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Review
. 2011 Apr;13(4):252-7.
doi: 10.1111/j.1751-7176.2011.00446.x.

Pathophysiology, prevention and management of chronic kidney disease in the hypertensive patient with diabetes mellitus

Anna Solini  1 , Ele Ferrannini
Affiliations
Review

Pathophysiology, prevention and management of chronic kidney disease in the hypertensive patient with diabetes mellitus

Anna Solini et al. J Clin Hypertens (Greenwich). 2011 Apr.

Abstract

The authors concisely review the main clinical issues arising in the management of the hypertensive patient with type 2 diabetes, in whom chronic kidney disease is prevalent and heralds increased cardiovascular morbidity and mortality. Special attention is paid to the clinical meaning, relevance and limits of albumin excretion and glomerular filtration rate, the two widely used markers of reduced kidney function during the course of chronic diseases like diabetes and hypertension. The main therapeutic strategies involving blood pressure and glycemic control, treatment of dyslipidemia and improvement of lifestyle are discussed from the viewpoint of a general practitioner dealing with the clinical complexity of these patients.

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Figures

Figure 1
Figure 1
The clinical triad of diabetic nephropathy. GFR indicates glomerular filtration rate; GBM, glomerular basement membrane; BP, blood pressure; T2DM, type 2 diabetes mellitus; ESRD, end‐stage renal disease.
Figure 2
Figure 2
Estimated glomerular filtration rate (eGFR) (by the Chronic Kidney Disease Epidemiology Collaboration [CKD‐EPI] formula) in type 2 diabetic patients with or without hypertension by category of urinary albumin excretion. Data from the Renal Insufficiency and Cardiovascular Events (RIACE) study (ClinicalTrials.gov, NCT00715481).
Figure 3
Figure 3
Interpretation of increased albumin excretion (UAE) and reduced glomerular filtration rate (GFR) in kidney disease of type 2 diabetes. Hyperglycemia leads to increased UAE through the typical glomerular lesions (glomerular membrane thickening, podocyte loss). Aging and associated comorbidities (hypertension and dyslipidemia) lead to mostly atherosclerotic vascular damage, which per se reduces GFR. The two “hits” cross each other, as atherosclerotic vascular damage is also a long‐term consequence of chronic hyperglycemia and microvascular dysfunction is known to be associated with hypertension and dyslipidemia even in nondiabetic individuals.
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References

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