Diabetic nephropathy overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Diabetic nephropathy from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Ali Poyan Mehr, M.D. [2] Associate Editor(s)-in-Chief: Olufunmilola Olubukola M.D.[3]

Overview

Diabetic kidney disease (Diabetic Nephropathy) is the most common cause of chronic kidney disease and end stage renal disease (ESRD) in the United States [1] . Due to the ongoing world wide increase in the incidence of diabetes mellitus, Diabetic nephropathy (DN) is increasingly a major cause of ESRD disease worldwide [2].

Diabetic Nephropathy affects male and female patients equally. The incidence of DN in African-Americans, Native Americans and people of Mexican origins is greater than the incidence in white Americans [3]. Currently, the main goal in the treatment of diabetic nephropathy is to slow the progression of chronic kidney disease. This is achieved by excellent control of hyperglycemia, dyslipidemia, and blood pressure. Antiproteinuric therapy through renin-angiotensin-aldosterone system Inhibitors is considered to be a major pillar of the treatment [4]. Renin-angiotensin-aldosterone system inhibition it thought to be beneficial in the early stages of diabetic nephropathy through decreasing proteinuria and progression [5]. Therefore, early diagnosis and institution of prompt treatment is very important in the management of diabetes nephropathy. Also, the role of diabetes prevention becomes paramount patients at high risk (e.g. metabolic syndrome, impaired glucose tolerance).

Diabetic nephropathy (DN) is characterized by the presence of proteinuria or decreased renal function in patients with diabetes mellitus[6][7][8] however, diabetic nephropathy can also present in form of non-proteinuric decline in GFR. Nonetheless, proteinuria remains the hallmark of diagnosis for diabetic nephropathy, despite emerging trends suggestive of non proteinuric diabetic nephropathy. [9]

Early Diabetic Nephropathy

The range of proteinuria in early DN is shown below[6][7][8]:

  • Males: Microalbuminuria in the range of 30-300 mg/24 hrs or a spot urinary albumin/creatinine ratio of 30-300 mg/g
  • Females: Microalbuminuria in the range of 30-300 mg/24 hrs or a spot urinary albumin/creatinine ratio of 20-200 mg/g

Overt Diabetic Nephropathy

Overt DN is defined according to the presence of proteinuria or according to renal function. The following ranges in overt DN are shown below[6][7][8]:

  • Proteinuria > 500 mg/24 hrs or albuminuria > 300 mg/24 hrs.
  • Estimated glomerular filtration rate (eGFR) < 60 ml/min/1.73m2

Historical Perspective

Diabetic nephropathy was first described by Clifford Wilson and Paul Kimmelstiel in 1936.

Classification

Diabetic nephropathy can be classified according to the type of underlying diabetes mellitus or the histopathological findings of the disease.

Pathophysiology

Diabetic nephropathy is a serious complication in patients with long standing Type 1 or Type 2 Diabetes Mellitus. It usually occurs in about 10 to 15 years following the onset of diabetes mellitus. Poor glycemic control, dyslipidemia, smoking, and environmental and genetic factors play important roles in the development of diabetic nephropathy.

Causes

The exact cause of diabetic nephropathy is unknown. However, it is thought that hyperfiltration through the renal glomeruli may be responsible for the manifestations of the disease.

Differentiating Diabetic nephropathy from other Diseases

Diabetic nephropathy should be differentiate from other causes of glomerular disease such as nephritic syndromenephrotic syndromeFabry's disease, poststreptococcal glomerulonephritis, lupus nephritisantiglomerular basement membrane disease (goodpasture's syndrome)CryoglobulinemiaHenoch-Schönlein purpuraamyloidosis, pulmonary-renal syndromes (vasculitis), thin basement membrane diseaseAlport's Syndromeanti-GBM Diseasehypertensive nephrosclerosis, and subacute bacterial endocarditis. The various types of glomerular diseases may be differentiated from each other based on associations, presence of pitting edema, hemeturia, hypertensionhemoptysisoliguria, peri-orbital edema, hyperlipidemia, type of antibodieslight and electron microscopic features.

Epidemiology and Demographics

In the United States, prevalence of diabetic nephropathy (DN) has increased from 7.4% to 9.6% within a 20 years period (1988 to 2008), and this trend will likely continue due to the increasing incidence of diabetes in the American populace . Studies by de Boer et al showed that DN accounts for 44% of new ESRD cases with 6% attributed to type 1 DM, 38% attributed to type 2 DM, and a projected increase of 3 million cases over the course of 20 years. This increased incidence and prevalence of DN is notably greater among African Americans, Asians, and Native Americans than it is among Caucasians.

Risk Factors

Risk factors of diabetic nephropathy can be modifiable such as hypertensiondyslipidemia, and smoking or non-modifiable such as advanced age and positive family history.

Screening

Microalbuminuria is an excellent tool for the early detection of diabetic nephropathy.

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Patients with diabetic nephropathy can develop the manifestations of renal failure such as edema and unintentional weight gain late in the course of the disease.

Physical Examination

The majority of patients with diabetic nephropathy are asymptomatic. However, patients may present with other signs of diabetes mellitus or chronic renal failure.

Laboratory Findings

Microalbuminuria, as defined by an urinary albumin-to-creatinine ratio of >30mg/g is an early diagnostic clue to diabetic nephropathy. Some patients may go on to develop high-grade nephrotic range proteinuria, while others may develop diabetic nephropathy without any measurable albuminuria.

Other Diagnostic Studies

The diagnosis of diabetic nephropathy is based on history, physical examination and laboratory investigations. Renal imaging, such as ultrasound, is often done to rule out other kidney and urinary tract pathologies. However, the ultrasound findings in diabetic nephropathy are highly non-specific and may be normal. Some of the findings in chronic kidney disease due to diabetic nephropathy or other causes include: reduced renal length, reduced renal cortical thickness, increased renal cortical echogenicity, poor visibility of the renal pyramids and the renal sinus, marginal irregularities, papillary calcifications.

Treatment

Medical Therapy

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 drugs, which usually reduce glomerular hypertension, proteinuria levels, systemic hypertension and slow the progression of diabetic nephropathy.

Primary Prevention

Primary prevention of diabetic nephropathy is aimed at preventing diabetes in the first place.

Secondary Prevention

Once diabetic nephropathy develops, secondary prevention to halt the progression of the disease is aimed at strict control of blood pressure, blood glucose levels, as well as lipids.

References

  1. John S (2016). "Complication in diabetic nephropathy". Diabetes Metab Syndr. 10 (4): 247–249. doi:10.1016/j.dsx.2016.06.005. PMID 27389078.
  2. Tuttle KR, Bakris GL, Bilous RW, Chiang JL, de Boer IH, Goldstein-Fuchs J; et al. (2014). "Diabetic kidney disease: a report from an ADA Consensus Conference". Diabetes Care. 37 (10): 2864–83. doi:10.2337/dc14-1296. PMC 4170131. PMID 25249672.
  3. Baudy A, Batuman V (2015). "Non-diabetic renal disease in diabetic patients: How to identify? When to biopsy?". J Diabetes Complications. 29 (5): 613–4. doi:10.1016/j.jdiacomp.2015.04.015. PMID 25957005.
  4. Lozano-Maneiro L, Puente-García A (2015). "Renin-Angiotensin-Aldosterone System Blockade in Diabetic Nephropathy. Present Evidences". J Clin Med. 4 (11): 1908–37. doi:10.3390/jcm4111908. PMC 4663476. PMID 26569322.
  5. Kasiske BL, Kalil RS, Ma JZ, Liao M, Keane WF (1993). "Effect of antihypertensive therapy on the kidney in patients with diabetes: a meta-regression analysis". Ann Intern Med. 118 (2): 129–38. PMID 8416309.
  6. 6.0 6.1 6.2 Mogensen CE, Christensen CK (1984). "Predicting diabetic nephropathy in insulin-dependent patients". N Engl J Med. 311 (2): 89–93. doi:10.1056/NEJM198407123110204. PMID 6738599.
  7. 7.0 7.1 7.2 Mogensen CE (1984). "Microalbuminuria predicts clinical proteinuria and early mortality in maturity-onset diabetes". N Engl J Med. 310 (6): 356–60. doi:10.1056/NEJM198402093100605. PMID 6690964.
  8. 8.0 8.1 8.2 Reutens AT, Atkins RC (2011). "Epidemiology of diabetic nephropathy". Contrib Nephrol. 170: 1–7. doi:10.1159/000324934. PMID 21659752.
  9. MacIsaac RJ, Panagiotopoulos S, McNeil KJ, Smith TJ, Tsalamandris C, Hao H; et al. (2006). "Is nonalbuminuric renal insufficiency in type 2 diabetes related to an increase in intrarenal vascular disease?". Diabetes Care. 29 (7): 1560–6. doi:10.2337/dc05-1788. PMID 16801579.

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