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Overview of hypertension in acute and chronic kidney disease

Johannes FE Mann, MD
Section Editors
George L Bakris, MD
Norman M Kaplan, MD
Deputy Editor
John P Forman, MD, MSc


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.


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.

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Literature review current through: Nov 2017. | This topic last updated: Jul 28, 2016.
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  1. Bakris GL, Ritz E. The message for World Kidney Day 2009: hypertension and kidney disease: a marriage that should be prevented. Kidney Int 2009; 75:449.
  2. Catapano F, Chiodini P, De Nicola L, et al. Antiproteinuric response to dual blockade of the renin-angiotensin system in primary glomerulonephritis: meta-analysis and metaregression. Am J Kidney Dis 2008; 52:475.
  3. Rodríguez-Iturbe B, Colic D, Parra G, Gutkowska J. Atrial natriuretic factor in the acute nephritic and nephrotic syndromes. Kidney Int 1990; 38:512.
  4. Valentin JP, Qiu C, Muldowney WP, et al. Cellular basis for blunted volume expansion natriuresis in experimental nephrotic syndrome. J Clin Invest 1992; 90:1302.
  5. Buerkert J, Martin DR, Trigg D, Simon EE. Sodium handling by deep nephrons and the terminal collecting duct in glomerulonephritis. Kidney Int 1991; 39:850.
  6. Zolty E, Ibnou-Zekri N, Izui S, et al. Glomerulonephritis and sodium retention: enhancement of Na+/K+-ATPase activity in the collecting duct is shared by rats with puromycin induced nephrotic syndrome and mice with spontaneous lupus-like glomerulonephritis. Nephrol Dial Transplant 1999; 14:2192.
  7. Whaley-Connell AT, Sowers JR, Stevens LA, et al. CKD in the United States: Kidney Early Evaluation Program (KEEP) and National Health and Nutrition Examination Survey (NHANES) 1999-2004. Am J Kidney Dis 2008; 51:S13.
  8. Buckalew VM Jr, Berg RL, Wang SR, et al. Prevalence of hypertension in 1,795 subjects with chronic renal disease: the modification of diet in renal disease study baseline cohort. Modification of Diet in Renal Disease Study Group. Am J Kidney Dis 1996; 28:811.
  9. Neumann J, Ligtenberg G, Klein II, et al. Sympathetic hyperactivity in chronic kidney disease: pathogenesis, clinical relevance, and treatment. Kidney Int 2004; 65:1568.
  10. Raine AE, Bedford L, Simpson AW, et al. Hyperparathyroidism, platelet intracellular free calcium and hypertension in chronic renal failure. Kidney Int 1993; 43:700.
  11. Passauer J, Pistrosch F, Büssemaker E, et al. Reduced agonist-induced endothelium-dependent vasodilation in uremia is attributable to an impairment of vascular nitric oxide. J Am Soc Nephrol 2005; 16:959.
  12. London G, Guerin A, Pannier B, et al. Increased systolic pressure in chronic uremia. Role of arterial wave reflections. Hypertension 1992; 20:10.
  13. Portaluppi F, Montanari L, Massari M, et al. Loss of nocturnal decline of blood pressure in hypertension due to chronic renal failure. Am J Hypertens 1991; 4:20.
  14. Parra G, Rodríguez-Iturbe B, Colina-Chourio J, García R. Short-term treatment with captopril in hypertension due to acute glomerulonephritis. Clin Nephrol 1988; 29:58.
  15. Minutolo R, Agarwal R, Borrelli S, et al. Prognostic role of ambulatory blood pressure measurement in patients with nondialysis chronic kidney disease. Arch Intern Med 2011; 171:1090.
  16. Agarwal R, Andersen MJ. Prognostic importance of ambulatory blood pressure recordings in patients with chronic kidney disease. Kidney Int 2006; 69:1175.
  17. Slagman MC, Waanders F, Hemmelder MH, et al. Moderate dietary sodium restriction added to angiotensin converting enzyme inhibition compared with dual blockade in lowering proteinuria and blood pressure: randomised controlled trial. BMJ 2011; 343:d4366.
  18. REUBI FC, COTTIER PT. Effects of reduced glomerular filtration rate on responsiveness to chlorothiazide and mercurial diuretics. Circulation 1961; 23:200.
  19. Wollam GL, Tarazi RC, Bravo EL, Dustan HP. Diuretic potency of combined hydrochlorothiazide and furosemide therapy in patients with azotemia. Am J Med 1982; 72:929.
  20. Sica DA. Chlorthalidone: has it always been the best thiazide-type diuretic? Hypertension 2006; 47:321.
  21. Khosla N, Kalaitzidis R, Bakris GL. The kidney, hypertension, and remaining challenges. Med Clin North Am 2009; 93:697.
  22. Buter H, Hemmelder MH, Navis G, et al. The blunting of the antiproteinuric efficacy of ACE inhibition by high sodium intake can be restored by hydrochlorothiazide. Nephrol Dial Transplant 1998; 13:1682.
  23. Wilmer WA, Rovin BH, Hebert CJ, et al. Management of glomerular proteinuria: a commentary. J Am Soc Nephrol 2003; 14:3217.
  24. Bakris GL, Weir MR, Secic M, et al. Differential effects of calcium antagonist subclasses on markers of nephropathy progression. Kidney Int 2004; 65:1991.
  25. Kent DM, Jafar TH, Hayward RA, et al. Progression risk, urinary protein excretion, and treatment effects of angiotensin-converting enzyme inhibitors in nondiabetic kidney disease. J Am Soc Nephrol 2007; 18:1959.
  26. Khosla N, Kalaitzidis R, Bakris GL. Predictors of hyperkalemia risk following hypertension control with aldosterone blockade. Am J Nephrol 2009; 30:418.
  27. Minutolo R, Gabbai FB, Borrelli S, et al. Changing the timing of antihypertensive therapy to reduce nocturnal blood pressure in CKD: an 8-week uncontrolled trial. Am J Kidney Dis 2007; 50:908.
  28. Hermida RC, Ayala DE, Mojón A, Fernández JR. Bedtime dosing of antihypertensive medications reduces cardiovascular risk in CKD. J Am Soc Nephrol 2011; 22:2313.
  29. Blood Pressure Lowering Treatment Trialists' Collaboration, Turnbull F, Neal B, et al. Effects of different regimens to lower blood pressure on major cardiovascular events in older and younger adults: meta-analysis of randomised trials. BMJ 2008; 336:1121.