Comparison of manual versus automated blood pressure measurements in treated hypertensive patients.

This study assesses differences in blood pressure (BP) levels prospectively between office (manual) measurement and ambulatory blood pressure monitoring (ABPM) in 70 treated, essential, hypertensive patients. The objective was to determine whether ABPM is superior to office measurement for assessing adequacy of therapy. Twenty-four patients received monotherapy and 46 received multiple therapy. Thirty-five patients were administered medication in the morning only, whereas 33 were administered medication in the morning and evening both. Mean systolic BP by manual method was identical to that obtained by ABPM (141.98 +/- 14.98 mm Hg versus 141.46 +/- 16.33 mm Hg, respectively). However, mean diastolic BP by manual method was significantly higher than that obtained by ABPM. (90.38 +/- 9.01 mm Hg versus 86.69 +/- 10.65 mm Hg, respectively; P < 0.001). Significant correlations (P < 0.01) were found between the BP levels measured by these two methods, although individual readings differed by 10 mm Hg or more systolic and by 5 mm or more diastolic in many subjects. No significant differences were noted in BP levels measured by either method for patients treated by monotherapy or multiple therapy, and none were noted whether they were taking medication in the morning or in both the morning and evening. In addition, no differences were noted in BP levels using either method for race. Thus, this study shows that the office measurement is grossly similar to ABPM for assessment of adequacy of therapy in treated hypertensive patients whose blood pressure is controlled adequately. However, ABPM is found to be superior to office measurement in identifying hypertensive patients whose blood pressure is not controlled adequately or is uncontrolled.

Incidence of atheroembolic renal failure after coronary angiography. A prospective study.

Atheroembolic renal failure (AERF) is often seen after vascular procedures in elderly atherosclerotic patients. To estimate the incidence of AERF after coronary angiography, all patients undergoing coronary angiography at the V.A. Medical Center, Dayton, were prospectively evaluated for AERF. Since, unlike contrast nephropathy, AERF develops about a week after the vascular procedure and persists or progresses over weeks and months, serum creatinine was measured just prior to and 3 weeks after coronary angiography. Peripheral signs of cholesterol emboli were also looked for at follow-up visits. Two hundred sixty-seven patients underwent coronary angiography over a fifteen-month period. Most of the patients were sixty years old or older. Mean serum creatinine in these patients prior to coronary angiography was 1.2 mg/dL. Mean serum creatinine after coronary angiography was unchanged (1.2 mg/dL). Only 7 patients had serum creatinine > 2 mg/dL prior to coronary angiography. Two patients died within a week of coronary angiography and 2 did not return for follow-up. Of the remaining 263 patients, 5 had a serum creatinine increase by 0.5 mg/dL or more at three weeks after coronary angiography. Three of 5 had a serum creatinine increase by 1.0 mg/dL or more. Two of these 3 patients eventually died of renal failure. None of these 5 patients had peripheral signs of cholesterol emboli. In selected patients, the incidence of AERF after coronary angiography appears to be very low (< 2%).

Medical management of nephrolithiasis.

About 1 out of 14 males and 1 out of 30 females are afflicted with kidney stones. In many of these patients, the disease is recurrent. Fortunately, our understanding of the disease and ability to treat renal stone disease has increased in the last decade. Parenteral NSAIDs have been shown to be as effective as narcotics in treating renal colic. Dietary and drug therapy after proper metabolic evaluation of patients with recurrent stones is beneficial in reducing the recurrence rate. New understanding of the role of diet and many organic inhibitors of crystallization in urine will further broaden the scope of management of this common disease.

Predictive factors for high mortality in hypernatremic patients.

Hypernatremia (serum sodium level of > 145 mEq/L) is associated with high mortality. This study reports an analysis of mortality in 116 patients with hypernatremia from two large university-affiliated teaching hospitals. The purpose was to identify factors predictive of high mortality in hypernatremic patients. Medical records were reviewed to obtain the following data: serum sodium (Na+) levels; systolic (S) and diastolic (D) blood pressure (BP) at the time of admission and throughout the hospital course; status of cognitive function; and type of fluid administered. The patients were divided into two groups: expired and survived. Seventy-seven of 116 patients (66%) expired, while 39 patients (34%) survived and were discharged from the hospital. The mean age and gender for patients who died (70.9 +/- 15.4 years, 90% men) were not different from those who survived (66.4 +/- 17.3 years, 87% men). For the serum Na+ levels recorded at three different times (early, peak, and late), mean late serum Na+ level during hospital course was significantly higher in patients who died than in those who survived (151.2 +/- 9.2 v 143.1 +/- 8.0 mEq/L, respectively; P < .001). Mean admission serum Na+ level (154.9 +/- 5.5 v 155.1 +/- 7.7 mEq/L, respectively) and mean peak serum Na+ level (157.5 +/- 6.5 v 156.8 +/- 9.4 mEq/L, respectively) were not different between the two groups. Both SBP and DBP at the time of admission (P < .05) and throughout the hospital course (P < .001) were significantly lower in the patients who died than in those who survived. The cognitive abnormalities consisting of confusion, obtundation, and speech abnormality were significantly (P < .05) higher in the expired patients than in those who survived. Normal (isotonic) saline was used significantly more frequently (P < .00001) in patients who expired than in those who survived. Thus, this study suggests that a persistently elevated serum Na+ level (possibly caused by prolonged infusion of normal saline) in association with protracted hypotension portends a dismal prognosis in hospitalized hypernatremic patients.

Diffuse histoplasmosis in a patient with sarcoidosis.

A case is presented of a woman with a long history of sarcoidosis who developed diffuse histoplasmosis. Although association between these two entities has been described before, there are only a few case reports of histoplasmosis among sarcoid patients. Diagnosis was finally established by bone marrow biopsy which saved the patient's life.

IgA deposition in the skin of patients with alcoholic liver disease.

In patients with alcoholic liver disease, IgA deposits are often found in the liver, kidneys and skin. The present study was undertaken to determine the specificity, sensitivity and characteristics of IgA deposition in the skin of a group of alcoholic patients with or without overt liver disease, and compare these with findings in non-alcoholic cirrhotics. Twenty-six out of 28 patients with alcoholic cirrhosis had IgA deposition in the skin. In contrast, only 6 out of 11 patients who were alcoholic without any clinical liver disease and 3 out of 13 patients with non-alcoholic cirrhosis of the liver had IgA deposition. In the control group, only 1 out of 52 patients with various dermatoses (excluding IgA dermatoses) had this IgA deposition. Unlike other IgA dermatoses, such as Henoch-Schoenlein purpura or dermatitis herpetiformis, IgA deposition in alcoholic liver disease is characterized by its presence in the basement membrane of the eccrine secretory coils. This particular pattern of IgA deposition can be helpful in the diagnosis of alcoholic liver disease or alcoholism since the specificity is 100% with a sensitivity of 75%.

Hemolytic uremic syndrome as a presenting form of HIV infection.

Human immunodeficiency virus (HIV) infection has been associated with several renal disorders. Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS) were also described in several patients with overt AIDS. We describe a patient who presented with HUS and only subsequent investigation to find the cause of HUS led to the diagnosis of HIV infection. HIV infection should be suspected in patients presenting with microangiopathic renal failure.

Heparin-induced endothelial cell cytoskeletal reorganization: a potential mechanism for vascular relaxation.

We have previously shown that heparin given subcutaneously on a daily basis lowers blood pressure in hypertensive rat models, and that this blood pressure lowering effect is endothelium-dependent. The present study describes the effects of heparin on endothelial cell (EC) apical surface structures and cytoskeletal elements, namely, actin and vimentin as well as EC proliferative activity. The EC line (CRL 1998) was cultured, treated with different concentrations of heparin (0, 50, 100, 500 U/ml) for 4, 24 or 48 hours, and fixed for scanning electron microscopy (SEM), and immunofluorescence microscopy (IFM) studies. Enzyme-linked immunosorbent assays (ELISA) and flow cytometric analysis were performed on EC monolayers treated with different concentrations of heparin for quantitative detection of actin and vimentin. By SEM study the cell surface showed generalized smoothing as a result of blunting of surface microvilli with increasing time of exposure and dosage of heparin. By IFM study, the detectable actin signal within ECs became progressively reduced in both its cellular distribution and the apparent number of cells that remained reactive. By 48 hr/500 U heparin, the actin signal was almost undetectable. Vimentin showed a moderate reduction in the cellular distribution of labeling. Quantitatively, actin was significantly reduced after the 24 hour treatment with a higher dose of heparin (500 U/ml), from a baseline optical density (OD) of 1.12 +/- 0.060 to 0.866 +/- 0.008 (P < 0.0027). After 48 hours of treatment at both 100 U/ml and 500 U/ml heparin, actin was significantly reduced from a baseline OD of 1.347 +/- 0.063 to 1.090 +/- 0.039 (P < 0.0039) and 0.844 +/- 0.074 (P < 0.008), respectively. However, vimentin was significantly reduced only after 48 hours of treatment with a high dose of heparin (500 U/ml), from baseline OD 1.82 +/- 0.052 to 1.41 +/- 0.004 (P < 0.002). The flow cytometric findings were virtually identical to the ELISA data for actin and vimentin. These qualitative and quantitative changes in actin and vimentin are consistent with apparent smoothing and relaxation of the EC's apical surface. Labeling with the cell cycle marker MIB-1 (monoclonal antibody Ki-67), showed a progressive reduction in the observed intensity in heparin treated cells with substantially fewer cells being positive. After a 48 hour treatment with heparin (500 U/ml), most ECs displayed only dim labeling of the nucleolus. This finding is consistent with an antiproliferative effect. Overall, these findings are additive to our previous observations, and demonstrate that heparin causes EC cytoskeletal reorganization which is a potential mechanism for vascular relaxation.

Increased nitric oxide production in patients with hypotension during hemodialysis.

OBJECTIVE: To determine the involvement of nitric oxide production in hemodialysis-induced hypotension. DESIGN: Examination of nitric oxide synthesis, cyclic guanosine 3'5'-monophosphate (cGMP) levels, and endothelin-1 levels in plasma before and after hemodialysis. SETTING: Veterans Affairs medical center. PATIENTS: 13 patients with end-stage renal failure who were receiving hemodialysis: Six patients had hypotensive episodes during dialysis and 7 did not. INTERVENTION: Patients received heparin at a bolus dose of 2000 U at the initiation of dialysis followed by 1000 U/h during 4-hour hemodialysis sessions. RESULTS: Nitric oxide production markedly increased during hemodialysis-induced hypotensive episodes; this increase was not seen in patients who did not have a hypotensive episode. In both groups, the plasma cGMP and endothelin-1 levels decreased after hemodialysis. According to multiple regression analysis, standard coefficients of nitric oxide production, plasma cGMP levels, and endothelin-1 levels with mean blood pressure after hemodialysis were -0.743, -0.07, and 0.31, respectively. CONCLUSION: Nitric oxide production increased in patients who had a hypotensive episode during hemodialysis but did not increase in those who did not have a hypotensive episode.

In-hospital cardiopulmonary resuscitation. Survival in 1 hospital and literature review.

Cardiopulmonary resuscitation (CPR) has been used extensively in the hospital setting since its introduction over 3 decades ago. We reviewed the CPR records at 1 hospital during a 2-year period and the results from 113 published reports of inpatient CPR with a total patient population of 26,095. We compared the survival rates of patients following CPR and the pre-arrest and intra-arrest factors related to survival. At the hospital where CPR records were reviewed, 44% of patients initially survived following CPR, and the 1-year survival rate was 5%. Patients with shorter durations of CPR and those administered fewer procedures and medications during CPR survived longer than patients with prolonged CPR. Patients with witnessed cardiac arrests were more likely to survive than those with unwitnessed arrests. Also, patients with respiratory arrests had much better survival than patients with cardiopulmonary arrests. Worldwide, 113 studies showed a survival to discharge rate of 15.2% (United States = 15%, Canada = 16%, United Kingdom = 17%, other European countries = 14%). Patients were more likely to survive to discharge if they were treated in a community hospital (versus a teaching or Veterans Affairs hospital) or were younger. Patients with ventricular tachycardia or fibrillation were more likely to survive than those with asystole or electromechanical dissociation. Patient's location was related to outcome, with emergency room and coronary care unit patients more likely to survive than intensive care unit and general ward patients. Other factors related to better survival rates were respiratory arrest, witnessed arrest, absence of comorbidity, and short duration of CPR. Knowledge of the likelihood of survival following CPR for subgroups of the hospital population based on pre-arrest and intra-arrest factors can help patients, their families, and their physicians decide, with compassion and conviction, in what situations CPR should be administered.

Animal model of spinal cord infarction induced by cholesterol embolization.

Though several animal models of ischemic brain infarction have been developed, no animal model of purely ischemic spinal cord infarction exists. In humans, such paralysis often occurs as a complication of aortic surgery. While working on an animal model of cholesterol embolic renal disease, the authors produced an animal model of ischemic spinal paralysis by direct intraaortic injection of cholesterol suspension. With histologic examination of spinal cords of the paralyzed rats, prominent cholesterol crystals were found obliterating the lumen of the anterior and/or posterior spinal arteries. Spinal cord infarction was seen most prominently in the lateral columns and anterior horns, though other areas also were affected. Permanent paraplegia developed in most rats, but transient paralysis developed in a few, followed by partial or full recovery. This model of spinal infarction in nonanesthetized rats can be used to study the pathophysiology and therapy of spinal infarction.

Diuretics potentiate angiotensin converting enzyme inhibitor-induced acute renal failure.

Previous studies suggest that angiotensin converting enzyme (ACE) inhibitors cause reversible acute renal failure (ARF) in patients with hypertension, congestive heart failure (CHF), and renal disease. These patients often receive diuretics concomitantly with ACE inhibitors. The purpose of this study was to examine whether ACE inhibitors alone produce ARF or whether they do so when used in combination with diuretics. The medical records of patients taking ACE inhibitors without or with diuretics were reviewed. Complete data from 74 patients were obtained and the data were analyzed. These 74 patients had a diagnosis of hypertension, CHF or diabetes mellitus. BUN and serum creatinine values before, during, and after discontinuation of ACE inhibitor therapy for a mean period of 8.7 months were collected. Seventy-four patients were divided into two groups: Group A (n = 41) patients who received ACE inhibitors alone; Group B (n = 33) patients who received a combination of an ACE inhibitor and a diuretic. ARF developed in 1 of 41 (2.4%) Group A patients compared to 11 of 33 (33%) Group B patients. This group difference was highly significant (P < .001). In Group A, mean serum creatinine before (1.24 +/- .34 mg/dl) was identical to that 1.23 +/- .33 mg/dl) after 8.7 months of ACE inhibitor therapy, whereas in Group B, post-mean serum creatinine (3.11 +/- 2.27 mg/dl) was significantly (P < .01) higher than pre-mean serum creatinine (1.65 +/- .85 mg/dl). CHF patients had a higher rate of ARF than patients with other diagnoses. Urinary electrolytes showed that 4 of 6 Group B patients had chloride concentration less than 20 mEq/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired cystic disease of kidney associated with renal cell carcinoma in chronic dialysis patients.

We describe 2 cases of acquired cystic disease of the kidney (ACDK) associated with renal cell carcinoma in patients treated with long-term hemodialysis. Both patients have had dialysis for five and eight years, respectively. Renal cell carcinomas of these patients are small, averaging 2 cm in diameter. They are clear cell type. Atypical epithelial hyperplasia arising from cystic areas can be seen intermingling with carcinoma. This confirms that atypical epithelial hyperplasia is a precursor of renal cell carcinoma. Although the incidence of renal cell carcinoma arising in ACDK is on the rise, the issue of how to manage patients with ACDK remained unsettled and required further study.

An electron microscopy study of urinary sediment: relationship between myeloid body excretion and gentamicin nephrotoxicity in the rat.

We studied renal function, urinary enzymes, urinary sediment, and renal histopathology in Fischer 344 rats that were treated with one dose of mercuric chloride (HgCl2) alone, HgCl2 followed by gentamicin, gentamicin alone, or gentamicin, followed by HgCl2. HgCl2 was administered intraperitoneally at 1 mg/kg body weight. Gentamicin was injected subcutaneously at 40 mg/kg body weight. Renal function was assessed by creatinine clearance. Urinary sediment was examined using transmission electron microscopy; particular attention was given to the numbers by myeloid bodies in the urinary sediment. Renal tissue was assessed using light microscopy for acute tubular necrosis (ATN). In either HgCl2- or saline-treated rats urinary sediment showed no myeloid bodies, and renal morphology was essentially normal. The rats given HgCl2 48 h prior to initiation of gentamicin therapy showed significant decrease of myeloid bodies excretion. This was accompanied by significantly less impairment of renal function, mild renal lesion, and no necrotic tubule cells in urinary sediment. The rats treated with either gentamicin alone or gentamicin followed by HgCl2 developed significant impairment of renal function in association with marked elevation of the urinary enzymes, and variable extent of ATN. In both of these groups, urinary sediment showed a profusion of free myeloid bodies and many necrotic renal tubule cells. The urinary sediment findings, however, did not aid in distinguishing between these two treatment groups. From these data we conclude that (1) a tentative relationship exists between the concentration of the urinary myeloid bodies and severity of gentamicin nephrotoxicity; (2) prior treatment with compound(s) analogous to HgCl2 which could minimize urinary excretion of the myeloid bodies might be useful in the mitigation of gentamicin nephrotoxicity.

CAPD peritonitis. Incidence, pathogens, diagnosis, and management.

Peritonitis is a frequent complication of CAPD. Sixty percent of all patients on CAPD will have at least one episode of peritonitis during the first year of this mode of dialysis. Most of the episodes of peritonitis are caused by touch contamination of the dialysis tubing or by extension of the catheter exit site or tunnel infection. Coagulase-negative and coagulase-positive Staphylococcus are the two most common organisms, accounting for 50% or more of all CAPD peritonitis. Other gram-positive and gram-negative bacteria and fungi account for the rest. Intraperitoneal antibiotic treatments are usually effective in eradicating the infection. The choice of antibiotics depends on organisms isolated from cultured dialysate. Fungal peritonitis and, occasionally, Pseudomonas peritonitis require removal of the catheter to eradicate the infection. Prompt identification and treatment of peritonitis are essential to ensure success of a CAPD program. Although with newer techniques, like Y-connector or ultraviolet light system, the rate of peritonitis has declined; however, it has still remained the major complication of the CAPD program.