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Dive into the research topics where William P. Argy is active.

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Featured researches published by William P. Argy.


The American Journal of Medicine | 1978

Acute renal failure following drip infusion pyelography

Alejandro Carvallo; Thomas A. Rakowski; William P. Argy; George E. Schreiner

Abstract Acute renal failure is a well-known complication of intravenous pyelography in patients with diabetes mellitus or multiple myeloma. We describe 10 patients in whom acute renal failure developed after drip infusion pyelography (DIP). Of these patients, only four were diabetic and none had multiple myeloma. All patients had preexisting renal disease. Serum creatinine was higher than 1.5 mg/dl in eight. Proteinuria, vascular disease, dehydration and fluid overload were all seen in the group. An increase in serum creatinine was noted in all patients within 48 hours following DIP. Urine volume decreased in eight patients within 24 hours after the examination. Renal function returned to the levels pre-DIP in three patients in periods ranging from eight to 10 days. In five others, serum creatinine decreased almost to the prestudy levels but remained elevated by 0.7 to 1.4 mg/dl at the time of the last observation. No patient died of acute renal failure. The data indicate that (1) preexisting renal insufficiency in the setting of systemic disease is the most prevalent predisposing factor to acute renal failure after DIP; (2) renal hypoperfusion of various types seemed to render these patients susceptible to acute renal failure after DIP; (3) in some patients, acute renal failure was not typical of acute tubular necrosis; and (4) recovery of renal function toward base line after a short period of oliguria frequently occurred. In 10 patients acute renal failure developed after drip infusion pyelography (DIP). Six had neither diabetes mellitus nor multiple myeloma. All patients had preexisting renal disease. Proteinuria, vascular disease, fluid overload and volume contraction were noted. All patients had elevated serum creatinine levels and eight were oliguric. Return of renal function toward base line was frequently seen. The prevalent predisposing cause of acute renal failure after DIP was preexisting renal disease on a background of systemic disease.


Annals of Internal Medicine | 1971

Diabetic Glomerulosclerosis in the Absence of Glucose Intolerance

Frank G. Strauss; William P. Argy; George E. Schreiner

Abstract A patient with the nephrotic syndrome had a renal biopsy specimen that showed typical well-formed mesangial nodules and occasional fibrin cap lesions, as are found in diabetes mellitus. Th...


Nephron | 1976

Evaluation of Percutaneous Kidney Biopsy in Advanced Renal Failure

John J. Curtis; Thomas A. Rakowski; William P. Argy; George E. Schreiner

As more information is gained on the long-term survival in chronic dialysis and transplant patients, it is unacceptable to be satisfied with a clinical impression of the etiology of the end stage renal failure in each case. It becomes important to know the histological diagnosis in patients who present with terminal renal failure. In the past there was little to offer such individuals in terms of therapeutics, and their prognosis was uniformly poor. Thus, biopsy for other than academic reasons was difficult to justify. This is no longer true and presented here is a series of 28 such patients in whom percutaneous renal biopsy was performed. The complications and diagnostic yield are reported. It is further demonstrated that the added knowledge of histological diagnosis can be of benefit to the individual patient.


Annals of the New York Academy of Sciences | 2006

Clinical evaluation of carisoprodol in cerebral palsy.

William P. Argy

A review of the literature on carisoprodol indicates satisfactory results with regard to muscle relaxation and The only untoward reactions noted in these reports were drowsiness and in rare instances the occurrence of a rash. To date, the exact mode of action of drugs such as carisoprodol has been rather confusingly and vaguely defined. Concurrently with a vast number of so-called tranquilizers that have been flooding the field, we have references to internuncial blocking agents, acetylcholine neutralizers, and amine oxidase inhibitors. On the whole, the exact nature of the reactions involved, in my opinion, has been difficult to understand and appreciate. From a clinical standpoint, there are many factors in favor of the theory of Spears and Phelps2 that carisoprodol produces a kinesthetic block in the cerebellum. Much work needs to be done before definite proof of this theory is obtained. Other mechanisms may be what might be called inhibition of excessive facilitation and facilitation of decreased inhibition. Either of these actions could take place in the reticular system of the brain stem. In two cases, children who were receiving 350 mg. carisoprodol twice daily developed tremor within a few days. In one instance the parents refused to continue the drug. In the other case, the tremor disappeared when the dose was increased to 700 mg. twice daily. Both of these children were athetoids with compensatory muscle spasm. The observed tremor may result from drug action of the following types: stimulation of the activating areas, sufficient stimulation to release a tremor, or sufficient relaxation of the spastic muscle to permit the rhythmic contractions of the antagonistic muscles. Two of the children had Jacksonian convulsions during the period of drug administration. One had rigidity and the other spasticity; both patients were topographically quadriplegic. We did not attribute these convulsions to the action of carisoprodol because they existed before the onset of this treatment. In one instance, phenobarbital administration had been discontinued because of a possible conflict with carisoprodol; the convulsions stopped when phenobarbital was resumed. Furthermore, no other children developed convulsive a t tacks. It was decided that improvement could be measured in terms of degrees of relaxation of the muscles involved. Inoreases in the range of passive movement could be gauged with the protractor or by the patient’s ability to lock the braces. In addition to this, the patient’s over-all response to therapy could also be of value. A 250-mg. capsule, and later a 350-mg. capsule, of carisoprodol was administered twice daily. The dose was then increased to 700 mg. twice daily and in one instance 1050 mg. was given three times a day with no untoward results. I t was decided to give all new cases initial doses of 700 mg. twice daily. In a


Archive | 1986

Creatine Kinase, Amylase, and Parathyroid Hormone in Stable CAPD and Hemodialysis Patients

J. Rahmat; J. F. McAnally; James F. Winchester; Thomas A. Rakowski; N. Perri; William P. Argy; George E. Schreiner

Since there are conflicting reports on elevation of plasma creatine kinase and amylase above normal in dialysis patients we studied total and isoenzyme fractions of creatine kinase and amylase. In addition since hyperparathyroidism and pancreatitis are associated we also studied plasma-n-terminal parathyroid hormone levels. Studies were performed in 35 stable CAPD patients, and creatine kinase alone was studied in 11 stable hemodialysis patients. Total creatine kinase was elevated in nine of 35 CAPD patients (25.7%); elevated isoenzyme fractions of CK were as follows: nine of nine patients had elevated MM band, one of nine had elevated MB and one of nine had elevated BB band. In the hemodialysis patients two of 11 had elevated CK (MM bands). Total amylase was elevated in 17 of 26 CAPD patients with ten of these patients having an elevated pancreatic isoenzyme fraction; in six of 17, the salivary isoenzyme fraction equalled the pancreatic enzyme fraction in one patient. Parathyroid hormone was elevated in 24 of 35 CAPD patients, but no correlation existed between parathyroid hormone levels, creatine kinase and amylase, although there was a significant correlation between creatine kinase and amylase levels in CAPD patients (r = 0.4, n = 23, p < 0.05). These findings suggest a common etiology for elevated creatine and amylase in otherwise stable CAPD patients such as inadequate dialysis, subclinical skeletal myopathy, or metabolic complications. These findings warrant further study.


Archive | 1986

The Telephone—An Underestimated Resource for CAPD Nursing Management

W. F. Barnard; N. Kloberdanz; William P. Argy; Thomas A. Rakowski; James F. Winchester

Telephone communication between CAPD nursing staff and patients, avoids unnecessary delays in dealing with simple problems, giving support to patients, and judging whether patients have serious problems necessitating acute nursing/medical management. The telephone serves as a vital link between patient and nursing personnel.


Annals of Internal Medicine | 1982

Survival with End-Stage Renal Disease

Alexander C. Chester; William P. Argy; Thomas A. Rakowski; George E. Schreiner

Excerpt To the editor: Hutchinson and associates (1) make a substantial contribution to the type of analysis needed to understand the natural history of end-stage renal disease. Data such as these ...


Annals of Internal Medicine | 1972

Complications of Peritoneal Dialysis.

David M. Roxe; William P. Argy; George E. Schreiner

ABSTRACT: Peritoneal dialysis is an easily available therapeutic procedure. The complications noted in 490 dialyses over a six-year period in a university hospital have been reviewed. Seventeen major and 624 minor complications occurred. Only four deaths could be attributed to the procedure itself. Peritoneal dialysis is an effective procedure but one with a significant incidence of complications, though few of these are associated with mortality or morbidity for the patient. Various safeguards against these are discussed.


JAMA Internal Medicine | 1979

Hemodialysis in the eighth and ninth decades of life.

Alexander C. Chester; Thomas A. Rakowski; William P. Argy; Anna Giacalone; George E. Schreiner


JAMA | 1980

Fibrosing Uremic Pleuritis During Hemodialysis

Raul Rodelas; Thomas A. Rakowski; William P. Argy; George E. Schreiner

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Harry G. Preuss

Georgetown University Medical Center

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J. Rahmat

Georgetown University

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N. Perri

Georgetown University

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