jong PE and Coresh J: Chronic Kidney Disease Prognosis Consortium. Lower estimated glomerular filtration rate and higher albuminuria are associated with mortality and end-stage renal disease. A collaborative meta-analysis of kidney disease population cohorts. Kidney International 2011; 79(12): 1331-40. Van Der Velde M, Matsushita K, Coresh J, Astor BC, Woodward M, Levey AS, de Jong PE and Gansevoort RT: Chronic Kidney Disease Prognosis Consortium. Lower estimated glomerular filtration rate and higher albuminuria are associated with all-cause and cardiovascular mortality. A collaborative meta-analysis of high-risk population cohorts. Kidney international 2011; 79(12): 1341-52.
- Adler AI, Stevens RJ, Manley SE, Bilous RW, Cull CA and Holman RR: UKPDS Group. Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney international 2003; 63(1) 225-32.
- So WY, Kong AP, Ma RC, Ozaki R, Szeto CC, Chan NN, Ng V, Ho CS, Lam CW, Chow CC and Cockram CS: Glomerular filtration rate, cardiorenal end points, and all-cause mortality in type 2 diabetic patients. Diabetes care. 2006; 29(9): 2046-52.
- Alicic, Radica Z, Michele T. Rooney and Katherine R: Tuttle. "Diabetic kidney disease: difficulties, developments, and prospects." Clinical Journal of the American Society of Nephrology 12.12 2017; 2032-2045.
- Alicic RZ, Rooney MT and Tuttle KR: Diabetic kidney disease: challenges, progress, and possibilities. Clinical Journal of the American Society of Nephrology: CJASN. 2017; 12(12): 2032.
- Roshan B, Warram JH, Perkins BA, Ficociello LH and Krolewski AS: It may not always be necessary to move to proteinuria for people with type 1 diabetes and newly developed microalbuminuria to develop advanced chronic kidney disease. Int 2010; 77(1): 57–64.
- Krolewski AS: Progressive renal decline: the new paradigm of diabetic nephropathy in type 1 diabetes. Diabetes care. 2015; 38(6): 954-62.
- Thorn LM, Gordin D, Harjutsalo V, Hägg S, Masar R, Saraheimo M, Tolonen N, Wadén J, Groop PH, Forsblom CM. The presence and consequence of nonalbuminuric chronic kidney disease in patients with type 1 diabetes. Diabetes Care 2015; 38(11): 2128-33.
- Perkins BA, Ficociello LH, Ostrander BE, Silva KH, Weinberg J, Warram JH and Krolewski AS: Microalbuminuria and the risk for early progressive renal function decline in type 1 diabetes. Journal of the American Society of Nephrology 2007; 18(4): 1353-61.
- Rigalleau V, Lasseur C, Raffaitin C, Beauvieux MC, Barthe N, Chauveau P, Combe C and Gin H: Normoalbuminuric renal-insufficient diabetic patients: a lower-risk group. Diabetes Care 2007; 30(8): 2034-9.
- MacIsaac RJ and Jerums G: Diabetic kidney disease with and without albuminuria. Current opinion in nephrology and hypertension 2011; 20(3): 246-57.
- Solini A, Penno G, Bonora E, Fondelli C, Orsi E and Arosio M: Renal Insufficiency and Cardiovascular Events (RIACE) Study Group. Diverging association of reduced glomerular filtration rate and albuminuria with coronary and noncoronary events in patients with type 2 diabetes: the renal insufficiency and cardiovascular events (RIACE) Italian multicenter study. Diabet Care 2012; 35(1): 143–9.
- Thomas MC, Brownlee M, Susztak K, Sharma K, Jandeleit-Dahm KA, Zoungas S, Rossing P, Groop PH and Cooper ME: Diabetic kidney disease. Nature Reviews Disease primers 2015; 1(1): 1-20.
- Afkarian M, Zelnick LR, Hall YN, Heagerty PJ, Tuttle K, Weiss NS and De Boer IH: Clinical manifestations of kidney disease among US adults with diabetes 1988-2014. Jama. 2016; 316(6): 602-10.
- Porrini E, Ruggenenti P, Mogensen CE, Barlovic DP, Praga M, Cruzado JM, Hojs R, Abbate M and de Vries AP: ERA-EDTA Diabesity Working Group. Non-proteinuric pathways in loss of renal function in patients with type 2 diabetes. The Lancet Diabetes & Endocrinology 2015; 3(5): 382-91.
- Penno G, Solini A, Zoppini G, Orsi E, Zerbini G, Trevisan R, Gruden G, Cavalot F, Laviola L, Morano S and Nicolucci A: Rate and determinants of association between advanced retinopathy and chronic kidney disease in patients with type 2 diabetes: the Renal Insufficiency And Cardiovascular Events (RIACE) Italian multicenter study. Diabetes care 2012; 35(11): 2317-23.
- Lin YC, Chang YH, Yang SY, Wu KD and Chu TS: Update of pathophysiology and management of diabetic kidney disease. Journal of the Formosan Medical Association. 2018; 117(8): 662-75.
- Chen Y, Lee K, Ni Z and He JC: Diabetic kidney disease: challenges, advances, and opportunities. Kidney diseases. 2020; 6(4): 215-25.
- DCCT/Edic Research Group. Intensive diabetes therapy and glomerular filtration rate in type 1 diabetes. N Engl J Med. 2011 Dec 22; 365:2366-76.
- Finne P, Reunanen A, Stenman S, Groop PH and Grönhagen-Riska C: Incidence of end-stage renal disease in patients with type 1 diabetes. Jama 2005; 294(14): 1782-7.
- Pergola PE, Raskin P, Toto RD, Meyer CJ, Huff JW, Grossman EB, Krauth M, Ruiz S, Audhya P, Christ-Schmidt H, Wittes J. Bardoxolone methyl and kidney function in CKD with type 2 diabetes.New England Journal of Medicine 2011; 365(4): 327-36.
- Sharma K, Ix JH, Mathew AV, Cho M, Pflueger A, Dunn SR, Francos B, Sharma S, Falkner B, McGowan TA and Donohue M: Pirfenidone for diabetic nephropathy. Journal of the American Society of Nephrology: JASN. 2011; 22(6): 1144.
- Thakar CV, Christianson A, Himmelfarb J and Leonard AC: Acute kidney injury episodes and chronic kidney disease risk in diabetes mellitus. Clinical Journal of the American Society of Nephrology: CJASN 2011; 6(11): 2567.
- Monseu M, Gand E, Saulnier PJ, Ragot S, Piguel X, Zaoui P, Rigalleau V, Marechaud R, Roussel R, Hadjadj S and Halimi JM: Acute kidney injury predicts major adverse outcomes in diabetes: synergic impact with low glomerular filtration rate and albuminuria. Diabetes Care 2015; 38(12): 2333-40.
- Caramori ML, Parks A and Mauer M: Renal lesions predict progression of diabetic nephropathy in type 1 diabetes. Journal of the American Society of Nephrology: JASN 2013; 24(7): 1175.
- Hussain S, Singh A, Habib A and Najmi AK: Proton pump inhibitors use and risk of chronic kidney disease: evidence-based meta-analysis of observational studies. Clinical Epidemiology and Global Health 2019; 7(1): 46-52.
- Cheng D, Fei Y, Liu Y, Li J, Xue Q, Wang X and Wang N: HbA1C variability and the risk of renal status progression in diabetes mellitus: a meta-analysis. PLoS One 2014; 9(12): 115509.
- Pugliese G, Solini A, Bonora E, Fondelli C, Orsi E, Nicolucci A and Penno G: RIACE Study Group. Chronic kidney disease in type 2 diabetes: lessons from the Renal Insufficiency and Cardiovascular Events (RIACE) Italian Multicentre Study. Nutrition, Metabolism and Cardiovascular Diseases 2014; 24(8): 815-22.
- Ismail-Beigi F, Craven T, Banerji MA, Basile J, Calles J, Cohen RM, Cuddihy R, Cushman WC, Genuth S, Grimm Jr RH, Hamilton BP. Effect of intensive treatment of hyperglycaemia on microvascular outcomes in type 2 diabetes: an analysis of the ACCORD randomised trial. The Lancet 2010; 376(9739): 419-30.
- Duckworth W, Abraira C, Moritz T, Reda D, Emanuele N, Reaven PD, Zieve FJ, Marks J, Davis SN, Hayward R and Warren SR: Glucose control and vascular complications in veterans with type 2 diabetes. New England journal of medicine 2009; 360(2): 129-39.
- Wagnew and Fasil: “Diabetes patients in sub-Saharan countries with diabetic nephropathy and hypertension: a complete study and meta-analysis”. BMC Research Notes 2018; 1-7.
- Vidi SR: Role of hypertension in the progression of chronic kidney disease in children. Current Opinion in Pediatrics 2018; 30(2): 247-51.
- Wagnew F, Eshetie S, Kibret GD, Zegeye A, Dessie G, Mulugeta H and Alemu A: Diabetic nephropathy and hypertension in diabetes patients of sub-Saharan countries:a systematic review and meta-analysis. BMC research notes 2018; 11(1): 1-7.
- Castañeda R, Cáceres A, Cruz SM, Aceituno JA, Marroquín ES, Sosa AC, Strangman WK and Williamson RT: Nephroprotective plant species used in traditional Mayan Medicine for renal-associated diseases. Journal of Ethnopharmacology 2022: 115755.
- Priya SH, Kedari GS and Naidu MP: Higher serum Sirtuin 1 levels and GA heterozygote of SIRT1 gene polymorphism rs10823108 serve as an independent risk factor for diabetic nephropathy in women. Human Gene. 2022 Dec 1; 34:201084.
- Chehade JM, Gladysz M and Mooradian AD: Dyslipidemia in type 2 diabetes: prevalence, pathophysiology, and management. Drugs 2013; 73(4): 327-39.
- Raile K, Galler A, Hofer S, Herbst A, Dunstheimer D, Busch P and Holl RW: Diabetic nephropathy in 27,805 children, adolescents, and adults with type 1 diabetes: effect of diabetes duration, A1C, hypertension, dyslipidemia, diabetes onset, and sex. Diabetes care.2007; 30(10): 2523-8.
- Kimoto E, Shoji T, Emoto M, Miki T, Tabata T, Okuno Y, Ishimura E, Inaba M, Nishizawa Y. Effect of diabetes on uremic dyslipidemia. Journal of atherosclerosis and thrombosis. 2002;9(6):305-13.
- Senba H, Furukawa S, Sakai T, Niiya T, Miyake T, Yamamoto S, Ueda T, Torisu M, Minami H, Miyaoka H, Onji M. Serum lipoprotein (a) levels and diabetic nephropathy among Japanese patients with type 2 diabetes mellitus. Journal of Diabetes and its Complications. 2016 Jul 1;30(5):923-7.
- Hill CJ, Cardwell CR, Maxwell AP, Young RJ, Matthews B, O’Donoghue DJ, Fogarty DG. Obesity and kidney disease in type 1 and 2 diabetes: an analysis of the National Diabetes Audit. QJM: An International Journal of Medicine. 2013 Oct 1;106(10):933-42.
- Wuerzner G, Pruijm M, Maillard M, Bovet P, Renaud C, Burnier M, Bochud M. Marked association between obesity and glomerular hyperfiltration: a cross-sectional study in an African population. American Journal of kidney diseases. 2010; 56(2): 303-12.
- Thomson SC, Vallon V and Blantz RC: Kidney function in early diabetes: the tubular hypothesis of glomerular filtration. American Journal of Physiology-Renal Physiology 2004.
- Chen HJ, Lin CR. Simultaneous quantification of ethyl purine adducts in human urine by stable isotope dilution nanoflow liquid chromatography nanospray ionization tandem mass spectrometry. Journal of Chromatography A. 2013 Dec 27; 1322:69-73.
- Look AHEAD Research Group. Effect of a long-term behavioural weight loss intervention on nephropathy in overweight or obese adults with type 2 diabetes: a secondary analysis of the Look AHEAD randomised clinical trial. The Lancet Diabetes &Endocrinology 2014; 2(10): 801-9.
- Chakkarwar VA: Smoking in diabetic nephropathy: sparks in the fuel tank?World J of Diabetes 2012; 3(12): 86.
- Orth SR, Hallan SI. Smoking: a risk factor for progression of chronic kidney disease and for cardiovascular morbidity and mortality in renal patients—an absence of evidence or evidence of absence?Clinical Journal of the American Society of Nephrology 2008;3(1): 226-36..
- Feodoroff and Maija: "Smoking and progression of diabetic nephropathy in patients with type 1 diabetes." Acta diabetologica 2016; 525-533.
- Inzucchi SE and Sherwin RS: Type 2 diabetes mellitus. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier 2011.
- Alicic RZ, Rooney MT and Tuttle KR: Diabetic kidney disease: challenges, progress, and possibilities. Clinical Journal of the American Society of Nephrology: CJASN. 2017; 12(12):2032.
- Xia J, Wang L, Ma Z, Zhong L, Wang Y, Gao Y, He L and Su X: Cigarette smoking and chronic kidney disease in the general population: a systematic review and meta-analysis of prospective cohort studies. Nephrology Dialysis Transplantation 2017; 32(3): 475-87.
- Tuttle KR: Back to the future: glomerular hyperfiltration and the diabetic kidney. Diabetes 2017; 66(1):14-6.
- Heerspink HJ, Perkins BA, Fitchett DH, Husain M and Cherney DZ: Sodium-glucose cotransporter 2 inhibitors in the treatment of diabetes mellitus: cardiovascular and kidney effects, potential mechanisms, and clinical applications. Circulation 2016; 134(10): 752-72.
- Grabias BM and Konstantopoulos K: The physical basis of renal fibrosis: effects of altered hydrodynamic forces on kidney homeostasis. American Journal of Physiology-Renal Physiology 2014; 306(5): F473-85..
- Tuttle KR. Back to the future: glomerular hyperfiltration and the diabetic kidney. Diabetes. 2017 Jan 1;66(1):14-6.
- Grabias BM, Konstantopoulos K. The physical basis of renal fibrosis: effects of altered hydrodynamic forces on kidney homeostasis.American Journal of Physiology-Renal Physiology 2014;306(5): F473-85.
- AD Association. Diabetes medical care standards until 2014 Diabetes care 37. Suppl 1 (2014): S14-80.
- Bilous RW, Gonzalez-Campoy JM, Fradkin JE, Mauer M, Molitch ME, Narva AS, Nelson RG, Sharma K, Tuttle KR, Rocco MV, Berns JS. KDOQI clinical practice guideline for diabetes and CKD: 2012 update. American Journal of Kidney Diseases. 2012..
- American Diabetes Association. Standards of medical care in diabetes--2014. Diabetes care 2014; 37: 14-80.
- Tuttle KR, Bakris GL, Bilous RW, Chiang JL, De Boer IH, Goldstein-Fuchs J, Hirsch IB, Kalantar-Zadeh K, Narva AS, Navaneethan SD, Neumiller JJ. Diabetic kidney disease: a report from an ADA Consensus Conference. Diabetes care. 2014 Oct 1;37(10):2864-83.
- Bilous RW, Gonzalez-Campoy JM, Fradkin JE, Mauer M, Molitch ME, Narva AS, Nelson RG, Sharma K, Tuttle KR, Rocco MV, Berns JS. KDOQI clinical practice guideline for diabetes and CKD: 2012 update. American Journal of Kidney Diseases. 2012.
- de Boer IH: Results from the DCCT/EDIC [Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research] trial on the effects of intensive diabetes therapy on the glomerular filtration rate in type 1 diabetes are included in the abstract with the reference number LBOR05. Journal of the American Society of Nephrology 22. Abstracts (2011): 2B.
- Retnakaran R, Cull CA, Thorne KI, Adler AI and Holman RR: UKPDS Study Group. Risk factors for renal dysfunction in type 2 diabetes: UK Prospective Diabetes Study 74. diabetes 2006; 55(6): 1832-9.
- ADVANCE Collaborative Group."Intense blood glucose management and vascular outcomes in type 2 diabetic patients."New England Journal of Medicine 358.24 (2008): 2560-2572.
- Duckworth W, Abraira C, Moritz T, Reda D, Emanuele N, Reaven PD, Zieve FJ, Marks J, Davis SN, Hayward R and Warren SR: Glucose control and vascular complications in veterans with type 2 diabetes. New England Journal of Medicine 2009; 360(2): 129-39.
- Papademetriou V, Lovato L, Doumas M, Nylen E, Mottl A, Cohen RM, Applegate WB, Puntakee Z, Yale JF, Cushman WC. Chronic kidney disease and intensive glycemic control increase cardiovascular risk in patients with type 2 diabetes. Kidney international 2015; 87(3): 649-59.
- Wong MG, Perkovic V, Chalmers J, Woodward M, Li Q, Cooper ME, Hamet P, Harrap S, Heller S, MacMahon S and Mancia G: Long-term benefits of intensive glucose control for preventing end-stage kidney disease: ADVANCE-ON. Diabetes care 2016; 39(5): 694-700.
- Ismail-Beigi F, Craven T, Banerji MA, Basile J, Calles J, Cohen RM, Cuddihy R, Cushman WC, Genuth S, Grimm RH and Hamilton BP: Effect of intensive treatment of hyperglycaemia on microvascular outcomes in type 2 diabetes: an analysis of the ACCORD randomised trial. The Lancet 2010; 376(9739): 419-30.
- American Diabetes Association. Standards of medical care in diabetes—2010. Diabetes care 2010; 33(Supplement_1):S11-61.
- Bilous RW, Gonzalez-Campoy JM, Fradkin JE, Mauer M, Molitch ME, Narva AS, Nelson RG, Sharma K, Tuttle KR, Rocco MV and, Berns JS: KDOQI clinical practice guideline for diabetes and CKD: 2012 update. American Journal of Kidney Diseases 2012.
- James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, Lackland DT, LeFevre ML, MacKenzie TD, Ogedegbe O, Smith SC. 2014 Evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8) Jama 2014; 311(5): 507-20.
- Tuttle KR, Bakris GL, Bilous RW, Chiang JL, De Boer IH, Goldstein-Fuchs J, Hirsch IB, Kalantar-Zadeh K, Narva AS, Navaneethan SD and Neumiller JJ: Diabetic kidney disease: a report from an ADA Consensus Conference. Diabetes care 2014; 37(10): 2864-83.
- Brenner and Barry M: "Effects of losartan on renal and cardiovascular outcomes in patients with type 2 diabetes and nephropathy." New England Journal of Medicine 2001; 861-869.
- Mann JF, Schmieder RE, McQueen M, Dyal L, Schumacher H, Pogue J, Wang X, Maggioni A, Budaj A, Chaithiraphan S and Dickstein K: Renal outcomes with telmisartan, ramipril, or both, in people at high vascular risk (the ONTARGET study): a multicentre, randomised, double-blind, controlled trial.The Lancet 2008; 372(9638): 547-53.
- Fried LF, Emanuele N, Zhang JH, Brophy M, Conner TA, Duckworth W, Leehey DJ, McCullough PA, O'Connor T, Palevsky PM and Reilly RF: Combined angiotensin inhibition for the treatment of diabetic nephropathy. New England Journal of Medicine 2013; 369(20): 1892-903.
- Wright Jr JT, Whelton PK and Reboussin DM: A randomized trial of intensive versus standard blood-pressure control. The New England Journal of Medicine. 2016; 374(23): 2294.
- Perkovic V and Rodgers A: Redefining blood-pressure targets—SPRINT starts the marathon. N Engl J Me 2015; 373(22): 2175-8.
- Cushman WC, Evans GW and Cutler JA: Long-term cardiovascular effects of 4.9 years of intensive blood pressure control in type 2 diabetes mellitus: the action to control cardiovascular risk in diabetes follow-on blood-pressure study. American Heart Association 2015 7).
- Wright JT, Whelton PK and Reboussin DM: A randomized trial of intensive versus standard blood-pressure control. The New England Journal of Medicine 2016; 374(23): 2294-.
- Rocco MV and Cheung AK: A SPRINT to the finish, or just the beginning? Implications of the SPRINT results for nephrologists. Kidney International 2016; 89(2): 261-3.
- Cushman WC, Evans GW and Cutler JA: Long-term cardiovascular effects of 4.9 years of intensive blood pressure control in type 2 diabetes mellitus: the action to control cardiovascular risk in diabetes follow-on blood-pressure study. American Heart Association 2015; 7.
- Tuttle KR, Bakris GL, Toto RD, McGill JB, Hu K and Anderson PW: The effect of ruboxistaurin on nephropathy in type 2 diabetes. Diabetes care 2005; 28(11): 2686-90.
- Brosius FC, Tuttle KR and Kretzler M: JAK inhibition in the treatment of diabetic kidney disease. Diabetologia 2016; 59(8): 1624-7.
- Navarro-González and Juan F: "Effect of pentoxifylline on renal function and urinary albumin excretion in patients with diabetic kidney disease: the PREDIAN trial." Journal of the American Society of Nephrology 2015; 220-229.
- De Zeeuw D, Coll B, Andress D, Brennan JJ, Tang H, Houser M, Correa-Rotter R, Kohan D, Heerspink HJ, Makino H and Perkovic V: The endothelin antagonist atrasentan lowers residual albuminuria in patients with type 2 diabetic nephropathy. Journal of the American Society of Nephrology 2014; 25(5): 1083-93.
- Danielle P: SONAR: Study of Diabetic Nephropathy with Atrasentan NCTO1858532 describes the study as "A Randomized, Multicountry, Multicenter, Double-Blind, Parallel, Placebo-Controlled Study of the Effects of Altrasentan on Renal Outcomes in Subjects with Type 2 Diabetes and Nephropathy." Available at: Clinical Trials. gov. Accessed 2017.
- Bakris GL, Agarwal R, Chan JC, Cooper ME, Gansevoort RT, Haller H, Remuzzi G, Rossing P, Schmieder RE, Nowack C and Kolkhof P: Effect of finerenone on albuminuria in patients with diabetic nephropathy: a randomized clinical trial. Jama 2015; 314(9): 884-94.
How to cite this article:
Ansari Y, Patel A, Haldeniya K, Sharma R, Haneef M, Kosey S and Kumar R: Review on the impact of diabetes on kidney disease. Int J Pharm Sci & Res 2023; 14(11): 5098-09. doi: 10.13040/IJPSR.0975-8232.14(11).5098-09.
All © 2023 are reserved by International Journal of Pharmaceutical Sciences and Research. This Journal licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.
Yasir Ansari *, Akhilesh Patel, Kulbhushan Haldeniya, Rajesh Sharma, Mohd Haneef, Sourabh Kosey and Ramesh Kumar
Department of Pharmacy Practice, NIMS Institute of Pharmacy, NIMS University, Jaipur, Rajasthan, India.
22 February 2023
09 May 2023
31 May 2023
01 November 2023