Diabetes & The Body

Treating Hypertension in Diabetic Nephropathy

In Type 1 diabetes (IDDM), hypertension usually develops after renal impairment. The hypertension subsequently accelerates the decrease in renal function. Type 2 diabetes (NIDDM), the adult and most common type of diabetes, is associated with obesity. Diabetic nephropathy is generally accompanied by other diabetic complications including hypertension, retinopathy, and vascular (blood vessel) changes, although these may not be obvious during the early stages of nephropathy.

Nephropathy may be present for many years before nephrotic syndrome or chronic renal failure develops. It is often diagnosed when routine urinalysis shows protein in the urine. Uncontrolled diabetes causes damage to many tissues of the body. Kidney damage caused by diabetes most often involves thickening and hardening (sclerosis) of the internal kidney structures, particularly the glomerulus (kidney membrane).

Control of hypertension in patients with diabetic nephropathy improves mortality and slows progression to end-stage renal disease. However, blood pressure is difficult to treat; multiple drug combination therapy is required and treatment algorithms to establish this are lacking. Researchers used a stepped-care algorithm, centered on maximum doses of an ACE inhibitor or angiotensin II receptor blocker, to treat hypertension according to American Diabetes Association recommended blood pressure target goals (<130/80 mmHg) in patients with diabetic nephropathy.

About 49 consecutive patients were treated with diabetes (13 with type 1 and 36 with type 2), diabetic nephropathy, and proteinuria ³500 mg/24 h with a stepped-care blood pressure treatment algorithm. The level of blood pressure control achieved at most recent follow-up was assessed.

Patients were followed for a median of 18 months (range 9–48). Mean blood pressure achieved was 140/75 ± 23/14 mmHg in patients with type 1 diabetes and 146/76 ± 22/14 mmHg in patients with type 2 diabetes. Target blood pressure was reached in 16 (33%) patients, 6 of 13 patients with type 1 diabetes and 10 of 36 patients with type 2 diabetes, whereas systolic blood pressure remained above the target level in the remaining patients. There was no difference in baseline blood pressure, proteinuria, or serum creatinine level between patients who were treated to target and those who were not. Levels of blood pressure control similar to those achieved in clinical trials in diabetic nephropathy were obtained with a stepped-care algorithm. However, in most patients, systolic blood pressure was difficult to control despite the use of multiple drug combination therapy.

About 40% of people with insulin-dependent diabetes will eventually develop end-stage renal disease. 80% of people with diabetic nephropathy as a result of IDDM have had this diabetes for 18 or more years. At least 20% of people with NIDDM will develop diabetic nephropathy, but the time course of development of the disorder is much more variable than in IDDM. The risk is related to the control of the blood-glucose levels. Risk is higher if glucose is poorly controlled than if the glucose level is well controlled. The management of the hypertensive diabetic patient involves a three-prong approach: 1) control of blood pressure, 2) control of glucose and 3) control of lipids. The middle-aged or older diabetic patient is assumed to have underlying coronary heart disease. The dyslipidemia should be vigorously treated to reduce the LDL cholesterol below 100 mg/dl. Glycemic control can also improve abnormal lipid levels, especially triglycerides.

This vigorous treatment of the hypertensive diabetic patient can yield gratifying results in lowering cardiovascular complications, but it is expensive and beyond the reach of many in developing countries. However, even small decreases in blood pressure can reduce complications, therefore control of hypertension is the most effective way of slowing kidney damage from diabetic nephropathy.