Control of Hypertension in Patients with Chronic Renal Failure

REVIEW ARTICLE Control of hypertension in patients with chronic renal failure ROBERT J. HEYKA, MD AND DONALD G. VIDT, MD • Hypertension related to renal parenchymal disease is the most common cause of secondary hypertension. Poor control of renal hypertension is associated with an increased risk for progressive atherosclerosis and progressive renal failure. This review discusses the prevalence, significance, and pathophysiology of renal hypertension. Treatment options, both dietary and pharmacologic, are reviewed. Special emphasis is given to important pharmacokinetic changes in chronic renal failure. Treatment of hypertensive urgen- cies and emergencies in this population is also reviewed. • INDEX TERMS: HYPERTENSION; KIDNEY DISEASES • CLEVE CLIN J MED 1989; 56:65-76 YPERTENSION and chronic renal failure PREVALENCE AND VARIATION may be related in one of two ways. First, es- sential or idiopathic hypertension may cause Chronic renal disease is the most common cause of renal parenchymal damage. The kidney may secondary hypertension accounting for 2.5% to 5% of all bHe more victim than culprit in this situation. It is impor- hypertension. Renal parenchymal hypertension is more tant to break the cycle of idiopathic hypertension with prevalent than the hypertension due to renovascular adequate control of the hypertension, thus preventing disease or endocrine abnormalities such as Cushing's progressive renal damage. Second, chronic renal failure syndrome, primary hyperaldosteronism, or pheochro- is frequently accompanied by hypertension. Here the mocytoma, which account for 0.5% to 3% of all hyper- kidney may be more the culprit but is also a victim of its tension.1 own dysfunction. Hypertension secondary to chronic A recent study compared 3,090 determinations of renal failure presents certain unique challenges to the glomerular filtration rate (GFR) using the isotope clinician. We will consider several important aspects of iothalamate 1-131 with the corresponding serum creat- this latter association, including differences in preva- inine levels. In patients aged 41 to 50 years, a GFR of 50 lence with various renal diseases, risks associated with mL/min/1.73 m2 was seen with an average serum creat- deteriorating renal function and atherosclerosis, as well inine value of 1.5 mg/dL in females and 1.7 mg/dL in as pathogenesis and treatment. males. With a GFR of 25 mL/min/1.73 m2, the average serum creatinine values were 2.2 and 2.8 mg/dL, respec- tively. In patients aged 61 to 70 years, the serum creatinine value averaged 1.2 and 1.6 mg/dL for females and From the Department of Hypertension and Nephrology, The 2 Cleveland Clinic Foundation. Submitted for publication Nov 1988; males with a GFR of 50 mL/min/1.73 m (Hall P, unpub- accepted Nov 1988. lished data). Address reprint requests to R.J.H., Department of Hypertension Thus the serum creatinine value can be falsely reas- and Nephrology, The Cleveland Clinic Foundation, One Clinic suring, and significant renal failure can be present even Center, 9500 Euclid Avenue, Cleveland, Ohio 44195. JANUARY • FEBRUARY 1989 CLEVELAND CLINIC JOURNAL OF MEDICINE 65 Downloaded from www.ccjm.org on September 30, 2021. For personal use only. All other uses require permission. HYPERTENSION WITH CHRONIC RENAI. FAILURE • HEYKA AND VIDI TABLE 1 This concept is still disputed and several authors have PREVALENCE OF HYPERTENSION AND ETIOLOGY OF CHRONIC found no risk from chronic renal failure that is inde- RENAL FAILURE* pendent of other known risk factors.7,8 Nevertheless, Common atherosclerotic cardiovascular disease is the most com- Vascular disease mon cause of death in patients with chronic renal Systemic lupus erythematosis failure. Many factors can potentially contribute to this Scleroderma 9 Polyarteritis problem. As with any patient at risk for atherosclerotic Glomerular disease disease, patients with chronic renal failure should be Postinfectious (short-lived) glomerulonephritis strongly encouraged to discontinue tobacco use, lipids Crescentic (rapidly progressive) glomerulonephritis should be regularly monitored, and dietary or pharmaco- Focal segmenal glomerulosclerosis Diabetic nephropathy logic treatment should be initiated if necessary. Glucose Tubo-interstitial disease levels should be tightly controlled in patients with in- Autosomal dominant polycystic kidney disease sulin-dependent diabetes mellitus. Of all the potential Analgesic abuse nephropathy (geographic variation) atherosclerotic risk factors in patients with chronic Uncommon renal failure, hypertension is probably the most impor- Membranous glomerulonephritis tant.10,11 This emphasizes the need for aggressive and Membrano-proliferative glomerulonephritis IgA nephropathy adequate control of blood pressure in patients with Chronic pyelonephritis chronic renal failure. *Data derived from Blythe2 and McDonald.3 Progression of renal failure with modest increases in serum creatinine levels. The second major consideration for treatment of hy- The prevalence of hypertension in patients with pertension is related to prevention of progressive renal chronic renal failure varies with the etiology and sever- damage. In many instances, progression to end-stage ity of the renal disease (Table I). Diseases that involve renal disease occurs despite the spontaneous or ther- the small renal vessels, including systemic lupus erythe- apeutic resolution of the initial renal insult. Worsening matosus, scleroderma or vasculitis, and certain glomer- renal function can be seen in such diverse disorders as ulopathies such as diabetic nephropathy and rapidly pro- acute tubular necrosis, analgesic nephropathy, vesi- gressive glomerulonephritis (RPGN), are associated coureteral reflux, and post-streptococcal glomerulone- with rates of hypertension approaching 90%-100% in phritis, even with adequate treatment of the primary patients with end-stage renal failure.4 In postinfectious renal problem.12 Once a critical percentage of renal glomerulonephritis, hypertension occurs in approxi- function is lost (approximately 80%), progression to mately 75% of patients but is transient, lasting an aver- end-stage renal disease with need for dialysis or trans- age of one to six weeks. In other disorders, such as plantation is very likely, regardless of the initial renal in- vasculitis or RPGN, the hypertension persists and signif- sult.13 icantly worsens the renal damage if not controlled. Among renal disorders associated with tubular or inter- How does treatment of hypertension help preserve stitial diseases, autosomal dominant polycystic kidney renal function? disease and analgesic-abuse nephropathy are frequently In the past, it was thought that renal arteriolar con- complicated by hypertension, with a prevalence restriction and vascular sclerosis (as is seen with malig- 2 ported between 40% and 75%. An important con- nant hypertension) were the major pathologic mecha- sideration is that both the incidence and severity of hy- nisms in the continued destruction of renal tissue. pertension worsen with chronic renal failure of any Emphasis has recently shifted to the concept that it is etiology as renal function deteriorates. The overall prev- the transmission of increased hemodynamic pressures alence rate of hypertension approaches 80% in predialy- and flows to the glomerular vessels that is a major mech- 5 sis patients. anism in continued renal damage.14 Particular agents, especially angiotension-converting enzyme (ACE) in- SIGNIFICANCE AND SURVIVAL hibitors, may have a more beneficial effect on preserva- tion of residual glomerular function than other antihy- Atherosclerosis pertensive agents. By decreasing efferent arteriolar Chronic renal failure may itself be a risk factor for constriction, these agents reduce intraglomerular pres- atherosclerosis—so called "accelerated atherosclerosis."6 sures and thus may offer protection for the damaged kid- 66 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 56 NUMBER 1 Downloaded from www.ccjm.org on September 30, 2021. For personal use only. All other uses require permission. HYPERTENSION WITH CHRONIC RENAI. FAILURE • HI-;YKA AND VIDT ney.15 It is argued that this protection may be lacking activity showed significant correlation with hyperten- with "nonspecific" control of systemic blood pressure sion. The best correlation was with hypertension and unless intraglomerular pressures are also lowered. the product of duration of hypertension, plasma renin Several studies have shown a protective effect against activity, and either NaE or blood volume, demonstrating progression of renal damage with use of "nonspecific" the interdependent roles played by sodium, fluid status, agents. In one dietary study, patients enrolled in the circulating renin, and the duration of hypertension.19 control phase had slowed progression of chronic renal An interesting and unsettled question is whether the failure simply with more frequent office visits and better relation between sodium/volume and elevated blood control of blood pressure.16 This occurred independent pressure is a direct one via volume expansion and an in- of any dietary protein restriction. The antihypertensive creased cardiac output or an indirect one mediated by drugs used were diuretics, as well as other nonspecified other pressor mechanisms. In the latter situation, agents. sodium would function as a marker of volume or as a Although hypertension in chronic renal disease is possible inducer of other pressor mechanisms but not as only a single factor in the progression of

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