Stephen G. Rostand

Renal insufficiency in treated essential hypertension

We analyzed the clinical courses of 94 patients with treated primary hypertension and initially normal serum creatinine concentrations (less than or equal to 133 mumol per liter [less than or equal to 1.5 mg per deciliter]) who were followed for a mean (+/- SD) of 58 +/- 34 months (range, 12 to 174) to determine the frequency with which renal function deteriorated and the factors associated with deterioration. Fourteen patients (15 percent) had an increase in serum creatinine concentrations (greater than or equal to 35 mumol per liter [greater than or equal to 0.4 mg per deciliter]); in 16 percent of the 61 patients with apparently good control of blood pressure, the serum creatinine concentration rose 59 +/- 33 mumol per liter (0.67 +/- 0.38 mg per deciliter). Despite good control of diastolic blood pressure (less than or equal to 90 mm Hg), black patients were twice as likely as white patients to have elevations in serum creatinine (23 percent vs. 11 percent). Stepwise discriminant function analysis showed that a significant rise in the serum creatinine concentration was most likely to occur in association with older age, black race, a higher number of missed office visits, and employment as a laborer. We conclude that although renal function was preserved in 85 percent of patients with treated hypertension, it may deteriorate in some patients despite good blood-pressure control. Our observations may partly explain why hypertension, particularly among black persons, remains a leading cause of renal disease in the United States.

Treatment of Uremic Pericarditis and Pericardial Effusion

Pericarditis occurred 161 times in 136 of 1,058 patients undergoing chronic dialysis during a period of 13.7 years. Cardiac tamponade occurred during 27 episodes, while pretamponade occurred in 30. Tamponade was less frequent and resolution of pericarditis without invasive intervention more frequent when pericarditis occurred within 2 weeks of initiation of chronic dialysis. Similarly, resolution with conservative therapy was more frequent with first episodes than with recurrences, and when pericarditis occurred within 3 months of initiation of chronic dialysis. The overall survival was 89.7% and was the same irrespective of the duration of dialysis or whether the pericarditis was a first episode or a recurrence. We recommend that patients with pericarditis and no hemodynamic alterations receive intensive hemodialysis, with careful hemodynamic and echocardiographic monitoring, as primary treatment. Invasive intervention is indicated if cardiac tamponade or pretamponade develops, if a pericardial effusion increases progressively in size, or if a large effusion persists after ten to 14 days of intensive dialysis. In our experience, the invasive intervention of choice is either formal pericardiectomy or subxiphoid pericardiotomy with intrapericardial steroid instillation. In our experience, pericardiocentesis has proven to be a high-risk procedure. It is reserved for emergency circumstances, and then is preferably performed in the operating room just prior to induction of anesthesia for definitive surgical drainage.

Changing patterns of end-stage renal disease due to hypertension

We analyzed the records of all residents of Jefferson County, Alabama, accepted for renal replacement therapy between 1982 and 1987 and compared them with those accepted between 1974 and 1978 to determine any changes in the distribution and frequency of end-stage renal disease (ESRD) due to hypertension (H-ESRD). H-ESRD increased from 6.4 to 9.6 per 100,000 in blacks and from 0.36 to 0.62 per 100,000 in whites. Smoothed age- and race-specific yearly H-ESRD rates decreased in blacks under age 50. Peak incidence of H-ESRD shifted from age 40 to 49 in 1974 through 1978 to age 50 to 59 in 1982 through 1987 (P less than 0.0001). Blacks were referred for care with significantly higher blood pressure levels and serum creatinine concentrations than whites, and had more severe retinal vascular disease. Factors significantly associated with a shorter time from referral to renal replacement therapy were black race, female gender, blood urea nitrogen and serum creatinine concentrations, carbohydrate intolerance, and the use of alpha-agonist and/or angiotensin-converting enzyme (ACE) inhibitor. We conclude that racial distribution and risk for H-ESRD have not changed. Peak rates of H-ESRD have been delayed nearly a decade, suggesting a possible effect of better awareness and treatment of hypertension.

Treatment of secondary hyperparathyroidism in patients with chronic renal failure by total parathyroidectomy and parathyroid autograft.

Sixty-one patients with chronic renal failure and secondary hyperparathyroidism underwent total parathyroidectomy and parathyroid autograft. Symptoms relieved by parathyroidectomy included bone pain, pruritus, soft tissue calcification, muscle weakness and healing of fractures. Serum parathormone levels measured before and after operation in 48 patients returned to normal in all but two patients. Serum alkaline phosphatase levels also returned toward normal after operation, except in one patient with a retained parathyroid gland. Complete radiographic studies before and after operation were available in 30 of 61 patients. Twenty-three of 24 patients with osteitis fibrosa had evidence of healing, and in one patient no change occurred. Osteosclerosis noticed in 23 patients improved slightly in eight patients, did not change in 14 and became worse in one. Pathologic examinations revealed 45 patients to have diffuse hyperplasia and 16 nodular hyperplasia. There were two early postoperative deaths, in the first 30 days, and 16 late postoperative deaths, from four months to four years afterward. In no case did the operation contribute to the death. Some patients required the administration of supplemental calcium after operation, but in no instance did profound hypocalcemia occur. No patient developed recurrent hyperparathyroidism.

The Management of Coronary Artery Disease in Patients with End-Stage Renal Disease

Ischemic heart disease (IHD) has been a leading cause of death for more than two decades in patients undergoing chronic dialysis for end-stage renal disease (ESRD). While the reasons for this are debated [1–5], it is generally accepted that dialysis patients have an increased prevalence of coronary risk factors [2–11], including hypertension, left ventricular hypertrophy (LVH), and abnormalities of serum lipoproteins. Furthermore, the mean age of new patients receiving renal replacement therapy has increased, as has the prevalence of diabetes mellitus [12]. As a result, clinical nephrologists must make diagnostic and therapeutic decisions in an aging and increasingly sick patient population with ESRD and chest pain. In this chapter, we review the problems of diagnosis and management of IHD in patients undergoing chronic dialysis.

Effect of reduced chloride reabsorption on renin release in the isolated rat kidney

To investigate the relationship between tubular reabsorption of chloride and renal renin release in the isolated perfused rat kidney, perfusate renin activity was measured during substitution of either nitrate or thiocyanate for varying amounts of perfusate chloride but with maintained perfusate sodium concentration. Renin rose significantly as perfusate chloride fell; there was a sevenfold increase between perfusion with normal chloride and almost complete substitution of chloride by nitrate. With a normal perfusate chloride the addition of furosemide 10−4 M to the perfusate also led to an increase in renin and a reduction in tubule chloride reabsorption. For all these experiments there was a significant negative correlation between renin and absolute tubular reabsorption of chloride (r=−0.68,P<0.001), but no such relationship with absolute sodium reabsorption. Renin release in a nonfiltering kidney, produced by elevating perfusate albumin concentration, increased approximately 40-fold. Thus increasing plasma oncotic pressure elevates renin by mechanisms additional to cessation of tubular chloride absorption. However, substitution of chloride in the perfusate by nitrate in this nonfiltering kidney did not further elevate renin release. We conclude that renin release is influenced by a signal dependent on, and inversely proportional to, chloride reabsorption in the thick ascending limb of the Loop of Henle.

Ischemic Heart Disease in Chronic Renal Failure: Demography, Epidemiology, and Pathogenesis

Cardiac diseases, especially ischemie heart disease, remain a leading cause of death among patients receiving renal replacement therapy with either dialysis or transplantation. Although a recent report [1] suggests that heart disease mortality in the dialysis population may have decreased during the past 15 years, this same study and another [1,2] show that all-cause cardiac mortality has not changed appreciably from that reported previously [3,4]. Thus, heart disease mortality has remained nearly constant, representing 30% to 50% of all deaths in dialysis populations, with myocardial infarction causing about 10% to 15% of all deaths [3–5]. In renal-transplant populations, myocardial infarction and ischemic heart disease occur in about 8% and 11% of patients, respectively [6]. Myocardial infarction is the second leading cause of death in this group. The fact that sustained high mortality rates from ischemie heart disease persist in the end-stage renal disease (ESRD) population is not surprising given its demographic characteristics, the high rates of nonfatal symptomatic ischemie heart disease, and the clustering within these patients of numerous disease- and treatment-associated alterations in hemodynamics, metabolism, and cardiac structure that affect myocardial performance, perfusion, and oxygenation (figure 4–1).

Cardiovascular problems in acute renal failure

Little has been written of the relationship between acute renal failure (ARF) and cardiovascular disease, in comparison with chronic renal failure (CRF) where cardiovascular disease is the leading cause of death [1]. However, ARF with severely impaired renal function certainly may cause cardiovascular dysfunction, due to fluid and electrolyte abnormalities or uremic pericarditis. Moreover, certain populations, such as the elderly and diabetics, have a predilection to develop both ARF and cardiovascular disease. The vulnerability of the elderly to ARF relates, in part, to a high prevalence of polypharmacy, and an age-associated reduction in renal and hepatic function, resulting in decreased detoxification and disposal of nephrotoxic drugs. Also, the prevalence of conditions likely to cause both chronic renal disease and significant cardiovascular dysfunction rises with increasing age. These conditions include diabetes mellitus, hypertension, atherosclerotic peripheral and coronary vascular disease, left ventricular hypertrophy (LVH) of any cause, hypothyroidism, and hyperlipidemia.