no diabetes1


no diabetes1


Titrate to diastolic BP Optimal BP Suboptimal BP

<140/85 <150/90

< 80 <130/80 < 140/85

<125/75 < 130/80

ABM = Ambulatory blood pressure monitoring.

1 In those with high cardiovascular risk and initial BP 140-159/90-99 mm Hg there could be a case for adopting the targets for diabetic patients (British Hypertension Society 1999).

ABM = Ambulatory blood pressure monitoring.

1 In those with high cardiovascular risk and initial BP 140-159/90-99 mm Hg there could be a case for adopting the targets for diabetic patients (British Hypertension Society 1999).

1970s and has subsequently produced several guidelines, the first in 1975. New guidelines have recently appeared also related to hypertension in diabetes. Several of these new guidelines have a similar approach. There is a clear emphasis on early and effective antihypertensive treatment in patients with diabetes suggesting a lower threshold for the start of the treatment and also a lower goal during treatment. ACE inhibitors are often preferred as initial agents but combination therapy is often warranted. In view of the recent observation that different types of drugs (ACE-I, p-blockers, calcium channel blockers and diuretics) reduce cardiovascular risks in type 2 diabetes, there are different treatment options. In diabetic renal disease, ACE-I is however preferred. We should aim to achieve a BP around 135/85 mmHg during treatment, or lower.

The British Hypertension Society proposes: (1) 'The threshold for antihypertensive treatment in type 1 diabetes is > 140/90 mm Hg. The target BP is <130/80 mmHg, or lower (<125/75 mmHg) when there is proteinuria > 1 g/24 h'. And (2): 'Trials support treatment of all patients with type 2 diabetes and BP > 140/90 mm Hg, aiming for a target BP < 130/80 mm Hg. BPs < 140/85 mm Hg on treatment should be considered suboptimal.' (3) ' Thus there is evidence from outcome trials in hypertensive patients with diabetes for the efficacy and safety of ACE inhibitors, p-blockers, dihydropyrid-ines, and low-dose thiazides. The choice among these drug classes should be made using the criteria set out for nondiabetic patients. BP control will usually require more than one antihypertensive drug, and about 30% of hypertensive patients with diabetes need three or more agents in combination.' A similar approach is seen in table 6.

The problem is that it may be difficult to achieve such BP with patients with proteinuria and overt renal disease and also in others with cardiovascular problems. Therefore, it is strongly advocated to start treatment early, e.g. with development of microalbuminuria, even in patients with normal BP. It has also been proposed to start treatment even before microalbuminuria. Since complications are so closely associated with BP increase (also in the normal range) this could easily be recommended in future guidelines as we now have effective treatment modalites with rather limited side effects.

Summary Notes

This chapter clearly documents that excess albuminuria, often accompanied by increased BP, is associated with actual or subsequent organ damage, not only in the kidney but also in other organs, especially in the eyes and in the heart. In the kidney, abnormal albuminuria starting in the microalbumi-nuric range reflects more advanced glomerular structural lesions, although the exact location of the permeability defect has not been defined at an ultrastructural level. BP elevation may not initiate the glomerular permeability defect but high systemic BP aggravates the course of established lesions and clinical disease. Transition from micro- to macroalbuminuria is associated with a reduction in GFR, the key parameter in evaluation of renal function.

Biochemical and hemodynamic hypotheses have been put forward supported by animal models, but these notions are difficult to substantiate in humans, where isolated phenomena cannot be studied, and direct measurement of e.g. glomerular wall charge and intraglomerular pressure is not feasible. A unifying concept would be attractive, comprising biochemical aberrations, such as charge defects, changes in enzymatic activities and glycation phenomena as well as hemodynamic changes such as hyperfiltration with elevated glomerular pressure, aggravated by early systemic BP rise. This may be seen along with vascular and endothelial changes, reflected by increases in von Willebrand factor, circulating prorenin as well as increased transcapillary escape rate of albumin and dyslipidemia. Antioxidant status may also play a role. A common pathway explaining all or most of these abnormalities should be pursued, with the basis in prolonged hyperglycemia and related biochemical changes, characteristic for the diabetic state.

However, when diabetic complications are evolving as a consequence of hyperglycemia, increasing BP remains a decisive factor in promoting organ damage in the kidney, and antihypertensive treatment seems to be the therapeutic cornerstone in ameliorating deterioration in organ function. A low protein diet may also reduce albuminuria and the fall rate in GFR. However, strict antihypertensive therapy may limit the need for any dramatic reduction of the protein content of the diet.

Suggested Reading

American Diabetes Association: Diabetic nephropathy. Diabetes Care 2000;23(suppl 1): 69-72.

Charurvedi N: HOPE and extension of the indications for ACE-inhibitors? Lancet 2000;355, in press.

Curb JD, Pressel SL, Cutler JA, Savage PJ, Applegate WB, Black H, et al: Effect of diuretic-based antihypertensive treatment on cardiovascular disease risk in older diabetic patients with isolated systolic hypertension. Systolic Hypertension in the Elderly Program Cooperative Research Group. JAMA 1996;276:1886-1892.

Estacio RO, Jeffers BW, Hiatt WR, Biggerstaff SL, Gifford N, Schrier RW: The effect of nisoldipine as compared with enalapril on cardiovascular outcomes in patients with non-insulin-dependent diabetes and hypertension. N Engl J Med 1998;338:645-652.

Feldt-Rasmussen B, Mathiesen ER, Jensen T, Lauritzen T, Deckert T: Effect of improved metabolic control on loss of kidney function in type 1 (insulin-dependent) diabetic patients: An update of the Steno studies. Diabetologia 1991;34:164-170.

Forsblom C, Trenkwalder P, Dahl K, Mulder H, on behalf of the Multicenter Study Group: Angiotensin II receptor blockers in type 2 diabetic patients with microalbuminuria. Nephrol Dial Transplant 1998;13:1069.

Gsde P, Vedel P, Parving HH, Pedersen O: Intensified multifactorial intervention in patients with type 2 diabetes mellitus and microalbuminuria: The Steno type 2 randomised study. Lancet 1999;353: 617-622.

Guidelines (1999) for the management of hypertension: Memorandum from a World Health Organization/ International Society of Hypertension Meeting. J Hypertens 1999;17:151-183.

Hansson L, Lindholm LH, Niskanen L, et al: Effect of angiotensin-converting enzyme inhibition compared with conventional therapy on cardiovascular morbidity and mortality in hypertension: The Captopril Prevention Project (CAPPP) Randomised Trial. Lancet 1999;353:611-616.

Hansson L, Zanchetti A, Carruthers SG, et al, for the HOT Study Group: Effects of intensive BP lowering and low-dose aspirin in patients with hypertension: Principal results of the Hypertension Optimal Treatmen (HOT) randomised trial. Lancet 1998;351:1755-1762.

Jacobsen P, Rossing K, Rossing P, Tartow L, Mallet C, Poirier O, Cambien F, Parving HH: Angiotensin converting enzyme gene polymorphism and ACE inhibition in diabetic nephropathy. Kidney Int 1998;53:1002-1006.

Lewis EJ, Hunsicker LG, Bain RP, Rhode RD: The effect of angiotensin-converting-enzyme inhibition on nephropathy. N Engl J Med 1993;329:1456-1462.

Mathiesen ER, Hommel E, Hansen HP, Parving HH: Preservation of normal GFR in type 1 diabetic patients with microalbuminuria under long-term (8 years) ACE inhibition. Nephrol Dial Transplant 1998;13:1062.

Microalbuminuria Collaborative Study Group, UK: Intensive therapy and progression to clinical albuminuria in patients with insulin-dependent diabetes mellitus and microalbuminuria. BMJ 1995;311: 973-977.

Mogensen CE: Combined high BP and glucose in type 2 diabetes: Double jeopardy (editorial). BMJ 1998;317:693-694.

Mogensen CE (ed): The Kidney and Hypertension in Diabetes mellitus. Boston, Kluwer Academic, 2000.

Mogensen CE: Microalbuminuria, blood pressure and diabetic renal disease: Origin and development of ideas. Diabetologia 1999;42:263-285.

Mogensen CE, Keane WF, Bennett PH, Jerums G, Parving HH, Passa P, Steffes MW, Striker GE, Viberti GC: Prevention of diabetic renal disease with special reference to microalbuminuria. Lancet 1995; 346:1080-1084.

Mogensen CE, Mau Pedersen M, Ebbeh0j E, Poulsen PL, Schmitz A: Combination therapy in hypertension-associated diabetic renal disease. Int J Clin Pract 1997;90(suppl):52-58.

N0rgaard K, Rasmussen E, Jensen T, Giese J, Feldt-Rasmussen B: Essential hypertension and type 1 diabetes. Am J Hypertens 1993;6:830-836.

Nyberg G, Norden G, Attman PO, Aurell M, Uddebom G, Lenner RA, Isaksson B: Diabetic nephropathy: Is dietary protein harmful? J Diabetes Complications 1987;1:37-40.

0sterby R, Schmitz A, Nyberg G, Asplund J: Renal structural changes in insulin-dependent diabetic patients with albuminuria. Comparison of cases with onset of albuminuria after short or long duration. APMIS 1998;106:361-370.

Parving HH: Renoprotection in diabetes: Genetic and non-genetic risk factors and treatment. Diabetologia 1998;41:745-759.

Ravid M, Brosh D, Levi Z, Bar-Dayan Y Ravid D, Rachmani R: Use of enalapril to attenuate decline in renal function in normotensive patients with type 2 diabetes mellitus. A randomized controlled trial. Ann Intern Med 1998;128:982-988.

Tarnow L, Gluud C, Parving HH: Diabetic nephropathy and the insertion/deletion polymorphism of the angiotensin-converting enzyme gene. Nephrol Dial Transplant 1998;13:1125-1130.

Tatti P, Pahor M, Byington RP, Di Mauro P, Guarisco RG, Strollo G, Strollo F: Outcome results of the fosinopril versus amlodipine cardiovascular events randomized trials (FACET) in patients with hypertension and NIDDM. Diabetes Care 1998;21:597-603.

Turner R, Holman R, Stratton I, Cull C, Frighi V, Manley S, et al, for United Kingdom Prospective Diabetes Study Group: Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: United Kingdom Prospective Diabetes Study 38. BMJ 1998;317: 703-713.

UKPDS 34: Effect of an intensive blood glucose control policy with metformin on complications in type 2 diabetic patients. Lancet 1998;352:854-865.

Zeller K, Whittakerm E, Sullivan L, Raskin P, Jacobson HR: Effect of restricting dietary protein on the progression of renal failure in patients with insulin-dependent diabetes mellitus. N Engl J Med 1991;324:78-84.

Carl Erik Mogensen, Medical Department M (Diabetes and Endocrinology), Kommunehospitalet, Arhus University Hospital, DK-8000 Arhus C (Denmark) Tel. +45 89492011, Fax +45 86137852, E-Mail [email protected]

Belfiore F, Mogensen CE (eds): New Concepts in Diabetes and Its Treatment. Basel, Karger, 2000, pp 174-185

Chapter XII

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