Editing Diabetic nephropathy

{{Short description|Chronic loss of kidney function}}
{{Lead too long|date=May 2025}}
{{Infobox medical condition
| name            = Diabetic nephropathy
| synonyms        = Diabetic kidney disease
| image           = Nodular_glomerulosclerosis.jpeg
| caption         = Two glomeruli in diabetic nephropathy: the acellular light purple areas within the capillary tufts are the destructive mesangial matrix deposits.
| pronounce       =
| field           =
| symptoms        = [[Albuminuria]],<ref name="dmsj2019">{{cite journal |last1=Alamo |first1=A. |last2=Campagna |first2=D. |last3=Di Pino |first3=A. |last4=Russo |first4=C. |last5=Calogero |first5=A. E. |last6=Polosa |first6=R. |last7=Purrello |first7=F. |date=October 2019 |title=Smoking and diabetes: dangerous liaisons and confusing relationships |url=https://dmsjournal.biomedcentral.com/track/pdf/10.1186/s13098-019-0482-2.pdf |journal=Diabetology & Metabolic Syndrome |publisher=[[BioMed Central]] |volume=11 |issue=85 |page=85 |doi=10.1186/s13098-019-0482-2 |doi-access=free |issn=1758-5996 |pmc=6813988 |pmid=31666811 |s2cid=204882089 |access-date=20 August 2021}}</ref> [[peripheral edema]],<ref name="dmsj2019"/> high blood pressure,<ref name="dmsj2019"/> tiredness<ref name="nih22"/>
| complications   =
| onset           =
| duration        =
| types           =
| causes          =
| risks           = High blood pressure, [[tobacco smoking]],<ref name="dmsj2019"/> unstable blood glucose<ref name="nih22"/>
| diagnosis       = Abnormal levels of urinary albumin<ref name="lewis2014">{{cite journal | vauthors = Lewis G, Maxwell AP | title = Risk factor control is key in diabetic nephropathy | journal = The Practitioner | volume = 258 | issue = 1768 | pages = 13–7, 2 | date = February 2014 | pmid = 24689163 }}</ref>
| differential    =
| prevention      = [[Smoking cessation]]<ref name="dmsj2019"/>
| treatment       = ACE inhibitors<ref name="ace">{{cite journal | vauthors = Lim AK | title = Diabetic nephropathy – complications and treatment | journal = [[International Journal of Nephrology and Renovascular Disease]] | volume = 7 | pages = 361–81 | date = 2014 | pmid = 25342915 | pmc = 4206379 | doi = 10.2147/IJNRD.S40172 | doi-access = free }}</ref>
| medication      =
| prognosis       =
| frequency       =
| deaths          =
}}

'''Diabetic nephropathy''', also known as '''diabetic kidney disease''',<ref>{{cite book|title=Nutrition Therapy for Chronic Kidney Disease|vauthors=Kittell F|publisher=CRC Press|year=2012|veditors=Thomas LK, Othersen JB|page=198|chapter=Diabetes Management|isbn=9781439849491|chapter-url=https://books.google.com/books?id=DreAtq_hKmcC&pg=PA198}}</ref> is the chronic loss of [[kidney function]] occurring in those with [[diabetes mellitus]]. Diabetic nephropathy is the leading cause of [[chronic kidney disease]] (CKD) and end-stage renal disease (ESRD) globally. The triad of protein leaking into the urine (proteinuria or albuminuria), rising blood pressure with hypertension and then falling renal function is common to many forms of CKD. [[Proteinuria|Protein loss in the urine]] due to damage of the [[Glomerulus (kidney)|glomeruli]] may become massive, and cause a low [[serum albumin]] with resulting [[Anasarca|generalized body swelling (edema)]] so called [[nephrotic syndrome]]. Likewise, the estimated [[glomerular filtration rate]] (eGFR) may progressively fall from a normal of over 90 ml/min/1.73m<sup>2</sup> to less than 15, at which point the patient is said to have [[end-stage renal disease]].<ref>{{cite book|last1=Longo|first1=Dan|title=Harrison's manual of medicine|last2=Fauci|first2=Anthony|last3=Kasper|first3=Dennis|last4=Hauser|first4=Stephen|last5=Jameson|first5=J.|last6=Loscalzo|first6=Joseph|date=2013|publisher=McGraw-Hill Medical|isbn=978-0-07-174519-2|edition=18th|location=New York|page=2982|name-list-style=vanc}}</ref> It usually is slowly progressive over years.<ref>{{cite journal|vauthors=Afkarian M, Zelnick LR, Hall YN, Heagerty PJ, Tuttle K, Weiss NS, de Boer IH|date=August 2016|title=Clinical Manifestations of Kidney Disease Among US Adults With Diabetes, 1988–2014|journal=JAMA|volume=316|issue=6|pages=602–10|doi=10.1001/jama.2016.10924|pmc=5444809|pmid=27532915}}</ref>

Pathophysiologic abnormalities in diabetic nephropathy usually begin with long-standing poorly controlled blood glucose levels. This is followed by multiple changes in the filtration units of the kidneys, the [[nephron]]s. (There are normally about 750,000–1.5 million nephrons in each adult kidney).<ref>{{cite book|last1=Hall|first1=John|title=Textbook of Medical Physiology|last2=Guyton|first2=Arthur|date=2005|publisher=W.B. Saunders|isbn=978-0-7216-0240-0|edition=11th|location=Philadelphia|page=310|name-list-style=vanc}}</ref> Initially, there is constriction of the [[efferent arterioles]] and dilation of [[afferent arterioles]], with resulting glomerular capillary hypertension and hyperfiltration particularly as nephrons become obsolescent and the adaption of hyperfiltration paradoxically causes further [[shear stress]] related damage to the delicate glomerular capillaries, further proteinuria, rising blood pressure and a vicious circle of additional nephron damage and decline in overall renal function.<ref>{{Cite journal |last1=Hostetter |first1=T. H. |last2=Olson |first2=J. L. |last3=Rennke |first3=H. G. |last4=Venkatachalam |first4=M. A. |last5=Brenner |first5=B. M. |date=July 1981 |title=Hyperfiltration in remnant nephrons: a potentially adverse response to renal ablation |url=https://pubmed.ncbi.nlm.nih.gov/7246778/ |journal=The American Journal of Physiology |volume=241 |issue=1 |pages=F85–93 |doi=10.1152/ajprenal.1981.241.1.F85 |issn=0002-9513 |pmid=7246778|s2cid=1553863 }}</ref><ref>{{cite web|title=diabetic nephropathy|url=http://medical-dictionary.thefreedictionary.com/diabetic+nephropathy|access-date=2015-06-27}}</ref> Concurrently, there are changes within the glomerulus itself: these include a thickening of the [[basement membrane]], a widening of the slit membranes of the [[podocytes]], an increase in the number of [[mesangial cell]]s, and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces deposits called Kimmelstiel-Wilson nodules. The mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration.<ref name="Schlöndorff_20092">{{cite journal|vauthors=Schlöndorff D, Banas B|date=June 2009|title=The mesangial cell revisited: no cell is an island|journal=Journal of the American Society of Nephrology|volume=20|issue=6|pages=1179–87|doi=10.1681/ASN.2008050549|pmid=19470685|doi-access=free}}</ref><!--Prevention and Treatment-->

The status of diabetic nephropathy may be monitored by measuring two values: the amount of protein in the urine - [[proteinuria]]; and a blood test called the serum [[creatinine]]. The amount of the proteinuria reflects the degree of damage to any still-functioning glomeruli. The value of the [[serum creatinine]] can be used to calculate the [[estimated glomerular filtration rate]] (eGFR), which reflects the percentage of glomeruli which are no longer filtering the blood. {{citation needed|date=December 2017}} Treatment with an [[angiotensin converting enzyme inhibitor]] or [[angiotensin receptor blocker]], which dilates the [[arteriole]] exiting the glomerulus, thus reducing the [[blood pressure]] within the glomerular capillaries, may slow (but not stop) progression of the disease. Three classes of diabetes medications – [[GLP-1 agonist]]s, [[DPP-4 inhibitor]]s, and [[SGLT2 inhibitor]]s– are also thought to slow the progression of diabetic nephropathy.<ref>{{cite journal|vauthors=de Boer IH|date=August 2017|title=A New Chapter for Diabetic Kidney Disease|journal=The New England Journal of Medicine|volume=377|issue=9|pages=885–887|doi=10.1056/nejme1708949|pmid=28854097}}</ref><!--Epidemiology-->

Diabetic nephropathy is the most common cause of end-stage renal disease and is a serious complication that affects approximately one quarter of adults with diabetes in the United States.<ref name="Fernandez201422">{{cite journal|vauthors=Mora-Fernández C, Domínguez-Pimentel V, de Fuentes MM, Górriz JL, Martínez-Castelao A, Navarro-González JF|date=September 2014|title=Diabetic kidney disease: from physiology to therapeutics|journal=The Journal of Physiology|volume=592|issue=18|pages=3997–4012|doi=10.1113/jphysiol.2014.272328|pmc=4198010|pmid=24907306}}</ref><ref name="Ding201522">{{cite journal|vauthors=Ding Y, Choi ME|date=January 2015|title=Autophagy in diabetic nephropathy|journal=The Journal of Endocrinology|volume=224|issue=1|pages=R15–30|doi=10.1530/JOE-14-0437|pmc=4238413|pmid=25349246}}</ref> Affected individuals with end-stage kidney disease often require [[hemodialysis]] and eventually [[kidney transplantation]] to replace the failed kidney function.<ref name="ReferenceB22">{{cite journal|vauthors=Lizicarova D, Krahulec B, Hirnerova E, Gaspar L, Celecova Z|year=2014|title=Risk factors in diabetic nephropathy progression at present|journal=Bratislavske Lekarske Listy|volume=115|issue=8|pages=517–21|doi=10.4149/BLL_2014_101|pmid=25246291|doi-access=free}}</ref> Diabetic nephropathy is associated with an increased [[Mortality rate|risk of death]] in general, particularly from [[cardiovascular disease]].<ref name="Fernandez201422"/><ref name="Pálsson R 201422">{{cite journal|vauthors=Pálsson R, Patel UD|date=May 2014|title=Cardiovascular complications of diabetic kidney disease|journal=Advances in Chronic Kidney Disease|volume=21|issue=3|pages=273–80|doi=10.1053/j.ackd.2014.03.003|pmc=4045477|pmid=24780455}}</ref>

==Signs and symptoms==
The onset of symptoms is 5 to 10 years after the disease begins.<ref name="nih22">{{Cite web|title=Diabetes and kidney disease: MedlinePlus Medical Encyclopedia|url=https://www.nlm.nih.gov/medlineplus/ency/article/000494.htm|website=www.nlm.nih.gov|access-date=2015-06-27}}</ref> A usual first symptom is frequent urination at night: [[nocturia]]. Other symptoms include [[tiredness]], [[headache]]s, a [[Malaise|general feeling of illness]], [[nausea]], [[vomiting]], frequent daytime urination, [[Anorexia (symptom)|lack of appetite]], [[Pruritus|itchy skin]], and [[Edema|leg swelling]].<ref name="nih22"/> The clinical presentation of diabetic nephropathy (DN) is characterized by proteinuria (protein in the urine), hypertension and progressive loss of kidney function. The process may be initially indolent, making regular screening for diabetic nephropathy in patients with diabetes mellitus of great importance.<ref>{{Cite journal|last=Kussman|first=M. J.|date=1976-10-18|title=The clinical course of diabetic nephropathy|journal=Journal of the American Medical Association|volume=236|issue=16|pages=1861–1863|doi=10.1001/jama.236.16.1861|pmid=989537|issn=0098-7484}}</ref>

==Risk factors==
Not all patients with diabetes go on to develop diabetic nephropathy. The main risk factors that increase the likelihood of developing diabetic nephropathy are:<ref name="nih22"/>
* Poor control of blood glucose
* Uncontrolled [[Hypertension|high blood pressure]]
* [[Type 1 diabetes mellitus]], with onset before age 20
* Past or current [[Tobacco smoking|cigarette use]]<ref>{{cite journal|vauthors=Jiang N|title=Smoking and the risk of diabetic nephropathy in patients with type 1 and type 2 diabetes: a meta-analysis of observational studies
|journal=Oncotarget|date=Nov 2017|volume=8|issue =54|pages=93209–93218
|doi=10.18632/oncotarget.21478|pmid=29190990|pmc=5696256
}}</ref>
* A family history of diabetic nephropathy- certain genes have been identified that are associated with DN. ( However, no direct correlation has been established yet.<ref>{{Cite journal|last1=Freedman|first1=Barry I.|last2=Bostrom|first2=Meredith|last3=Daeihagh|first3=Pirouz|last4=Bowden|first4=Donald W.|date=2007-10-17|title=Genetic Factors in Diabetic Nephropathy|journal=Clinical Journal of the American Society of Nephrology|volume=2|issue=6|pages=1306–1316|doi=10.2215/cjn.02560607|pmid=17942768|issn=1555-9041|doi-access=free}}</ref> One of these genes is APOL1, which has been found to be associated with nephropathy in African American individuals.<ref>{{Cite journal|last1=Kruzel-Davila|first1=Etty|last2=Wasser|first2=Walter G.|last3=Aviram|first3=Sharon|last4=Skorecki|first4=Karl|date=March 2016|title=APOL1 nephropathy: from gene to mechanisms of kidney injury|journal=Nephrology, Dialysis, Transplantation|volume=31|issue=3|pages=349–358|doi=10.1093/ndt/gfu391|issn=1460-2385|pmid=25561578|doi-access=free}}</ref>)
* Certain racial groups (African Americans, Mexican Americans, and Pima Indians are at higher risk).

==Pathophysiology==
[[File:Physiology of Nephron.png|250px|thumb|right|Diagram showing the basic outline of nephron structure and function: diabetic nephropathy is associated with changes in the afferent and efferent arterioles, causing capillary hypertension; and damage to the glomerular capillaries of multiple causes, including mesangial matrix deposition]]
{{See also|Renal physiology|l1=Review of normal Renal Physiology}}

The disease progression of diabetic nephropathy involves various clinical stages: hyperfiltration, microalbuminuria, macroalbuminuria, nephrotic proteinuria to progressive chronic kidney disease leading to end-stage renal disease (ESRD). The damage is exerted on all compartments of the kidney: the glomerulus, the renal tubules, the vasculature (afferent and efferent renal arterioles) and the interstitium. Renal fibrosis is the final common pathway of DN. This fibrosis is a product of multiple mechanisms including renal hemodynamic changes, glucose metabolism abnormalities associated with oxidative stress as well as inflammatory processes and an overactive [[Renin–angiotensin system|renin-angiotensin-aldosterone system]] (RAAS).{{citation needed|date=May 2020}}

The pathophysiology of diabetic nephropathy is thought to involve an interaction between hemodynamic and metabolic factors.<ref>{{Cite journal|last1=Lin|first1=Yi-Chih|last2=Chang|first2=Yu-Hsing|last3=Yang|first3=Shao-Yu|last4=Wu|first4=Kwan-Dun|last5=Chu|first5=Tzong-Shinn|date=2018-08-01|title=Update of pathophysiology and management of diabetic kidney disease|journal=Journal of the Formosan Medical Association|language=en|volume=117|issue=8|pages=662–675|doi=10.1016/j.jfma.2018.02.007|pmid=29486908|issn=0929-6646|doi-access=free}}</ref>

Hemodynamic factors include an increase in systemic and intraglomerular pressure, as well as the over-activation of the RAAS. Studies have shown that in the setting of diabetes, various factors stimulate the RAAS, which is one of the most important pathways in diabetic nephropathy pathophysiology. Due to the higher load of filtered glucose, there is an up-regulation in the sodium-glucose cotransporter 2 (SGLT2) in the proximal tubules, which cotransports sodium and glucose back into circulation. This leads to a decrease in the delivery of sodium chloride to the macula densa in the distal tubules, promoting the release of renin and over-activating RAAS.<ref>{{Citation|last1=Anderson|first1=Sharon|title=Pathogenesis of Diabetic Glomerulopathy: The Role of Glomerular Hyperfiltration|date=1988|work=The Kidney and Hypertension in Diabetes Mellitus|pages=139–146|publisher=Springer US|isbn=978-1-4757-1976-5|last2=Brenner|first2=Barry M.|doi=10.1007/978-1-4757-1974-1_17}}</ref> Hyperfiltration is one of the earliest features of DN. Several mechanisms have been proposed to cause hyperfiltration. One of these mechanisms is that as glomeruli becomes hypertrophied, filtration surface area initially increases. Another possible mechanism is that abnormal vascular control in diabetic nephropathy leads to a reduction in afferent glomerular arteriolar resistance and an increase in efferent glomerular arteriolar resistance, leading to a net increase in renal blood flow (RBF) and glomerular filtration rate (GFR).<ref>{{Cite journal|last=Hostetter|first=Thomas H.|date=March 2003|title=Hyperfiltration and glomerulosclerosis|url=https://pubmed.ncbi.nlm.nih.gov/12704579/|journal=Seminars in Nephrology|volume=23|issue=2|pages=194–199|doi=10.1053/anep.2003.50017|issn=0270-9295|pmid=12704579}}</ref> Glomerular hyperfiltration and an aberrant regulation of RAAS lead to increased intraglomerular pressure, causing stress on the endothelial cells, the mesangial cells and the podocytes. This exacerbates the dysfunction caused by the metabolic effects of hyperglycemia.{{citation needed|date=May 2020}}

Metabolic factors include the formation of [[advanced glycation end-product]]s (AGEs), which have a central role in the pathophysiology of many of the complications of diabetes mellitus, including cardiovascular complications.<ref>{{Cite journal|last1=Soldatos|first1=G.|last2=Cooper|first2=M. E.|date=2008-11-13|title=Diabetic nephropathy: Important pathophysiologic mechanisms|url=http://www.sciencedirect.com/science/article/pii/S0168822708004646|journal=Diabetes Research and Clinical Practice|series=The Shiga International Symposium on Diabetic Nephropathy|language=en|volume=82|pages=S75–S79|doi=10.1016/j.diabres.2008.09.042|pmid=18994672|issn=0168-8227|url-access=subscription}}</ref> AGEs are chemical groups that form when a reducing sugar (glucose in this case) reacts non-enzymatically with an amine group, predominantly lysine and arginine, which are attached on proteins, lipids and nucleic acids.<ref>{{Cite journal|last1=Wolffenbuttel|first1=B. H. R.|last2=Boulanger|first2=C. M.|last3=Crijns|first3=F. R. L.|last4=Huijberts|first4=M. S. P.|last5=Poitevin|first5=P.|last6=Swennen|first6=G. N. M.|last7=Vasan|first7=S.|last8=Egan|first8=J. J.|last9=Ulrich|first9=P.|last10=Cerami|first10=A.|last11=Levy|first11=B. I.|date=1998-04-14|title=Breakers of advanced glycation end products restore large artery properties in experimental diabetes|journal=Proceedings of the National Academy of Sciences|volume=95|issue=8|pages=4630–4634|doi=10.1073/pnas.95.8.4630|pmid=9539789|pmc=22541|bibcode=1998PNAS...95.4630W|issn=0027-8424|doi-access=free}}</ref> These [[glycation]] products accumulate on the proteins of vessel wall collagen, forming an irreversible complex of cross-linked AGEs. An important way AGEs exert their effect is through a receptor-mediated mechanism, most importantly by the receptor for advanced glycation end products (RAGE). RAGE is a signal transduction receptor found on a number of cell types including macrophages, endothelial cells, renal mesangial cells and podocytes in the glomerulus.<ref>{{Cite journal|last1=Yan|first1=Shi-Fang|last2=Ramasamy|first2=Ravichandran|last3=Bucciarelli|first3=Loredana G|last4=Wendt|first4=Thoralf|last5=Lee|first5=Larisse K|last6=Hudson|first6=Barry I|last7=Stenr|first7=David M|last8=Lalla|first8=Evanthia|last9=Du Yan|first9=Shi|last10=Rong|first10=Ling Ling|last11=Naka|first11=Yoshifumi|date=May 2004|title=RAGE and its ligands: a lasting memory in diabetic complications?|journal=Diabetes and Vascular Disease Research|volume=1|issue=1|pages=10–20|doi=10.3132/dvdr.2004.001|pmid=16305050|issn=1479-1641|doi-access=free}}</ref> Bindings of AGEs to RAGE receptors enhances production of cytosolic Reactive Oxygen Species (ROS) as well as stimulates intracellular molecules such as Protein Kinase C (PKC), NF-κB and the activation of growth factors TGF-B and vascular endothelial growth factor (VEGF). These factors, along with the hemodynamic changes that occur, lead to podocyte injury, oxidative stress, inflammation and fibrosis. As injury worsens, kidney function decreases and glomerular basement membrane (GBM) become more permeable and less efficient at filtration. This is accompanied by a steady decline in kidney function.{{citation needed|date=May 2020}}

==Diagnosis==
[[File:Ultrasonography of kidney with diabetic nephropathy - annotated.jpg|thumb|left|[[Medical ultrasonography|Ultrasonography]] showing [[Echogenicity|hyperechogenicity]] of the [[renal cortex]], visualized in the image as brighter than the liver.]]
Diagnosis is based on the measurement of abnormal levels of urinary albumin in an individual with diabetes <ref name="lewis20142">{{cite journal|vauthors=Lewis G, Maxwell AP|date=February 2014|title=Risk factor control is key in diabetic nephropathy|journal=The Practitioner|volume=258|issue=1768|pages=13–7, 2|pmid=24689163}}</ref> coupled with exclusion of other causes of albuminuria. Albumin measurements are defined as follows:<ref>{{Cite web|title=CDC – Chronic Kidney Disease – Glossary|url=http://nccd.cdc.gov/ckd/help.aspx?section=G|access-date=2015-07-02}}</ref>

:::::::::::* Normal [[albuminuria]]: urinary albumin excretion <30&nbsp;mg/24h;
:::::::::::* [[Microalbuminuria]]: urinary albumin excretion in the range of 30–299&nbsp;mg/24h;
:::::::::::* [[Macroalbuminuria]]: urinary albumin excretion ≥300&nbsp;mg/24h
::::::::::: Urinary albumin excretion can also be measured by urinary albumin/creatinine ratio in a spot urine sample, which is as accurate but more convenient than a 24-hour urine collection.<ref>{{Cite journal|last1=Umanath|first1=Kausik|last2=Lewis|first2=Julia B.|date=2018-06-01|title=Update on Diabetic Nephropathy: Core Curriculum 2018|journal=American Journal of Kidney Diseases|language=en|volume=71|issue=6|pages=884–895|doi=10.1053/j.ajkd.2017.10.026|pmid=29398179|issn=0272-6386|doi-access=free}}</ref>

It is recommended that individuals with diabetes have their albumin levels checked annually, beginning immediately after a diagnosis of type 2 diabetes and five years after a diagnosis of type 1 diabetes.<ref name="lewis20142" /><ref>{{cite journal|vauthors=Koroshi A|date=July 2007|title=Microalbuminuria, is it so important?|journal=Hippokratia|volume=11|issue=3|pages=105–7|pmc=2658722|pmid=19582202}}</ref> [[Medical imaging]] of the kidneys, generally by [[Medical ultrasonography|ultrasonography]], is recommended as part of a [[differential diagnosis]] if there is suspicion of [[urinary tract obstruction]], [[urinary tract infection]], [[kidney stone]]s or [[polycystic kidney disease]].<ref name="Grossde Azevedo20042">{{cite journal|vauthors=Gross JL, de Azevedo MJ, Silveiro SP, Canani LH, Caramori ML, Zelmanovitz T|date=January 2005|title=Diabetic nephropathy: diagnosis, prevention, and treatment|journal=Diabetes Care|volume=28|issue=1|pages=164–76|doi=10.2337/diacare.28.1.164|pmid=15616252|doi-access=free}}</ref> Conformation kidney biopsy should only be performed if non-diabetic kidney disease is suspected.{{citation needed|date=January 2021}}

Urine analysis in patients with diabetic kidney disease is often bland. In cases of severely increased microalbuminuria, hematuria might be present.<ref>{{Cite journal|last1=Jiang|first1=Shimin|last2=Wang|first2=Yining|last3=Zhang|first3=Zheng|last4=Dai|first4=Peilin|last5=Yang|first5=Yue|last6=Li|first6=Wenge|date=September 2018|title=Accuracy of hematuria for predicting non-diabetic renal disease in patients with diabetes and kidney disease: A systematic review and meta-analysis|journal=Diabetes Research and Clinical Practice|volume=143|pages=288–300|doi=10.1016/j.diabres.2018.07.027|pmid=30059756|s2cid=51880893|issn=0168-8227}}</ref> fat bodies might be present in patients who develop nephrotic-range proteinuria.
{|class="wikitable" style="float:right; margin-left:5px"
|+ Clinical staging<ref name="pmid224391552">{{cite book|url=https://www.ncbi.nlm.nih.gov/books/NBK84558/|title=Chronic Kidney Disease Stages 1–3: Screening, Monitoring, and Treatment [Internet]|vauthors=Fink HA, Ishani A, Taylor BC, Greer NL, MacDonald R, Rossini D, Sadiq S, Lankireddy S, Kane RL, Wilt TJ|chapter=Introduction |date=January 2012|publisher=Agency for Healthcare Research and Quality (US)|pmid=22439155|display-authors=6}}</ref>
!CKD<br>Stage
!eGFR level<br><small>(mL/min/1.73 m<sup>2</sup>)</small>
|-
|Stage 1
| style="text-align:center" |≥ 90
|-
|Stage 2
| style="text-align:center" |60–89
|-
|Stage 3
| style="text-align:center" |30–59
|-
|Stage 4
| style="text-align:center" |15–29
|-
|Stage 5
| style="text-align:center" |< 15
|}

===Staging===
To clinically stage the degree of damage in this (and any) kidney disease, the serum creatinine is determined and used to calculate the estimated glomerular filtration rate ([[Estimated Glomerular Filtration Rate|eGFR]]). Normal eGFR is equal to or greater than 90ml/min/1.73 m<sup>2</sup>.<ref>{{Cite web|title=Glomerular filtration rate: MedlinePlus Medical Encyclopedia|url=https://www.nlm.nih.gov/medlineplus/ency/article/007305.htm|website=www.nlm.nih.gov|access-date=2015-07-02}}</ref>
On biopsy, the following classification has been suggested by Tervaert ''et al.'':<ref name="pmid28316995">{{cite journal |last1=Qi |first1=Chenyang |last2=Mao |first2=Xing |last3=Zhang |first3=Zhigang |last4=Wu |first4=Huijuan |title=Classification and Differential Diagnosis of Diabetic Nephropathy |journal=Journal of Diabetes Research |date=2017 |volume=2017 |pages=8637138 |doi=10.1155/2017/8637138 |pmid=28316995 |pmc=5337846 |issn=2314-6745|doi-access=free }}  [[File:CC-BY icon.svg|50px]]  Text was copied from this source, which is available under a [https://creativecommons.org/licenses/by/4.0/  Creative Commons Attribution 4.0 International License].
</ref>
{|class=wikitable
|+Histopathologic staging
! Class !! Description and criteria
|-
| I || Mild or nonspecific changes on light microscopy and conformed GBM<br>thickening proven by electron microscopy: GBM > 395 nm (female), GBM > 430 nm (male).
|-
| IIa
|
* Mild mesangial expansion in >25% of the observed mesangium.
* Area of mesangial proliferation < area of capillary cavity.
|-
| IIb
|
* Severe mesangial expansion in >25% of the observed mesangium.
* Area of mesangial proliferation < area of capillary cavity.
|-
| III
| At least one convincing nodular sclerosis (Kimmelstiel-Wilson lesion).
|-
| IV
| Advanced diabetic glomerulosclerosis in >50% of glomeruli.
|}

=== Biomarkers ===
Although albuminuria is the most frequently used marker of DN, it has a limited sensitivity as many patients with diabetic nephropathy experience GFR loss and glomerulosclerosis without immediate elevation in albuminuria. Many novel markers are currently being studied that potentially detect diabetic nephropathy at earlier stages and identify progression risk. Cystatin C is a protein that is freely filtered in the glomeruli before it is reabsorbed and catabolized in the renal tubular cells. Its serum level is independent of muscle mass, making more accurate at estimating GFR than creatinine serum levels.{{citation needed|date=May 2020}}

== Treatment ==
The goals of treatment are to slow the progression of kidney damage and control related complications. Management of diabetic nephropathy currently centers over four main areas: Cardiovascular risk reduction, glycemic control, blood pressure control as well as inhibition of the RAAS system.{{citation needed|date=May 2020}}

Cardiovascular risk reduction: Patients with diabetes mellitus are at significantly increased risk of cardiovascular disease, which is also an independent risk factor for kidney failure. Therefore, it is important to aggressively manage cardiovascular risk factors in patients with diabetes mellitus and in particular those with diabetic nephropathy. The main components of managing cardiovascular disease is with tobacco cessation, lipid-lowering therapies (e.g., statins) as well as regular exercise and healthy eating.<ref>{{Cite journal|date=2008-06-12|title=Effects of Intensive Glucose Lowering in Type 2 Diabetes|journal=New England Journal of Medicine|volume=358|issue=24|pages=2545–2559|doi=10.1056/nejmoa0802743|pmid=18539917|pmc=4551392|issn=0028-4793|author1=Action to Control Cardiovascular Risk in Diabetes Study Group|last2=Gerstein|first2=H. C.|last3=Miller|first3=M. E.|last4=Byington|first4=R. P.|last5=Goff Jr|first5=D. C.|last6=Bigger|first6=J. T.|last7=Buse|first7=J. B.|last8=Cushman|first8=W. C.|last9=Genuth|first9=S.|last10=Ismail-Beigi|first10=F.|last11=Grimm Jr|first11=R. H.|last12=Probstfield|first12=J. L.|last13=Simons-Morton|first13=D. G.|last14=Friedewald|first14=W. T.}}</ref> In patients with kidney disease, atorvastatin is preferred over other statins as it does not require dose-adjustment based on GFR.<ref>{{Cite journal|last1=Bianchi|first1=Stefano|last2=Bigazzi|first2=Roberto|last3=Caiazza|first3=Alberto|last4=Campese|first4=Vito M.|date=2003-03-01|title=A controlled, prospective study of the effects of atorvastatin on proteinuria and progression of kidney disease|url=http://www.sciencedirect.com/science/article/pii/S0272638602692479|journal=American Journal of Kidney Diseases|language=en|volume=41|issue=3|pages=565–570|doi=10.1053/ajkd.2003.50140|pmid=12612979|issn=0272-6386|url-access=subscription}}</ref>

Glycemic control: Multiple studies have found a positive effect of improved glycemic control on clinical outcomes of patients with diabetic nephropathy.<ref>{{Cite journal|last1=DCCT/EDIC Research Group|last2=de Boer|first2=Ian H.|last3=Sun|first3=Wanjie|last4=Cleary|first4=Patricia A.|last5=Lachin|first5=John M.|last6=Molitch|first6=Mark E.|last7=Steffes|first7=Michael W.|last8=Zinman|first8=Bernard|date=2011-12-22|title=Intensive diabetes therapy and glomerular filtration rate in type 1 diabetes|journal=The New England Journal of Medicine|volume=365|issue=25|pages=2366–2376|doi=10.1056/NEJMoa1111732|issn=1533-4406|pmc=3270008|pmid=22077236}}</ref> Intensive glycemic control also reduces the rate of other DM complications, such as retinopathy and neuropathy. Glycemic control is maintained mainly with insulin in patients with Type 1 DM and with hypoglycemic agents and/or insulin in patients with type 2 DM. Studies showed a decrease in microvascular complications of diabetic nephropathy with a target goal HbA1c concentration of 7%. Further reduction in the HbA1c did not correlate with better outcomes and is thus not recommended in most patients as it could increase the risk of hypoglycemic episodes.<ref>{{Cite journal|date=2008-06-12|title=Intensive Blood Glucose Control and Vascular Outcomes in Patients with Type 2 Diabetes|journal=New England Journal of Medicine|volume=358|issue=24|pages=2560–2572|doi=10.1056/nejmoa0802987|pmid=18539916|issn=0028-4793|author1=ADVANCE Collaborative Group|last2=Patel|first2=A.|last3=MacMahon|first3=S.|last4=Chalmers|first4=J.|last5=Neal|first5=B.|last6=Billot|first6=L.|last7=Woodward|first7=M.|last8=Marre|first8=M.|last9=Cooper|first9=M.|last10=Glasziou|first10=P.|last11=Grobbee|first11=D.|last12=Hamet|first12=P.|last13=Harrap|first13=S.|last14=Heller|first14=S.|last15=Liu|first15=L.|last16=Mancia|first16=G.|last17=Mogensen|first17=C. E.|last18=Pan|first18=C.|last19=Poulter|first19=N.|last20=Rodgers|first20=A.|last21=Williams|first21=B.|last22=Bompoint|first22=S.|last23=De Galan|first23=B. E.|last24=Joshi|first24=R.|last25=Travert|first25=F.|url=https://espace.library.uq.edu.au/view/UQ:690128/UQ690128_OA.pdf|hdl=10072/26242|hdl-access=free}}</ref><ref>{{Cite journal|last1=Duckworth|first1=W.|last2=Abraira|first2=C.|last3=Moritz|first3=T.|date=April 2009|title=Glucose Control and Vascular Complications in Veterans with Type 2 Diabetes|journal=Journal of Vascular Surgery|volume=49|issue=4|pages=129–39|doi=10.1016/j.jvs.2009.02.026|pmid=19092145|issn=0741-5214|doi-access=free}}</ref>

Blood pressure control: Multiple randomized clinical trials have demonstrated a benefit of decreasing systolic blood pressure to <140 mmHg in patients with diabetic nephropathy. High blood pressure is associated with accelerated development of microalbuminuria, over proteinuria and declining kidney function. Angiotensin-converting-enzyme inhibitors, as well as angiotensin II receptor blockers, are particularly helpful in patients with diabetes to lower blood pressure and slow the progression of nephropathy.<ref>{{Cite journal|date=2010-04-29|title=Effects of Intensive Blood-Pressure Control in Type 2 Diabetes Mellitus|journal=New England Journal of Medicine|volume=362|issue=17|pages=1575–1585|doi=10.1056/nejmoa1001286|pmid=20228401|issn=0028-4793|author1=ACCORD Study Group|last2=Cushman|first2=W. C.|last3=Evans|first3=G. W.|last4=Byington|first4=R. P.|last5=Goff Jr|first5=D. C.|last6=Grimm Jr|first6=R. H.|last7=Cutler|first7=J. A.|last8=Simons-Morton|first8=D. G.|last9=Basile|first9=J. N.|last10=Corson|first10=M. A.|last11=Probstfield|first11=J. L.|last12=Katz|first12=L.|last13=Peterson|first13=K. A.|last14=Friedewald|first14=W. T.|last15=Buse|first15=J. B.|last16=Bigger|first16=J. T.|last17=Gerstein|first17=H. C.|last18=Ismail-Beigi|first18=F.|pmc=4123215}}</ref> More intensive blood pressure lowering (125-130/<80) in patients with diabetic mellitus has been shown to decrease the risk of progression of diabetic nephropathy as well as other diabetic complications.<ref>{{Cite journal|title=Faculty Opinions recommendation of BP Control and Long-Term Risk of ESRD and Mortality.|last=Ruilope|first=Luis|date=2017-04-19|doi=10.3410/f.726630344.793530925 |doi-access=free }}</ref> Some patients might require dual therapy to adequately control pressure, in which case calcium channel blockers or diuretics are a good second-line option.<ref>{{Cite journal|title=Faculty Opinions recommendation of Benazepril plus amlodipine or hydrochlorothiazide for hypertension in high-risk patients.|last=Townsend|first=Raymond|date=2009-01-07|doi=10.3410/f.1142854.599941 |doi-access=free }}</ref>

RAAS inhibition: Inhibition can be achieved with multiple therapies, mainly ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors, and mineralocorticoid antagonists. RAAS inhibition has been proven to be the most effective therapy to slow the progression of diabetic nephropathy in all stages.<ref>{{Cite journal|last1=Lewis|first1=Edmund J.|last2=Hunsicker|first2=Lawrence G.|last3=Bain|first3=Raymond P.|last4=Rohde|first4=Richard D|date=1993-11-11|title=The Effect of Angiotensin-Converting-Enzyme Inhibition on Diabetic Nephropathy|journal=New England Journal of Medicine|volume=329|issue=20|pages=1456–1462|doi=10.1056/nejm199311113292004|pmid=8413456|issn=0028-4793|doi-access=free}}</ref> Although RAAS blockade using more than one agent may further reduce proteinuria, the risk of adverse events (such as hyperkalemia, acute kidney injury) outweigh the potential benefits.<ref>{{Cite journal|last1=Fried|first1=Linda F.|last2=Emanuele|first2=Nicholas|last3=Zhang|first3=Jane H.|last4=Brophy|first4=Mary|last5=Conner|first5=Todd A.|last6=Duckworth|first6=William|last7=Leehey|first7=David J.|last8=McCullough|first8=Peter A.|last9=O'Connor|first9=Theresa|last10=Palevsky|first10=Paul M.|last11=Reilly|first11=Robert F.|date=2013-11-14|title=Combined Angiotensin Inhibition for the Treatment of Diabetic Nephropathy|journal=New England Journal of Medicine|volume=369|issue=20|pages=1892–1903|doi=10.1056/nejmoa1303154|pmid=24206457|s2cid=205095632 |issn=0028-4793|doi-access=free}}</ref> Therefore, it is recommended that only one agent is used in patients with DM who have hypertension or any signs of microalbuminuria or diabetic nephropathy.<ref>{{Cite journal|last1=Brenner|first1=Barry M.|last2=Cooper|first2=Mark E.|last3=de Zeeuw|first3=Dick|last4=Keane|first4=William F.|last5=Mitch|first5=William E.|last6=Parving|first6=Hans-Henrik|last7=Remuzzi|first7=Giuseppe|last8=Snapinn|first8=Steven M.|last9=Zhang|first9=Zhonxin|last10=Shahinfar|first10=Shahnaz|date=2001-09-20|title=Effects of Losartan on Renal and Cardiovascular Outcomes in Patients with Type 2 Diabetes and Nephropathy|journal=New England Journal of Medicine|volume=345|issue=12|pages=861–869|doi=10.1056/nejmoa011161|pmid=11565518|hdl=2445/122643|issn=0028-4793|hdl-access=free}}</ref>

About half of insulin is metabolized and cleared by the kidneys. This means that as kidney function worsens in the setting of DN, some patients with insulin-dependent DM may find that their regular insulin doses are lasting longer than normal, or that they are experiencing an increasing frequency of hypoglycemic episodes. It is also crucial to closely monitor kidney function to properly dose medications that are cleared by the kidneys. Some of the most commonly used nephrotoxic medications are non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen.<ref>{{Cite journal|last1=Khan|first1=Kanwar Nasir M.|last2=Burke|first2=Allen|last3=Stanfield|first3=Kristina M.|last4=Harris|first4=Richard K.|last5=Baron|first5=David A.|date=2001-01-01|title=Expression of Cyclooxygenase-2 in the Macula Densa of Human Kidney in Hypertension, Congestive Heart Failure, and Diabetic Nephropathy|journal=Renal Failure|volume=23|issue=3–4|pages=321–330|doi=10.1081/JDI-100104716|pmid=11499548|s2cid=11727215|issn=0886-022X|doi-access=free}}</ref>
With worsening kidney function, it might also be necessary to follow a renal-diet to avoid complications such as hyperkalemia and metabolic acidosis. Some evidence suggests that limiting dietary protein could slow the progression of DN, but further evidence is needed to confirm this benefit.<ref>{{Cite journal|last1=Hansen|first1=Henrik P.|last2=Tauber-Lassen|first2=Ellis|last3=Jensen|first3=Berit R.|last4=Parving|first4=Hans-Henrik|date=July 2002|title=Effect of dietary protein restriction on prognosis in patients with diabetic nephropathy|journal=Kidney International|volume=62|issue=1|pages=220–228|doi=10.1046/j.1523-1755.2002.00421.x|pmid=12081581|issn=0085-2538|doi-access=free}}</ref> Patients with diabetic nephropathy might go on to develop end stage renal disease and require kidney transplantation or hemodialysis.{{citation needed|date=May 2020}}

=== Emerging therapies ===
A relatively new medication that has been approved for treatment for DM is sodium glucose cotransporter 2 (SGLT2) inhibitors. The mechanism of action of this drug is to the sodium-glucose uptake cotransporter in the proximal tubule, thereby generating natriuresis and glucosuria. In multiple clinical trials, SGLT2 inhibitors showed improved cardiovascular outcomes in patients with DM as well a positive effect on kidney outcomes, mainly a reduction in albuminuria and progression of renal damage.<ref>{{Cite journal|last1=Heerspink|first1=Hiddo J.L.|last2=Perkins|first2=Bruce A.|last3=Fitchett|first3=David H.|last4=Husain|first4=Mansoor|last5=Cherney|first5=David Z. I.|date=2016-09-06|title=Sodium Glucose Cotransporter 2 Inhibitors in the Treatment of Diabetes Mellitus|journal=Circulation|volume=134|issue=10|pages=752–772|doi=10.1161/circulationaha.116.021887|pmid=27470878|issn=0009-7322|doi-access=free}}</ref><ref>{{Cite journal|last1=Wanner|first1=Christoph|last2=Inzucchi|first2=Silvio E.|last3=Lachin|first3=John M.|last4=Fitchett|first4=David|last5=von Eynatten|first5=Maximilian|last6=Mattheus|first6=Michaela|last7=Johansen|first7=Odd Erik|last8=Woerle|first8=Hans J.|last9=Broedl|first9=Uli C.|last10=Zinman|first10=Bernard|date=2016-07-28|title=Empagliflozin and Progression of Kidney Disease in Type 2 Diabetes|journal=New England Journal of Medicine|volume=375|issue=4|pages=323–334|doi=10.1056/nejmoa1515920|pmid=27299675|issn=0028-4793|doi-access=free}}</ref> Other classes of diabetic medications that have been shown to have a positive effect on the progression of diabetic nephropathy are GLP-1 agonists and DPP-4 inhibitors.<ref>{{Cite journal |last=Panchapakesan |first=Usha |last2=Mather |first2=Amanda |last3=Pollock |first3=Carol |date=2012-09-07 |title=Role of GLP-1 and DPP-4 in diabetic nephropathy and cardiovascular disease |url=https://portlandpress.com/clinsci/article-abstract/124/1/17/69079/Role-of-GLP-1-and-DPP-4-in-diabetic-nephropathy |journal=Clinical Science |volume=124 |issue=1 |pages=17–26 |doi=10.1042/CS20120167 |issn=0143-5221|url-access=subscription }}</ref>

=== Education and self-management ===
The success of diabetic nephropathy management depends greatly upon the ability of individuals to self-manage this condition, encompassing glycaemic control, and the adoption of healthy lifestyles. Appropriate self-management often requires patient education and behavioural counselling. However, there is still insufficient evidence to draw conclusions regarding the effects, regarding both benefits and harms, of educational programmes for people with diabetic nephropathy.<ref>{{Cite journal|last1=Li|first1=Ting|last2=Wu|first2=Hong Mei|last3=Wang|first3=Feng|last4=Huang|first4=Chang Quan|last5=Yang|first5=Ming|last6=Dong|first6=Bi Rong|last7=Liu|first7=Guan J|date=2011-06-15|editor-last=Cochrane Kidney and Transplant Group|title=Education programmes for people with diabetic kidney disease|url=https://doi.wiley.com/10.1002/14651858.CD007374.pub2|journal=Cochrane Database of Systematic Reviews|issue=6|pages=CD007374|language=en|doi=10.1002/14651858.CD007374.pub2|pmid=21678365|url-access=subscription}}</ref>

==Prognosis==
Diabetic nephropathy in type 2 diabetes can be more difficult to predict because the onset of diabetes is not usually well established. Without intervention, 20–40 percent of patients with type 2 diabetes/microalbuminuria, will evolve to macroalbuminuria.<ref>{{Cite journal|last=Shlipak|first=Michael|date=2011-03-15|title=Clinical Evidence Handbook: Diabetic Nephropathy: Preventing Progression – American Family Physician|url=http://www.aafp.org/afp/2011/0315/p732.html|journal=American Family Physician|volume=83|issue=6|pages=732|access-date=2015-06-27|name-list-style=vanc}}</ref> Diabetic nephropathy is the most common cause of [[end-stage kidney disease]],<ref name="Fernandez201422"/><ref name="Ding201522"/> which may require [[hemodialysis]] or even [[kidney transplantation]].<ref name="ReferenceB22"/> It is associated with an increased [[Mortality rate|risk of death]] in general, particularly from [[cardiovascular disease]].<ref name="Fernandez201422" /><ref name="Pálsson R 201422"/>

== Epidemiology ==
Diabetic nephropathy affects approximately a third of patients with type 1 and type 2 diabetes mellitus. Diabetic nephropathy is responsible for about a third of cases of ESRD worldwide, and an even larger fraction in the developed countries.<ref>{{Cite journal|last1=Zimmet|first1=Paul|last2=Alberti|first2=K. G. M. M.|last3=Shaw|first3=Jonathan|date=December 2001|title=Global and societal implications of the diabetes epidemic|journal=Nature|volume=414|issue=6865|pages=782–787|doi=10.1038/414782a|pmid=11742409|bibcode=2001Natur.414..782Z|s2cid=4384190|issn=0028-0836|url=https://repositorio.unal.edu.co/handle/unal/79579}}</ref> Worldwide, the prevalence of diabetes is projected to increase from 382 million in 2013, to over 592 million by 2035. This increase is projected to be sharpest in developed countries. The prevalence of type 2 DM is particularly increasing due to the rising prevalence of obesity worldwide.<ref>{{Cite journal|last1=Cameron|first1=Adrian J|last2=Zimmet|first2=Paul Z|last3=Atkins|first3=Robert C|last4=Shaw|first4=Jonathan E|date=2007|title=The Australian Diabetes, Obesity and Lifestyle Study – Profiling Diabetes and Cardiovascular Disease Risk in the Nation|journal=European Endocrinology|issue=2|pages=20|doi=10.17925/ee.2007.00.02.20|issn=1758-3772|doi-access=free}}</ref> Diabetic kidney disease progression could lead to ESRD as well as an increased risk of cardiovascular complications, all of which cause a substantial economic burden. The estimated cost of management of patients with ESRD due to diabetic nephropathy in the US is US$39.35 billion in 2010.<ref>{{Cite journal|last1=Trivedi|first1=Hariprasad S.|last2=Pang|first2=Michael M.H.|last3=Campbell|first3=Anne|last4=Saab|first4=Paulette|date=April 2002|title=Slowing the progression of chronic renal failure: Economic benefits and patients' perspectives|journal=American Journal of Kidney Diseases|volume=39|issue=4|pages=721–13|doi=10.1053/ajkd.2002.31990|pmid=11920337|issn=0272-6386}}</ref> Within developed countries, certain ethnic groups such as African Americans and Native Americans are at higher risk of developing diabetic nephropathy and ESRD.<ref>{{Cite journal|last=Disease|first=Ethnicity &|date=2018-10-17|title=Correction: Ethn Dis. 2010;20:[Suppl 1]:S1-60-S1-64|journal=Ethnicity & Disease|volume=28|issue=4|pages=586|doi=10.18865/ed.28.4.586|doi-broken-date=14 February 2025 |pmid=30405305|pmc=6200305|issn=1945-0826|doi-access=free}}</ref>

== See also ==
* [[Diabetic diet]]
* [[Hyperbaric medicine]]
* [[Nephrology]]

== References ==
{{Reflist|32em}}

== Further reading ==
{{refbegin|32em}}
* {{Cite web|title = Effects of renin-angiotensin system blockers on renal outcomes and all-cause mortality in patients with diabetic nephropathy: an updated meta-analysis|url = http://www.crd.york.ac.uk/CRDWeb/ShowRecord.asp?AccessionNumber=12009100199|website = www.crd.york.ac.uk|access-date = 2015-07-02}}
* {{cite journal | vauthors = Gross JL, de Azevedo MJ, Silveiro SP, Canani LH, Caramori ML, Zelmanovitz T | title = Diabetic nephropathy: diagnosis, prevention, and treatment | journal = Diabetes Care | volume = 28 | issue = 1 | pages = 164–76 | date = January 2005 | pmid = 15616252 | doi = 10.2337/diacare.28.1.164 | doi-access = free }}
* {{cite journal | vauthors = Tziomalos K, Athyros VG | title = Diabetic Nephropathy: New Risk Factors and Improvements in Diagnosis | journal = The Review of Diabetic Studies | volume = 12 | issue = 1–2 | pages = 110–8 | year = 2015 | pmid = 26676664 | pmc = 5397986 | doi = 10.1900/RDS.2015.12.110 }}
* {{cite journal | vauthors = Kume S, Koya D, Uzu T, Maegawa H | title = Role of nutrient-sensing signals in the pathogenesis of diabetic nephropathy | journal = BioMed Research International | volume = 2014 | pages = 315494 | date = 2014 | pmid = 25126552 | pmc = 4122096 | doi = 10.1155/2014/315494 | doi-access = free }}
* {{cite journal | vauthors = Doshi SM, Friedman AN | title = Diagnosis and Management of Type 2 Diabetic Kidney Disease | journal = Clinical Journal of the American Society of Nephrology | volume = 12 | issue = 8 | pages = 1366–1373 | date = August 2017 | pmid = 28280116 | pmc = 5544517 | doi = 10.2215/CJN.11111016  }}
{{refend}}

== External links ==
{{Medical resources
|  DiseasesDB      =
|  ICD10           = E10.2, E11.2, E12.2, E13.2, E14.2
|  ICD9            = {{ICD9|250.4}}
|  ICDO            =
|  OMIM            =
|  MedlinePlus     = 000494
|  eMedicineSubj   =
|  eMedicineTopic  =
|  MeshID          = D003928
}}
{{Scholia|topic}}
{{Glomerular disease}}

{{Diabetes}}

{{Authority control}}

{{DEFAULTSORT:Diabetic Nephropathy}}
[[Category:Kidney diseases]]
[[Category:Vascular diseases]]
[[Category:Complications of diabetes]]