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Diabetes mellitus and the kidney 

Diabetes mellitus and the kidney

Diabetes mellitus and the kidney

Rudolf Bilous


July 30, 2015: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.


Discussion modified to reflect (1) recent debate as to the benefit of intensive glucose control in people with type 2 diabetes; (2) the possibility of harm being caused by reducing blood pressure below standard target values; (3) the fact that multiple blockade of the renin-angiotensin system is no longer recommended.

Updated on 28 Nov 2013. The previous version of this content can be found here.
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date: 29 April 2017

Diabetic nephropathy is the commonest cause of endstage renal disease in the developed world, causing 44% of prevalent cases requiring renal replacement therapy in the United States of America in 2010 and 15.2% in the United Kingdom in 2011. Incident rates have been stable in the UK at around 24% of all new patients accepted onto RRT for the last few years. Most patients have type 2 diabetes, and in some countries the proportion with endstage renal disease who have type 1 diabetes is falling.

Aetiology and pathology—causation is related to glycaemic control (e.g. glycation of proteins, oxidative stress, sorbitol overproduction, alteration in growth factors), hypertension, genetic factors, and dietary and other environmental factors. Pathological hallmarks are thickening of the glomerular basement membrane and mesangial expansion, with or without nodule formation, secondary to an accumulation of extracellular matrix.

Staging and natural history—is classically described in terms of urinary albumin excretion rate (UAER): (1) normoalbuminuria—UAER less than 20 µg/min, albumin/creatinine ratio (ACR) less than 2.5 mg/mmol (men), less than 3.5 mg/mmol (women); (2) microalbuminuria (also called incipient nephropathy)—UAER 20 to 200 µg/min, ACR 2.5 to 30 mg/mmol (men), 3.5 to 30 mg/mmol (women); and (3) clinical proteinuria (sometimes called clinical nephropathy or overt nephropathy)—UAER greater than 200 µg/min, ACR greater than 30 mg/mmol. This staging maps better to the latest classification of chronic kidney disease based upon estimated glomerular filtration rate (eGFR) (see Chapters 21.4 and 21.6).

Clinical features—most patients (>60%) will have a normal UAER throughout their diabetic life, but 1 to 2% of the remainder develop persistent microalbuminuria each year. Once UAER exceeds 200 µg/min, there tends to be a relentless increase in proteinuria, occasionally into the nephrotic range, and GFR declines progressively at a rate that largely depends on blood pressure control.

Prevention—in both type 1 and type 2 diabetes, tight glycaemic control can prevent microalbuminuria. Whether intensive blood pressure control using angiotensin converting enzyme (ACE) inhibitors can prevent microalbuminuria is controversial. In both type 1 and type 2 diabetes, intensive blood pressure control using ACE inhibitors or angiotensin II receptor blockers (ARBs) slows progression from microalbuminuria to clinical proteinuria and slows the rate of decline in GFR in those with clinical proteinuria.

Management—aims for: (1) good control of glycaemia (typical recommendations are for HbA1c level <7.5% (58 mmol/mol) (NICE) and <7.0% (53 mmol/mol) (American Diabetes Association) in type 1 and 6.5–7.5% (48 – 58 mmol/mol) in type 2); (2) good control of hypertension (<130/80 mmHg) using an ACE inhibitor or an ARB; and (3) other interventions, including some or all of serum lipid lowering, low-dose aspirin, smoking cessation and reduction of dietary protein and salt.

Prognosis—mortality is higher for people with diabetes and increased albuminuria compared to those with normoalbuminuria. In type 2 diabetes, the annual mortality is almost 5% for patients with clinical proteinuria, and almost 20% for those with a serum creatinine greater than 175 µmol/litre or in endstage renal disease. Survival on dialysis remains worse for patients with diabetes compared to those without, although overall rates are improving. Cardiovascular disease is the commonest cause of death, and multifactorial cardiovascular risk-factor intervention has been shown to reduce mortality and morbidity in people with type 2 diabetes and microalbuminuria, and is recommended for all patients with diabetic nephropathy.

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