Overview of hypertension in acute and chronic kidney disease
- Johannes FE Mann, MD
Johannes FE Mann, MD
- Professor of Medicine
- Friedrich Alexander University of Erlangen-Nürnberg
- International Scholar, Population Health Research Institute, McMaster University, Canada
- Section Editors
- George L Bakris, MD
George L Bakris, MD
- Editor-in-Chief — Nephrology
- Section Editor — Hypertension
- Professor of Medicine
- The University of Chicago
- Norman M Kaplan, MD
Norman M Kaplan, MD
- Editor-in-Chief — Nephrology
- Section Editor — Hypertension
- Clinical Professor of Internal Medicine
- University of Texas Southwestern Medical Center
Hypertension is a frequent finding in both acute and chronic kidney disease, particularly with glomerular or vascular disorders . 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 . 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 . Although these changes are most prominent with severe disease, the incidence of hypertension is increased even in patients with a normal serum creatinine concentration . 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 . 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 . 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.To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- PATHOGENESIS OF HYPERTENSION IN KIDNEY DISEASE
- Acute glomerular disease
- Acute vascular disease
- Chronic kidney disease
- TREATMENT OF HYPERTENSION IN ACUTE GLOMERULAR OR VASCULAR DISEASE
- TREATMENT OF HYPERTENSION IN CHRONIC KIDNEY DISEASE
- Goal blood pressure
- - Technique of blood pressure measurement
- Benefits of sodium restriction
- Use of diuretics and goal of therapy
- Choice of antihypertensive therapy
- - Sequence of antihypertensive therapy in proteinuric CKD
- First-line therapy in proteinuric CKD
- Second- and third-line therapy in proteinuric CKD
- - Sequence of antihypertensive therapy in nonproteinuric CKD
- - Fourth-line therapy with other agents
- Possible benefit from nocturnal therapy
- Maintenance dialysis
- SUMMARY AND RECOMMENDATIONS