Vincent J. Canzanello

Renal duplex sonography: Evaluation of clinical utility

With the exception of conventional angiography, no previously proposed screening test has the necessary sensitivity/specificity to guide further evaluation for correctable renovascular disease. Recently, renal duplex sonography has been suggested as a useful substitute in such screening for renovascular disease. This report analyzes our data collected over the past 10 months in evaluation of renal duplex sonography to examine its diagnostic value. The study population for renal duplex sonography validity analysis consisted of 74 consecutive patients who had 77 comparative renal duplex sonography and standard angiographic studies of the arterial anatomy to 148 kidneys. Renal duplex sonography results from six kidneys (4%) were considered inadequate for interpretation. This study population contained 26 patients (35%) with severe renal insufficiency (mean 3.6 mg/dl) and 67 hypertension (91%). Fourteen patients (19%) had 20 kidneys with multiple renal arteries. Bilateral disease was present in 22 of the 44 patients with significant renovascular disease. Renal duplex sonography correctly identified the presence of renovascular disease in 41 of 44 patients with angiographically proven lesions, and renovascular disease was not identified in any patient free of disease. When single renal arteries were present (122 kidneys), renal duplex sonography provided 93% sensitivity, 98% specificity, 98% positive predictive value, 94% negative predictive value, and an overall accuracy of 96%. These results were adversely affected when kidneys with multiple (polar) renal arteries were examined. Although the end diastolic ratio was inversely correlated with serum creatinine (r = -0.3073, p = 0.009), low end diastolic ratio in 35 patients submitted to renovascular reconstruction did not preclude beneficial blood pressure or renal function response. We conclude from this analysis that renal duplex sonography can be a valuable screening test in the search for correctable renovascular disease causing global renal ischemia and secondary renal insufficiency (ischemic nephropathy). Renal duplex sonography does not, however, exclude polar vessel renovascular disease causing hypertension alone nor does it predict hypertension or renal function response after correction of renovascular disease.

Percutaneous transluminal renal angioplasty in management of atherosclerotic renovascular hypertension: results in 100 patients.

The long-term effect of percutaneous transluminal renal angioplasty (PTRA) on blood pressure and renal function was assessed in 100 consecutive patients with atherosclerotic renovascular hypertension. Technical success rates (complete plus partial) of a first PTRA averaged 76.2%, 74.1%, and 67.7% for the unilateral (n=42), bilateral (n=27), and solitary (n=31) groups, respectively. Of the technical successes, 59% (43/73) experienced sustained blood pressure benefit (mostly amelioration) during a mean follow-up period of 29 months. Rates of blood pressure benefit were similar in the three groups. Ostial lesions comprised the majority of blood pressure benefit failures. Repeat angioplasty in 14 patients resulted in a 71% technical success rate and a 50% blood pressure benefit rate during a mean follow-up period of 22 months. Long-term stability of mean serum creatinine level was observed after technically successful angioplasty in all three groups. Acute renal insufficiency, which was reversible in all but one patient, complicated 26% of the procedures. Mechanical complications occurred in 14% (20/145) of the arteries acted on; surgical intervention was required in five patients. The mortality rate was 2%. These results suggest that angioplasty is effective in both the long-term management of renovascular hypertension and the preservation of renal function hi a large fraction of patients with atherosclerotic renovascular hypertension.

A Race-Controlled Human Leukocyte Antigen Frequency Analysis in Lupus Nephritis

Systemic lupus erythematosus (SLE) has higher incidence and mortality rates in addition to a greater risk for nephropathy in African Americans (blacks), compared with whites. We analyzed the South-Eastern Organ Procurement Foundation (SEOPF) database from 1982 through 1986 to determine if variation in human leukocyte antigen (HLA) frequencies, beyond those normally present between the races, were associated with lupus nephritis (LN). HLA antigen frequencies in 271 black and 230 white renal transplant recipients with LN as the cause of end-stage renal disease (ESRD) were compared with 4,506 race-matched cadaveric kidney donor controls. Odds ratios (ORs) and chi-square values were computed to assess the prevalence of each HLA phenotype among the cases versus the controls separately for blacks and whites. HLA-B8 and -DR2 frequencies were increased, and HLA-DR4 frequency was decreased in cases of both races compared with race-matched controls (race-combined ORs, 1.68, 1.46, and 0.49, respectively; all P < 0.01). Race-specific analyses showed that HLA-DR6 was decreased in black cases versus black controls (OR, 0.48; P < 0.001) and HLA-DR3 was increased in white cases versus white controls (OR, 1.88; P < 0.001). HLA-B8 and DR2 are positively associated and HLA-DR4 is negatively associated with LN in patients of both races. HLA-DR3 and -DR6 demonstrate race-specificity in LN and place whites at a disadvantage relative to blacks. It is likely that non-HLA-mediated genetic factors and/or environmental factors contribute to the increased risk of nephritis observed in black patients with SLE.(ABSTRACT TRUNCATED AT 250 WORDS)

Management of renovascular hypertension in the elderly population

This article summarizes our experience with the operative management of renovascular hypertension in a contemporary population of elderly patients. During a recent 18-month period 35 of 74 patients (47%) undergoing an operation for renovascular hypertension at our center were in their seventh (21 patients) or eighth (14 patients) decade of life (mean age, 68 years). There were 17 men and 18 women with blood pressures ranging from 176/90 mm Hg to 280/215 mm Hg (mean, 213/121 mm Hg). Twenty-seven patients (77%) had renal insufficiency (serum creatinine ≥1.3 mg/dl). Nineteen patients had severe insufficiency (serum creatinine ≥2.0 mg/dl), with five of these patients being dependent on dialysis. Thirty-three of 35 patients (94%) had evidence of organ-specific atherosclerotic damage as manifested by cardiac disease (72%), cerebrovascular disease (37%), or renal insufficiency (77%). Operative management consisted of unilateral revascularization in 17 patients (includes three contralateral nephrectomies), bilateral renal revascularization in 17 patients, and primary nephrectomy in one. Simultaneous aortic replacement was performed in nine patients. There were two operative deaths (5.7%) and two postoperative graft thromboses (4%). Hypertension was cured (three) or improved (27) in 30 of the 33 survivors (91%). Renal function was improved in six and worsened in two patients with severe non-dialysis-dependent renal insufficiency. Three of five patients who were dependent on dialysis before surgery were removed from dialysis after renal revascularization. On follow-up (mean, 10.3 months) we found that five patients had died. This article emphasizes the complexity of atherosclerosis in the current population presenting for operative management of renovascular hypertension. Despite the complexity of disease in this elderly population, our experience suggests that operative management is beneficial and can be accomplished with acceptable albeit increased risk in properly selected elderly patients. (J Vasc Surg 1989;10:266–73.)

Hemodialysis‐Associated Muscle Cramps

Muscle cramps remain an important cause of temporary morbidity associated with the hemodialysis procedure. In addition to immediate physical discomfort, a long-term sequela of cramps may be underdialysis due to the not uncommon practice of premature “sign-off by the patient. At our institution, cramps account for approximately 15% of all “sign-offs” and result in an average of 27 minutes lost per hemodialysis treatment.* Finally, the cost and dialysis attendant time involved in the management of these cramps is considerable. This review will focus on the epidemiologic, clinical, and pathophysiologic features of hemodialysis-associated muscle cramps and will provide a detailed discussion of the prevention and treatment of this common problem.

Spurious assessment of acid-base status due to dilutional effect of heparin

A patient was encountered in whom clinically significant spurious hypocapnia and hypobicarbonatemia were diagnosed resulting from the dilutional effect of excessive amounts of sodium heparin solution in the blood sample. This report presents the relevant data in this patient, summarizes the effects of heparin on the determination of the acid-base status, and provides suggestions for avoiding this important pitfall in clinical practice.

Diabetic Neuropathy and HLA-DR3/4

Excerpt To the Editors:The identification of an HLA-DR3/4 phenotype association with diabetes mellitus-induced autonomic neuropathy is an important advance in the demonstration of a genetic basis f...

The Thomas Shunt Revisited

During a 10-year period, 57 external Thomas femoral shunts (TS) were placed in 43 patients for chronic hemodialysis access. Median shunt survival was 28 months (range, 0.5 to 132). Sixty-three percent (36/57) of shunts are presently functional or functioned until the time of patient death from unrelated cause or removal after renal transplantation. The remaining 37% (21/57) failed after a mean duration of 18 months (range, 2 to 40). Causes of failure were thrombosis (57%), refractory infection (24%), and failure during surgical revision (19%). There were no shunt-related deaths. Race, sex, the presence of diabetes mellitus or hypertension, and prior surgical revision of access did not adversely affect shunt survival. These results support the TS as a viable means of chronic vascular access for hemodialysis patients who cannot receive further upper arm accesses.

Captopril and Anemia

Exacerbation of the anemia associated with chronic renal failure has been well documented in hemodialysis patients treated with the angiotensinconverting enzyme inhibitor captopril(1-3). In one study (3), the anemia of 9 of 12 hemodialysis patients worsened during captopril therapy, with no correlation between the extent of anemia and the dose of the drug. Interestingly, two of the three patients who did not develop anemia were concurrently receiving anabolic steroids. Further evidence of a suppressive effect of captopril upon erythropoiesis has been a recent report of its successful use to reduce postrenal transplant erythrocytosis (4). The relationship between the renin angiotensin system and erythropoiesis has been examined in several studies (5-1 1). In male rats exposed to hypoxia, a positive correlation was found between the elevation of erythropoietin levels and plasma levels of renin, renin substrate, and angiotensin I ( I 1). In the same study, female rats did not develop elevated renin levels during hypoxia, but when renin was injected subcutaneously, their erythropoietin levels doubled. Captopril administered to renin-treated female rats reduced erythropoietin to undetectable levels while prior administration of angiotensin I1 prevented this suppression of erythropoietin levels. The observation that renin substrate levels paralleled those of erythropoietin suggested three potential explanations for the association: 1) renin substrate may be a carrier protein for erythropoietin, 2) renin substrate and erythropoietin possibly share a similar protein precursor, or 3) renin substrate might be modified into erythropoietin under hypoxic conditions (1 1). Captopril delays recovery of the hematocrit following hemorrhage in rats (12). In this study, captopril administration led to continuously suppressed angiotensin I1 levels followed subsequently by a decrease in erythropoietin levels. Considering human studies, captopril has been associated with anemia in hypertensive hemodialysis patients (2). This anemia was directly correlated to angiotensin I1 levels before, and following, captopril administration. There was no measurable change in erythropoietin levels despite the worsening of anemia; however, this may have reflected a lack of sensitivity in the erythropoietin assay. The authors suggested that angiotensin I1 might be a direct stimulant for erythropoietin production or alternatively, that captopril might reduce renal ischemia and, thereby, decrease erythropoietin production (2). Supporting the latter suggestion is the observation that vasodilators such as hydralazine and diazoxide prevent the expected increases of erythropoietin levels following renin administration, possibly due to decreased renal ischemia (7, 13). Enalapril has also been found to exacerbate anemia in patients with end-stage renal disease (1). In addition, enalapril has been associated with a decrease in hematocrit in patients with hypertension ( 1 4), chronic renal insufficiency (1 5) , and in renal transplant recipients (1 6, 17). In enalapril treated patients with congestive heart failure, erythropoietin levels, but not hematocrit, may decrease ( 1 8). We are not aware of data regarding the effects of lisinopril, ramipril, benazepril, or fosinopril upon hematopoiesis in patients with end-stage renal disease, but the clinician should be alert for this possible interaction. The mechanisms discussed for angiotensin-converting enzyme-inhibitor-related anemia do not suggest that these drugs will interfere with exogenous erythropoietin therapy; data, though, are unavailable on this point.