Overview of hypertension in acute and chronic kidney disease

INTRODUCTION

Hypertension is a frequent finding in both acute and chronic kidney disease, particularly with glomerular or vascular disorders [1]. The pathogenesis and preferred treatment of hypertension vary with the type of renal disease and its duration. This topic will summarize the pathogenesis and treatment of hypertension in patients with acute and chronic kidney disease and then direct the reader, when necessary, to more detailed discussions in other topics.  

PATHOGENESIS OF HYPERTENSION IN KIDNEY DISEASE

The pathogenesis of hypertension varies with the type of disease (eg, glomerular versus vascular) and with the duration of disease (acute versus chronic).

Acute glomerular disease — Patients with acute glomerular disease, such as poststreptococcal glomerulonephritis, tend to be volume expanded and edematous due to sodium retention [2]. As a result, the elevation in blood pressure is primarily due to fluid overload, as evidenced by suppression of the renin-angiotensin-aldosterone system and enhanced release of atrial natriuretic peptide [3]. Although these changes are most prominent with severe disease, the incidence of hypertension is increased even in patients with a normal serum creatinine concentration [4]. Both a familial predisposition to hypertension and subclinical volume expansion are thought to be important in this setting.

Experimental studies of the nephrotic syndrome or glomerulonephritis suggest that sodium retention in these disorders is due to increased reabsorption in the collecting tubules [5]. Two different abnormalities in collecting tubule function have been identified in glomerular disease, both of which could increase sodium reabsorption:

• Relative resistance to atrial natriuretic peptide, due at least in part to more rapid degradation of the second messenger cyclic GMP (guanosine monophosphate) by the enzyme phosphodiesterase [4]. In an animal model of nephrotic syndrome, infusion of a phosphodiesterase inhibitor largely reverses this defect and restores the normal natriuretic response to volume expansion.
• Increased activity of the Na-K-ATPase pump in the cortical collecting tubule but not other nephron segments [6]. This pump provides the energy for active sodium transport by pumping reabsorbed sodium out the cell into the peritubular capillary.