The relative antihypertensive potency of propranolol, oxprenolol, atenolol, and metoprolol given once daily. A double-blind, crossover, placebo-controlled study in ambulatory patients.

The antihypertensive effect of four beta-blocking agents given once daily was compared with that of placebo in a prospective, crossover, double-blind study of 150 patients. The preparations tested were slow-release propranolol hydrochloride, 160 mg, atenolol, 100 mg, slow-release oxprenolol hydrochloride, 160 mg, and metoprolol, 200 mg. Propranolol and atenolol produced a significant decline in lying, standing, and postexercise blood pressure and pulse rate values. The effects of oxprenolol and metoprolol were not significantly different from that of placebo.

Long-term renoprotective effect of angiotensin-converting enzyme inhibition in non-insulin-dependent diabetes mellitus. A 7-year follow-up study.

BACKGROUND: Diabetic nephropathy is the leading cause of end-stage renal disease in developed countries. Duration of diabetes, blood pressure values, and metabolic status are the major determinants of the course of nephropathy, and microalbuminuria is the hallmark of its onset. Angiotensin-converting enzyme inhibitors offer important renoprotection to hypertensive and normotensive patients with insulin-dependent diabetes mellitus and non-insulin-dependent diabetes mellitus. Our study extends previous observations for duration and the effect of angiotensin-converting enzyme inhibition on advanced nephropathy. METHODS: Double-blinded (first phase) and open (second phase) randomized controlled study of 7 years. Ninety-four normotensive patients with non-insulin-dependent diabetes mellitus whose serum creatinine levels were lower than 123.76 mumol/L (1.4 mg/dL) and who had microalbuminuria (30 to 300 mg/24 h) were given enalapril maleate, 10 mg/d, or placebo, for 5 years. For 2 more years they were followed up openly and given the choice to receive enalapril or no treatment. RESULTS: In the enalapril-treated patients, albuminuria remained stable for 7 years. An increase from (mean +/- SD) 123 +/- 58 to 310 +/- 167 mg/24 h occurred in the untreated group after 5 years, and a further increase to (mean +/- SD) 393 +/- 223 mg/24 h occurred after 7 years. Reciprocal creatinine was unchanged in treated patients for 7 years; in the untreated patients, the mean decline was 13% at 5 years and 16% at 7 years. Treatment with enalapril resulted in an absolute risk reduction of 42% for nephropathy to develop during 7 years (95% confidence interval, 15% to 69%; P < .001, Student's t test). Glycosylated hemoglobin and body mass index remained unchanged. CONCLUSIONS: Angiotensin-converting enzyme inhibition offers long-term protection against the development of nephropathy in normotensive patients with noninsulin-dependent diabetes mellitus who have microalbuminuria, and it stabilizes renal function in previously untreated patients with impaired renal function. Discontinuation of treatment results in renewed progression of nephropathy.

Main risk factors for nephropathy in type 2 diabetes mellitus are plasma cholesterol levels, mean blood pressure, and hyperglycemia.

BACKGROUND: The control of hyperglycemia is of major importance in the treatment of patients with type 1 diabetes mellitus. However, there is no consensus about the required degree of metabolic control in patients with type 2 diabetes mellitus and about the role of hyperglycemia in diabetic nephropathy and in the development of atherosclerosis in relation to other risk factors. PATIENTS AND METHODS: A prospective, long-term follow-up study was conducted on 574 patients, aged 40 to 60 years, with recent onset of type 2 diabetes mellitus. Patients were initially normotensive and had normal renal function and a normal urinary albumin excretion rate (<30 mg/24 h). The patients were followed up for 2 to 9 years (mean +/- SD, 7.8 +/- 0.9 years). Levels of hemoglobin A1c and plasma lipids, mean blood pressure, and body mass index (calculated as the weight in kilograms divided by the square of the height in meters) were determined periodically. Cigarette smoking and socioeconomic status were recorded. Renal status was evaluated by the logarithm of the final urinary albumin excretion rate and by the decline in reciprocal creatinine values. Definite clinical events including death, nonfatal myocardial infarction, angina pectoris, congestive heart failure, and peripheral vascular disease were recorded. RESULTS: At the end of the study the urinary albumin excretion rate remained normal (<30 mg/24 h) in 373 patients (65%), 111 (19%) had microalbuminuria (30-300 mg/24 h), and 90 (16%) had overt albuminuria (>300 mg/24 h). Logistic regression models demonstrated that the correlation between hemoglobin A1c levels and the risk of albuminuria is exponential. Multiple logistic regression analysis indicated that levels of total cholesterol, mean blood pressure, and hemoglobin A1c were the main factors associated with the decrease in renal function and with the increase in albuminuria. The combination of values higher than the 50th percentile of all 3 factors defined a high-risk patient population. These high-risk patients had an odds ratio of 43 (95% confidence interval, 25-106) for microalbuminuria and 15 (95% confidence interval, 9-25) for clinical events related to arteriosclerosis compared with the rest of the group. Low levels of high-density lipoprotein, body mass index, cigarette smoking, low socioeconomic status, and male sex were all significantly associated with diabetic nephropathy, as well as with the manifestations of arteriosclerosis. CONCLUSIONS: The combination of blood pressure values in the high-normal range with moderately elevated levels of total cholesterol and hemoglobin A1c defines a high-risk group for the progression to diabetic nephropathy and for clinical events related to arteriosclerotic cardiovascular disease.

Proteinuria, renal impairment, metabolic control, and blood pressure in type 2 diabetes mellitus. A 14-year follow-up report on 195 patients.

BACKGROUND: The deleterious effect of hypertension on the course of diabetic retinopathy and the protective influence of antihypertensive therapy are well known. There is, however, little information about the long-term effect of different levels of blood pressure within the normal range on the evolution of renal function in type II diabetes. METHODS: One hundred ninety-five young normotensive patients with recent-onset type II diabetes, normal renal function, and no proteinuria were followed up for 14 years. Plasma glucose, creatinine, and urinary protein levels and blood pressure were determined periodically. RESULTS: Thirty patients developed hypertension; among them, 18 developed proteinuria (0.3 g/L). Among 144 patients who remained normotensive, 30 developed proteinuria. The mean decline in renal function (decline in reciprocal creatinine [100/creatinine level], expressed as a percentage of the initial value) was 26% for normotensive patients, 43% for normotensive patients with nephropathy, 39% for hypertensive patients, and 52% for hypertensive patients with nephropathy. The degree of metabolic control was not associated with the presence of proteinuria or with the severity of renal impairment. There was a significant association between the mean blood pressure over the whole observation period and the degree of impairment in renal function. This association was significant also in the patients who remained normotensive with and without proteinuria. CONCLUSIONS: Minor elevation of blood pressure as well as values in the upper normal range may be associated with acceleration of renal damage in type II diabetes.

Intermittent dobutamine treatment in patients with chronic refractory congestive heart failure: a randomized, double-blind, placebo-controlled study.

BACKGROUND: Intravenous dobutamine administration improves short-term hemodynamics in patients with severe congestive heart failure (CHF). However, the clinical benefit of periodic administration remains controversial. OBJECTIVE: To evaluate the efficacy of intermittent dobutamine administration in patients with refractory CHF. METHODS: Nineteen patients with New York Heart Association class III/IV, ischemia-induced CHF participated in this double-blind, placebo-controlled study. All patients received intravenous dobutamine or placebo over a 24-hour period every 2 to 3 weeks for 6 months. They were also treated with angiotensin-converting enzyme inhibitors, digoxin, and diuretics. The number of admissions for CHF and mortality rate were compared. RESULTS: Ten patients received dobutamine and nine received placebo. The pretreatment characteristics were similar in both groups. No statistically significant difference was observed between the number of admissions for CHF (p = 0.11). The median survival after enrollment was 7.97 months in the placebo group and 4.6 months in the dobutamine group. The Kaplan-Meier survival curves overlay, with no statistically significant difference between the treatment arms (p = 0.7). CONCLUSION: Intermittent dobutamine infusions in patients with refractory CHF have no effect on the need for hospitalization or on survival.

Treatment of diabetic perforating ulcers (mal perforant) with local dimethylsulfoxide.

Perforating foot ulcers constitute a major problem in diabetics with peripheral neuropathy for which no specific therapy is available. Twenty patients with chronic, resistant mal perforant were treated by local application of dimethylsulfoxide (DMSO) solution. Complete healing of the ulcers was achieved in 14 patients following 4-15 weeks of daily treatment. Partial resolution was observed in another four patients, and in the remaining two there was no effect. A control group, equal in number, was treated conventionally. Complete healing of the ulcers took place in only two patients. The therapeutic effect of DMSO most probably results from an increase in tissue oxygen saturation via a combined mechanism of local vasodilatation, decreased thrombocyte aggregation, and increased oxygen diffusion. Local DMSO is effective, simple, devoid of systemic side effects, and inexpensive. It should be employed for diabetic foot ulcers prior to the consideration of surgical measures.

A clinical approach to "idiopathic" normocytic-normochromic anemia.

OBJECTIVES: Normocytic-normochromic anemia is frequently found in patients with chronic disorders. The pathogenesis, epidemiological and clinical characteristics of normocytic normochromic anemia of unknown cause are not well established. We evaluated the role of bone marrow examination and the clinical course of patients with "idiopathic" normocytic-normochromic anemia. DESIGN: Patients with normocytic-normochromic anemia underwent a noninvasive evaluation according to a predetermined protocol. Bone marrow aspiration and biopsy were performed in those patients in whom no explanation for the anemia was found. They were later followed at 3 to 6 month intervals. RESULTS: Thirty-one patients (23 females and 8 males) with "idiopathic" normocytic-normochromic anemia (mean hemoglobin concentration was 10.0 + 0.6 g/dL) were detected. No patient had symptoms related to the anemia. Twenty-nine bone marrow aspirations and 21 biopsies were performed. Iron deficiency and mild myelofibrosis were found in one patient each. The rest of the bone marrow examinations were normal. During 15.5 +/- 10.3 months of follow-up, the hemoglobin level rose marginally to 10.9 + 1.0 g/dL (P < .0002). No changes in clinical or laboratory variables that could be ascribed to anemia were detected. CONCLUSION: Normocytic-normochromic anemia of unknown cause is encountered infrequently in clinical practice and is found mainly in older patients. The evaluation should be noninvasive to exclude correctable causes of the anemia. Bone marrow examination is only rarely contributive in this setting. The prognosis of these patients is excellent.

Effect of enalapril and nifedipine on orthostatic hypotension in older hypertensive patients.

OBJECTIVE: To compare the effect of enalapril with long-acting nifedipine on orthostatic hypotension in older patients. DESIGN: A prospective, double blinded, cross-over study. SETTING: The outpatient clinic of a university hospital. PARTICIPANTS: Thirty-nine patients aged 65 years or older with systolic blood pressure (SBP) of 140-190 mm Hg and diastolic blood pressure (DBP) of 90-110 mm Hg. INTERVENTION: Enalapril 5-20 mg od or nifedipine 30-90 mg od for 8 weeks, followed by 4 weeks washout and cross-over for a second 8-week period. MEASUREMENTS: Supine and standing 0-, 1-, and 5-minutes blood pressure was recorded before and at the end of each treatment period. RESULTS: At baseline, SBP was 158.8 +/- 8.7 mm Hg, and DBP was 97.1 +/- 5.9 mm Hg. There was a decline in SBP of 6.1 +/- 2.7 mm Hg and 8.4 +/- 4.1 mm Hg after 1 and 5 minutes of standing, respectively. Both agents caused a significant decline in supine blood pressure. Enalapril: supine SBP 158.8 +/- 8.7 to 143 +/- 7.3 mm Hg; supine DBP 97.1 +/- 5.9 to 85.1 +/- 5.1 mm Hg (P = .0001). The drop in SBP after standing for 5 minutes was only 2.4 +/- 1.6 mm Hg with no change in diastolic values. A > or = 10 mm Hg drop in SBP was observed in only three patients, and no patient experienced a decline of 20 mm Hg or more. Nifedipine: supine SBP: 160.3 +/- 9 to 145.3 +/- 8.1 mm Hg; supine DBP: 96.3 +/- 5.7 to 86.3 +/- 5.8 (P = .0001). Nifedipine induced an orthostatic decline in SBP values; there was an 8.7 +/- 4.8 mm Hg difference between supine and 5 minutes standing values (P = .0005) without change in diastolic values. An orthostatic decline in SBP of > or = 10 mm Hg occurred in 13 patients, and there was a drop of > or = 20 mm Hg in six patients. The cross-over of enalapril and nifedipine reproduced the hypotensive effect and reversed the postural effect. (P = .0002 nifedipine vs enalapril) CONCLUSIONS: Enalapril and nifedipine were equipotent in reducing supine blood pressure levels. Enalapril also reduced the number of orthostatic episodes significantly, whereas nifedipine aggravated this phenomenon.

Incidence and origin of non-systemic microdeposits of amyloid.

In a general hospital, 391 consecutive necropsies in which at least seven organs were available, were examined retrospectively by polarizing microscopy of Congo-red-stained sections for the presence of local amyloid deposits.Non-systemic microdeposits of amyloid were encountered in 72 cases, an overall incidence of 18.4%. They were usually small and frequently detectable only by virtue of polarizing microscopy. There is no indication that these microdeposits of amyloid are of pathogenetic significance. Although they sometimes occur in more than one organ, such deposits can be readily distinguished from those of systemic amyloidosis by their histological features.

The protective effect of dimethyl sulfoxide in experimental ischemia of the intestine.

Experiments with two models of intestinal ischemia were performed in order to examine the protective effect of dimethyl sulfoxide (DMSO). Segmental ischemia of the small intestine for 150 minutes caused necrosis of the affected bowel in 90% of the animals. Intravenous administration of DMSO or impregnation of the peritoneum with this substance prevented the development of gangrene in 28 of 29 rats. 30 or 60 minutes of complete ischemia of the small intestine, produced by clamping of the superior mesenteric artery, resulted in partial or complete necrosis of bowel segments with a high incidence of perforation and peritonitis and a high mortality rate within the first 24 hours. Intravenous DMSO, given upon declamping of the artery, effectively protected the bowel from the ischemic damage. There were no deaths among DMSO-treated animals and at 24 h there was no evidence of ischemic damage to the intestine. Though the exact mechanism of action of DMSO is unknown, the results of these and other experiments may warrant clinical trials especially in cases of mesenteric thrombosis.

Dimethyl sulfoxide in acute ischemia of the kidney.

Renal ischemia was produced in rats by clamping of the renal artery for 1 h. Upon termination of the ischemic period a 20% solution of DMSO (5 g kg-1 b.w.) was given intravenously to 33 rats. Eighteen control animals received normal saline. All DMSO-treated animals survived while all control animals died within the subsequent seven days. At 24 h following the experiment, the mean blood urea of the control rats was 254 mg/100 ml and the mean plasma creatinine 7.2 mg/100 ml. By contrast, the DMSO-treated rats had a mean blood urea of 69 mg/100 ml and plasma creatinine of 1.6 mg/100 ml. In 17 animals the kidney was perfused with DMSO prior to the closure of the renal artery. All these rats survived the procedure and showed near normal kidney function at 24 h. The renal artery was clamped for 60 min in ten dogs. Five dogs received DMSO (3 g kg-1 b.w.) and the other five received an equivalent dose of normal saline. Three weeks later a contralateral nephrectomy was performed. Renal function was normal in the DMSO-treated dogs. One control dog died of uremia, in the remaining four a transient renal failure was observed. These experiments in two different animals highlight the protective effect of DMSO on the ischemic kidney when the drug is administered after the ischemic period.

Long-term effect of ACE inhibition on development of nephropathy in diabetes mellitus type II.

Ninety-four normotensive, type II diabetics with microalbuminuria and normal renal function were randomized to receive enalapril or placebo and were followed for five years. In the patients treated with enalapril, albuminuria decreased initially from 143 +/- 64 (mean +/- SD) mg/24 hours to 122 +/- 67 mg/24 hours, then a slow increase was observed to 140 +/- 134 mg/24 hours after five years. In the placebo group albuminuria increased from 123 +/- 58 mg/24 hours to 310 +/- 167 mg/24 hours after five years. The difference between the rates of change in albuminuria over time in the two groups was highly significant (P < 0.005). Kidney function, expressed as mean reciprocal creatinine, declined by 13% in the placebo group and remained stable (-1%) in the enalapril group (P < 0.05). The initial value of daily albuminuria was a good predictor of the subsequent decline in renal function (r = 0.86, P < 0.001 and r = 0.72, P < 0.001 for the enalapril and the placebo groups, respectively). Initial and subsequent mean values of cholesterol and LDL were lower in the enalapril than in the placebo group. There was a close correlation between mean cholesterol values and the decline in renal function (r = -0.58, P < 0.001). The mean blood pressure was stable in the enalapril group (initial group mean 99 +/- 2.1 mmHg, fifth year mean 100 +/- 3.2 mmHg) and increased in the placebo group from 97 +/- 3.2 mmHg to 102 +/- 3.4 mm Hg at the end of the study (P = 0.082).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-converting enzyme inhibitors and cough: a prospective evaluation in hypertension and in congestive heart failure.

Angiotensin-converting enzyme inhibitors (ACE-I) have become the mainstem of antihypertensive therapy and first-choice agents for vasodilatation in congestive heart failure (CHF). A typical dry cough is the main cause for discontinuation of ACE-I therapy. Data about the incidence, course, and clinical significance of this side effect are conflicting. This study determined the incidence of cough in ACE-I treated patients with hypertension and with CHF and to appreciate its clinical significance; 268 ACE-I treated patients, 164 with hypertension and 104 with CHF were prospectively followed for at least 1 year and specifically questioned about cough and other side effects. In those in whom cough developed, a second and then a third ACE-I were tried. Cough developed in 50 (18.6%) of the 268 patients; 23 patients with hypertension (14%) had coughs 24.7 +/- 17.1 (SD) weeks after initiation of therapy; 27 patients with CHF (26%) had coughs 12.3 +/- 12 (SD) weeks after the start of ACE-I therapy (P = 0.005). All but three patients had coughs also on the second and third ACE-I. The time from the beginning of therapy to the onset of cough was significantly shorter with the second than the first drug. ACE-I agents had to be discontinued in 50% of the patients in whom coughs developed, most of them in the CHF group. In the others, cough was well tolerated or disappeared during subsequent months. The incidence of cough, which necessitated discontinuation of ACE-I treatment, was 4% among patients with hypertension and 18% among patients with CHF (P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of enalapril to captopril by 24-hour ambulatory blood pressure monitoring.

The efficacy of a once-daily dose of enalapril was compared with a thrice-daily dose of captopril in an open-label, randomized parallel group study of 27 hypertensive patients. The patients were monitored using conventional measurements of blood pressure and with 24-hour ambulatory blood pressure monitoring at baseline and after 12 weeks of therapy. The end points were 24-hour, daytime, and nighttime mean blood pressure values and the percentage of elevated systolic and diastolic measurements, reflecting the "hypertensive load." Enalapril reduced mean 24-hour systolic blood pressure by 18 mmHg and diastolic blood pressure by 11 mmHg. The comparative values for captopril were 9 mmHg and 2 mmHg, respectively. The mean daytime systolic blood pressure was reduced by 20 mmHg with enalapril versus 7 mmHg with captopril; the diastolic values were lowered by 11 mmHg with enalapril versus 4 mmHg with captopril. The mean nighttime systolic blood pressure was lowered by 16 mmHg with enalapril versus 12 mmHg with captopril; the diastolic values were reduced by 10 mmHg with enalapril and 5 mmHg with captopril. No major side effects were recorded in either group. A single daily 20-mg dose of enalapril, therefore, proved to be equipotent or superior to 75 mg of captopril administered in three divided doses.

Detection of bcl rearrangements in B-CLL by fluorescence in situ hybridization.

Data concerning oncogene activation in CLL are very limited. When studied by Southern blot, rearrangements of bcl-1, bcl-2, and bcl-3 have been only infrequently reported. We evaluated the role of fluorescence in situ hybridization (FISH) in the detection of gene rearrangements in two CLL patients. We used multiple DNA probes, including those of chromosome 12, immunoglobulin heavy and light chains, and the oncogenes bcl-1, bcl-2, and bcl-3. Additionally, routine cytogenetic study was performed. In one patient, trisomy 12 and bcl-2 translocation were demonstrated by both methods, while trisomy 12 and bcl-1 translocation were seen in the second patient, who had a normal karyotype. Larger studies should evaluate the role of FISH in the detection of oncogene involvement in CLL and compare it with other molecular methods.

Fluorescence in situ hybridization (FISH) for retrospective detection of trisomies 3 and 7 in multiple myeloma.

The malignant plasma cells of multiple myeloma (MM) have a low proliferative activity and therefore cytogenetic studies of the disease have been severely limited. We evaluated the role of fluorescence in situ hybridization (FISH) in the detection of numerical chromosomal abnormalities in early stages of myeloma and the applicability of the method to stored archival slides. Old air-dried bone marrow smears from 15 myeloma patients obtained at presentation were probed with alpha satellite DNA sequences to chromosomes 3 and 7. Numerical chromosome aberrations were found in eight (53%) of the patients, including six (of 12) with trisomy 7, and two (of eight) with trisomy 3. This study demonstrates that FISH is a sensitive method for the detection of numerical aberrations in myeloma and for the study of old slides for retrospective analysis.

In situ hybridization: a simple and sensitive method for detection of trisomy 12 in chronic lymphocytic leukemia.

Chromosome aberrations are detected in only 50% of patients with chronic lymphocytic leukemia (CLL), owing usually to the low mitotic rate exhibited by the neoplastic lymphocytes. Fluorescence in situ hybridization (FISH) is a simple method for identifying numerical abnormalities of the target chromosome in interphase nuclei. Therefore, we used the FISH procedure with chromosome 12-specific a-satellite probe to evaluate 19 patients with CLL. Trisomy 12 was detected in interphase cells of 12 patients (63%). Cytogenetic analysis, performed in nine patients, yielded trisomy 12 in four (44%). FISH detected three patients with trisomy 12 in whom conventional cytogenetic method yielded a normal karyotype. FISH is a simple, reliable, and sensitive method for detection of trisomy 12 in patients with CLL.

Fluorescence in situ hybridization for the detection of trisomies 8 and 9 in polycythemia vera.

Trisomies 8 and 9 are the most common numerical chromosome abnormalities in polycythemia vera (PCV). Their role in the pathogenesis of the disease is unclear, however, as is their diagnostic or prognostic value. We evaluated fluorescent in situ hybridization as compared to chromosome analysis for the detection of trisomies 8 or 9 in peripheral blood cells of PCV patients. We demonstrated that FISH is a more sensitive method for the detection of the abnormalities. A positive correlation between the duration of the disease and trisomy 9 was found. FISH is a sensitive, convenient, and rapid method for the diagnosis and follow-up of chromosome aberrations in patients with PCV. The application of FISH to a larger cohort of patients may provide valuable information regarding the role of the chromosomal aberrations in the initiation and progression of this disease.

The BCL-1, BCL-2, and BCL-3 oncogenes are involved in chronic lymphocytic leukemia. Detection by fluorescence in situ hybridization.

The putative oncogenes BCL-1, BCL-2, and BCL-3 are commonly rearranged by translocations to the immunoglobulin genes in B-cell malignancies. However, Southern blotting rarely detected their involvement in chronic lymphocytic leukemia (CLL). This discrepancy could stem from some unique features of the oncogenesis of CLL or be due to shortcomings of Southern blotting. We have therefore evaluated the role of fluorescence in situ hybridization (FISH) in the detection of these oncogenes in CLL. Twenty consecutive CLL patients were studied by FISH for the detection of BCL-1, BCL-2, or BCL-3 rearrangement and for the presence of trisomy 12. Selected patients were also evaluated by classical cytogenetic techniques and by Southern blot analysis. Juxtaposition of JH and BCL-1 was demonstrated in 10 (50%), BCL-2 in three (15%), and BCL-3 in four (20%) of the patients. Trisomy 12 was detected by FISH in 11 (55%) patients. The coexistence of trisomy 12 and translocation of the BCL-1 oncogene was common. Three of the patients had chromosomal aberrations compatible with those detected by FISH. In contrast, in none of the five patients selected by their positive FISH findings was a rearrangement demonstrated by Southern blotting. We conclude that FISH is a sensitive method for the detection of oncogene involvement in CLL. Mainly BCL-1, but also BCL-2 and BCL-3, are commonly translocated to the immunoglobulin heavy chain locus on chromosome 14. These translocations are often associated with trisomy 12. These findings indicate that the BCL oncogenes are commonly involved in CLL and lend support to the multi-hit theory of cancer development.

Reversible renal hypertension due to renal hygroma.

A hygroma of the left kidney was found at surgery in a thirty-five-year-old woman, who presented with anemia, hypertension, and a left abdominal mass. There was a very high sedimentation rate and fine needle aspiration yielded bizarre cells which raised the possibility of malignancy. Compression of the kidney by the cystic structure probably interfered with renal blood flow and was responsible for the elevated blood pressure which receded to normal after removal of the cyst and the left kidney.