ESSENTIALS OF DIAGNOSIS
Evidence of diabetes mellitus, typically over 10 years.
Albuminuria usually precedes decline in GFR.
Other end-organ damage, such as retinopathy, is common.
Diabetic nephropathy is the most common cause of ESRD in the United States. The incidence is approximately 30% in both type 1 and type 2 diabetes mellitus. ESRD is much more likely to develop in persons with type 1 diabetes mellitus, in part due to fewer comorbidities and deaths before ESRD ensues. With the current epidemic of obesity and type 2 diabetes mellitus, rates of diabetic nephropathy are projected to continue to increase. Patients at higher risk include males, African Americans, Native Americans, and those with a family history of kidney disease. Mortality rates are higher for diabetics with kidney disease compared to those without CKD.
Diabetic nephropathy develops about 10 years after the onset of diabetes mellitus. It may be present at the time type 2 diabetes mellitus is diagnosed. The first stage of classic diabetic nephropathy is hyperfiltration with an increase in GFR, followed by the development of microalbuminuria (30–300 mg/day). With progression, albuminuria increases to greater than 300 mg/day and can be detected on a urine dipstick as overt proteinuria; the GFR subsequently declines over time. Yearly screening for microalbuminuria is recommended for all diabetic patients to detect disease at its earliest stage; however, diabetic nephropathy can, less commonly present as nonproteinuric CKD.
The most common lesion in diabetic nephropathy is diffuse glomerulosclerosis, but nodular glomerulosclerosis (Kimmelstiel-Wilson nodules) is pathognomonic. The kidneys are usually enlarged. Kidney biopsy is not required in most patients unless atypical findings are present, such as sudden onset of proteinuria, nephritic spectrum features (see above), massive proteinuria (greater than 10 g/day), urinary cellular casts, or rapid decline in GFR.
Patients with diabetes are prone to other renal diseases. These include papillary necrosis, chronic interstitial nephritis, and type 4 (hyporeninemic hypoaldosteronemic) renal tubular acidosis. Patients are more susceptible to AKI from many insults, including intravenous contrast material and concomitant use of an ACE inhibitor or ARB with NSAID. Diabetic patients with normal kidney function, however, do not appear to be at increased risk for contrast nephropathy. If a contrast study is essential for patients with CKD, adequate hydration can help prevent AKI. The PRESERVE trial supports the use of intravenous 0.9% (normal) saline, 1–3 mL/kg for 1–12 hours (usually 6 hours) administered both before and after the contrast. Patients at highest risk for radiographic contrast nephropathy are those with GFR less than 30 mL/min/1.73 m2.
With the onset of microalbuminuria, aggressive treatment is necessary. Strict glycemic control should be emphasized early in diabetic nephropathy, with recognition of risk of hypoglycemia as CKD becomes advanced (see CKD section). Recommended blood pressure goals should be tailored to the individual patient: based on the ACCORD trial, those with microalbuminuria (30–300 mg/day) and preserved GFR and those with significant CVD likely derive little ...