関: diabetic kidney disease、diabetic nephropathy、nodular glomerulosclerosis

WordNet

suffering from diabetes
someone who has diabetes
of or relating to or causing diabetes

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糖尿病の / 糖尿病患者

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/04/21 16:51:14」(JST)

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Diabetic nephropathy (or diabetic kidney disease^[1]) is a progressive kidney disease caused by damage to the capillaries in the kidneys' glomeruli.^[2] It is characterized by nephrotic syndrome and diffuse scarring of the glomeruli. It is due to longstanding diabetes mellitus, and is a prime reason for dialysis in many developed countries. It is classified as a small blood vessel complication of diabetes.^[3]

Signs and symptoms

During its early course, diabetic nephropathy often has no symptoms.^[4] Symptoms can take 5 to 10 years to appear after the kidney damage begins.^[4] These late symptoms include severe tiredness, headaches, a general feeling of illness, nausea, vomiting,frequent voiding, lack of appetite, itchy skin, and leg swelling.^[4]

Causes

Illustration depicting diabetic nephropathy

The cause of diabetic nephropathy is not well understood, but it is thought that high blood sugar, advanced glycation end product formation, and cytokines may be involved in the development of diabetic nephropathy.^[5]

Kidney damage is likely if one or more of the following is present:^[4]

Poor control of blood glucose
High blood pressure
Type 1 diabetes mellitus (before age 20)
History of cigarette smoking
A family history of kidney problems

Mechanism

Diabetes causes a number of changes to the body's metabolism and blood circulation, which likely combine to produce excess reactive oxygen species (chemically reactive molecules containing oxygen). These changes damage the kidney's glomeruli (networks of tiny blood vessels), which leads to the hallmark feature of albumin in the urine (called albuminuria).^[6] As diabetic nephropathy progresses, a structure in the glomeruli known as the glomerular filtration barrier (GFB) is increasingly damaged.^[7] This barrier is composed of three layers including the fenestrated endothelium, the glomerular basement membrane, and the epithelial podocytes.^[7] The GFB is responsible for the highly selective filtration of blood entering the kidney's glomeruli and normally only allows the passage of water, small molecules, and very small proteins (albumin does not pass through the intact GFB).^[7]

Diagnosis

CKD Stage^[8]	eGFR level (mL/min/1.73 m²)
Stage 1	≥ 90
Stage 2	60 – 89
Stage 3	30 – 59
Stage 4	15 – 29
Stage 5	< 15

Diagnosis is usually based on the measurement of high levels of albumin in the urine or evidence of reduced kidney function.^[9] Albumin measurements are defined as follows:^[10]

Normal albuminuria: urinary albumin excretion <30 mg/24h;
Microalbuminuria: urinary albumin excretion in the range of 30–299 mg/24h;
Clinical (overt) albuminuria: urinary albumin excretion ≥300 mg/24h.

People with diabetes are recommended to have their albumin levels checked annually, beginning immediately after diagnosis for type 2 diabetics, and five years after diagnosis for type 1 diabetics.^[9]^[11] To test kidney function, the person's estimated glomerular filtration rate (eGFR) is measured from a blood sample. Normal eGFR ranges from 90 to 120 ml/min/1.73 m².^[12]

Treatment

ACE inhibitor

The goals of treatment are to slow the progression of kidney damage and control related complications. The main treatment, once proteinuria is established, is ACE inhibitor medications, which usually reduce proteinuria levels and slow the progression of diabetic nephropathy.^[13] Other issues that are important in the management of this condition include control of high blood pressure and blood sugar levels (see diabetes management), as well as the reduction of dietary salt intake.^[14]

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.^[15]

Diabetic nephropathy is the most common cause of end-stage kidney disease,^[7]^[16] which may require hemodialysis or even kidney transplantation.^[17] It is associated with an increased risk of death in general, particularly from cardiovascular disease.^[7]^[18]

Epidemiology

In the U.S., diabetic nephropathy affected an estimated 6.9 million people during 2005–2008.^[19] The number of people with diabetes and consequently diabetic nephropathy is expected to rise substantially by the year 2050.^[20]

References

^ Kittell F (2012). "Diabetes Management". In Thomas LK, Othersen JB. Nutrition Therapy for Chronic Kidney Disease. CRC Press. p. 198.
^ "diabetic nephropathy". Retrieved 2015-06-27.
^ Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p.2982
^ ^a ^b ^c ^d "Diabetes and kidney disease: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-27.
^ "Diabetic Nephropathy: Background, Pathophysiology, Etiology". 2015-06-20.
^ Cao, Zemin; Cooper, Mark E (2011). "Pathogenesis of diabetic nephropathy". Journal of Diabetes Investigation 2 (4): 243–247. doi:10.1111/j.2040-1124.2011.00131.x. ISSN 2040-1116. PMC: 4014960. PMID 24843491.
^ ^a ^b ^c ^d ^e Mora-Fernández C, Domínguez-Pimentel V, de Fuentes MM, et al. (2014). "Diabetic kidney disease: from physiology to therapeutics". J. Physiol. (Lond.) 592 (Pt 18): 3997–4012. doi:10.1113/jphysiol.2014.272328. PMID 24907306.
^ Fink, Howard A.; Ishani, Areef; Taylor, Brent C.; Greer, Nancy L.; MacDonald, Roderick; Rossini, Dominic; Sadiq, Sameea; Lankireddy, Srilakshmi; Kane, Robert L. (2012). "Introduction".
^ ^a ^b Lewis G, Maxwell AP (2014). "Risk factor control is key in diabetic nephropathy". Practitioner 258 (1768): 13–7, 2. PMID 24689163.
^ "CDC - Chronic Kidney Disease - Glossary". Retrieved 2015-07-02.
^ Koroshi, A (2007). "Microalbuminuria, is it so important?". Hippokratia 11 (3): 105–107. ISSN 1108-4189. PMC: 2658722. PMID 19582202.
^ "Glomerular filtration rate: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-07-02.
^ Lim, Andy KH (2014). "Diabetic nephropathy – complications and treatment". International Journal of Nephrology and Renovascular Disease 7: 361–381. doi:10.2147/IJNRD.S40172. ISSN 1178-7058. PMC: 4206379. PMID 25342915.
^ "Diabetic Nephropathy Treatment & Management: Approach Considerations, Glycemic Control, Management of Hypertension". 2015-06-20.
^ Shlipak, Michael. "Clinical Evidence Handbook: Diabetic Nephropathy: Preventing Progression - American Family Physician". www.aafp.org. Retrieved 2015-06-27.
^ Ding Y, Choi ME (January 2015). "Autophagy in diabetic nephropathy". J Endocrinol 224 (1): R15–30. doi:10.1530/JOE-14-0437. PMC: 4238413. PMID 25349246.
^ Lizicarova D, Krahulec B, Hirnerova E, Gaspar L, Celecova Z (2014). "Risk factors in diabetic nephropathy progression at present". Bratisl Lek Listy 115 (8): 517–21. doi:10.4149/BLL_2014_101. PMID 25246291.
^ Pálsson R, Patel UD (2014). "Cardiovascular complications of diabetic kidney disease". Adv Chronic Kidney Dis 21 (3): 273–80. doi:10.1053/j.ackd.2014.03.003. PMC: 4045477. PMID 24780455.
^ Lerma, Edgar V. (2014-01-01). Diabetes and Kidney Disease. Springer. ISBN 9781493907939.
^ Lai, K. N.; Tang, S. C. W. (2011-06-08). Diabetes and the Kidney. Karger Medical and Scientific Publishers. ISBN 9783805597432.

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 糖尿病性腎症の概要 overview of diabetic nephropathy
2. 糖尿病性腎症の治療 treatment of diabetic nephropathy
3. 糖尿病性腎症における腎移植 renal transplantation in diabetic nephropathy
4. 糖尿病性腎疾患を有する女性における妊娠 pregnancy in women with diabetic kidney disease
5. 糖尿病性腎症における透析 dialysis in diabetic nephropathy

English Journal

Fatty Acid-Binding Protein 4 mediates apoptosis via endoplasmic reticulum stress in mesangial cells of diabetic nephropathy.

Yao F1, Li Z2, Ehara T3, Yang L4, Wang D5, Feng L5, Zhang Y5, Wang K5, Shi Y1, Duan H1, Zhang L6.
Molecular and cellular endocrinology.Mol Cell Endocrinol.2015 Aug 15;411:232-42. doi: 10.1016/j.mce.2015.05.003. Epub 2015 May 6.
Type 2 diabetes is characterized by hyperglycemia and deregulated lipid metabolism with increased plasma non-esterified fatty acids (NEFA). Apoptosis of glomerular cells is a hallmark in diabetic glomerulosclerosis. Fatty acid-binding protein 4 (FABP4), a carrier protein for fatty acids, has been li
PMID 25958041

Translational value of animal models of kidney failure.

Ortiz A1, Sanchez-Niño MD2, Izquierdo MC2, Martin-Cleary C3, Garcia-Bermejo L4, Moreno JA3, Ruiz-Ortega M5, Draibe J6, Cruzado JM6, Garcia-Gonzalez MA7, Lopez-Novoa JM8, Soler MJ9, Sanz AB10; Red de Investigacion Renal (REDINREN) and Consorcio Madrileño para investigación del fracaso renal agudo (CIFRA).
European journal of pharmacology.Eur J Pharmacol.2015 Jul 15;759:205-20. doi: 10.1016/j.ejphar.2015.03.026. Epub 2015 Mar 24.
Acute kidney injury (AKI) and chronic kidney disease (CKD) are associated with decreased renal function and increased mortality risk, while the therapeutic armamentarium is unsatisfactory. The availability of adequate animal models may speed up the discovery of biomarkers for disease staging and the
PMID 25814248

Predicting non-diabetic renal disease in type 2 diabetic adults: The value of glycated hemoglobin.

Pallayova M1, Mohammed A2, Langman G3, Taheri S4, Dasgupta I5.
Journal of diabetes and its complications.J Diabetes Complications.2015 Jul;29(5):718-23. doi: 10.1016/j.jdiacomp.2014.12.005. Epub 2014 Dec 13.
AIMS: The indications for renal biopsy in type 2 diabetes mellitus (T2D) are not well established. We investigated the prevalence, spectrum, and predictors of biopsy-proven non-diabetic renal disease (NDRD) in T2D.METHODS: An observational, single-center, retrospective study of T2D adults who underw
PMID 25633572

Japanese Journal

チアノーゼ腎症の病理

本田一穂,小田秀明,西川俊郎
東京女子医科大学雑誌 84(E2), E237-E243, 2014-03-31
チアノーゼ腎症(cyanotic nephropathy: CN)は、チアノーゼ型先天性心疾患(cyanotic congenital heart disease: CCHD)に合併する腎障害である。一般にCNの臨床症状は軽いが、ネフローゼ症候群を合併したり腎不全に進行したりする症例が稀に存在する。CNの腎糸球体形態変化は極めて顕著で、その発症機序に対する関心が高い。その特徴的な病理変化は、糸球体 …
NAID 110009770490

Expression of Toll-Like Receptor 4 in Glomerular Endothelial Cells under Diabetic Conditions

Takata Shunsuke,Sawa Yoshihiko,Uchiyama Takanobu,Ishikawa Hiroyuki
ACTA HISTOCHEMICA ET CYTOCHEMICA 46(1), 35-42, 2013
… Diabetic conditions promote glomerulosclerosis by mesangial cells but the mechanisms are not fully elucidated. … The present study evaluated the expression of toll-like receptor 4 in glomerular endothelial cells in the streptozotocin (STZ)-induced type 1 diabetic mouse (ICR-STZ) and the type 2 diabetic KK/TaJcl mouse which were fed a high fat diet feed (KK/Ta-HF). …
NAID 130003361070

糖尿病腎症の病理診断 (特集糖尿病腎症 : 成因,診断,治療法の最近の進歩)

守屋達美,小川惇郎,山岸貴洋
内分泌・糖尿病・代謝内科 34(6), 509-516, 2012-06
NAID 40019382372

Related Pictures

★リンクテーブル★

リンク元	「糖尿病性腎症」「diabetic kidney disease」
拡張検索	「nodular diabetic glomerulosclerosis」
関連記事	「diabetic」

「糖尿病性腎症」

Diabetic nephropathy
	Scarred glomeruli in the kidney of a person with diabetic nephropathy
Classification and external resources
Specialty	endocrinology
ICD-10	E10.2, E11.2, E12.2, E13.2, E14.2
ICD-9-CM	250.4
MedlinePlus	000494
MeSH	D003928
	[edit on Wikidata]

　　[★]

英: diabetic nephropathy
同: 糖尿病腎症。糖尿病性腎硬化症 diabetic nephrosclerosis、糖尿病性糸球体硬化症 diabetic glomerulosclerosis
関: 糖尿病、糸球体硬化糸球体硬化症、結節性糖尿病性糸球体硬化症

[show details]

糖尿病性腎症 : 約 281,000 件
糖尿病腎症 : 約 45,700 件

概念

糖尿病の三大合併症(糖尿病性網膜症・糖尿病性腎症・糖尿病性神経症)の一つ
糖尿病の細小血管病変を基礎ととして糖尿病性糸球体硬化症(結節性糸球体硬化症病変)を来たして蛋白尿、浮腫、高血圧、ついには腎不全をきたす病態。
透析療法導入の原因疾患の1位
顕性蛋白尿が出現するには糖尿病発症後6-10年程度は必要である。糖尿病発症後25-30年度には末期腎不全となる。(YN.D-99)

疫学

5-10年以上の糖尿病罹患者

1型糖尿病の場合は10年以上、2型の場合は5年以上の罹病期間の存在する傾向がある

女性に多い

病理

ひまん性結節性糸球体硬化症病変

糸球体病変の特徴：基底膜の肥厚、びまん性メサンギウム硬化症、結節性糸球体硬化症(BPT.782-783)

結節性糸球体硬化症病変が見られる →　キンメルスティール・ウィルソン病変(Kimmelstiel-Wilson lesion)
腎糸球体の内皮細胞の変性(glomerular lesion)、基底膜の肥厚による血流障害(renal vascular lesion, arteriolosclerosis, pyelonephritis inducing necrotizing papillitis)、血液成分の漏出が原因でメサンギウムが増生し、糸球体構造が破壊され、機能の障害が引き起こされる。

病態生理

糸球体内皮の変性、基底膜肥厚、血漿成分漏出　→　メサンギウム増生・フィブリン沈着、糸球体破壊、間質線維化、糸球体高血圧(→GFR増加、微量アルブミン尿)

経過

糖尿病の発症と主に(GFR,Ccrで代用)が増大(140ml/分)。
随時尿の蛋白30 mg/gクレアチニン超：腎臓に構造的問題が発生
随時尿の蛋白300 mg/gクレアチニン超：顕性腎症：尿蛋白持続陽性状態、GFR低下傾向の開始

症状

http://www.ikedaiin.com/img/keika.gif

治療

第1 期(腎症前期)　　：　　　血糖コントロール
第2 期(早期腎症)　　：厳格な血糖コントロール、降圧療法
第3A期(顕性腎症前期)：厳格な血糖コントロール、降圧療法、蛋白制限食
第3B期(顕性腎症後期)：　　　　　　　　　　　　厳格な降圧療法、蛋白制限食
第4 期(腎不全期　　)：　　　　　　　　　　　　厳格な降圧療法、蛋白制限食、透析療法導入
第5 期(透析療法期　)：透析療法、腎移植

降圧療法

降圧目標：130/80 mmHg (拡張期血圧の方が厳密)、尿蛋白1g/日以上では125/75mmHgを目指す
薬物：

アンジオテンシン転換酵素阻害薬、アンジオテンシンII受容体阻害薬　→　血清Ccr≧3mgの場合、腎機能悪化、高カリウム血症を惹起しうるので禁
カルシウム拮抗薬

蛋白制限

蛋白制限食(0.8g/kg以下)を第3A期から施行することで、尿蛋白の減少と腎障害の進行を抑制できる

透析導入

尿路感染症

糖尿病では尿路感染を伴うことが多い。

診断

以下の症状で見られる場合、糖尿病性腎症と診断できる
5-10年以上の糖尿病罹患者
糖尿病性網膜症
蛋白尿が主体の尿所見