Robert L. Winer
United States Department of Veterans Affairs
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Featured researches published by Robert L. Winer.
Clinical Immunology and Immunopathology | 1977
Robert L. Winer; Arthur H. Cohen; Ajit S. Sawhney; John T. Gorman
Abstract Renal functional abnormalities and evidence of interstitial nephritis are common in Sjogrens syndrome, and it has been suggested that the interstitial changes may be on an immunologic basis. We report a patient with the sicca complex variety of Sjogrens syndrome who presented with renal functional insufficiency and intense interstitial nephritis. Focal tubular basement membrane (TBM) deposits were observed, and immunofluorescence showed focal TBM deposits of IgG and C3. Glomeruli contained no deposits. Therapy with prednisone and cyclophosphamide was associated with marked clinical improvement and regression of tissue leukocyte infiltration. We propose local or in situ formation of immune complexes, as in the rabbit model of autologous immune-complex interstitial nephritis, and suggest that this mechanism may be operative in some patients with Sjogrens syndrome and tubulointerstitial renal disease. Immunosuppressive therapy may have helped to preserve renal function.
Nephron | 1979
Samia Aziz; Arthur H. Cohen; Robert L. Winer; Francisco Llach; Shaul G. Massry
The present study describes 3 patients with the simultaneous occurrence of diabetic nephropathy and immune-complex mediated glomerulonephritis. Renal manifestation included proteinuria and hematuria which were preceded by or co-existent with an infectious process. Renal manifestation included proteinuria and hematuria which were preceded by or co-existent with an infectious process. Renal histology showed the characteristic change of diabetic nephropathy along with those of immune complex glomerulonephritis. Immunofluorescence studies showed a linear pattern with a superimposed granular pattern of IgG and C3 deposits. Renal function and urinary findings improved in the 2 patients who were followed up.
American Journal of Kidney Diseases | 1987
Gaurang M. Shah; Robert L. Winer; Ralph E. Cutler; Allen I. Arieff; William G. Goodman; John W. Lacher; Patricia Schoenfeld; Jack W. Coburn; Arthur M. Horowitz
While the use of magnesium-containing compounds is usually contraindicated in dialysis patients, the risk of toxicity from hypermagnesemia can be reduced by lowering the magnesium concentration in dialysate. We examined the effects of a magnesium-free dialysate on both serum magnesium level and the peritoneal removal rate of magnesium over 12 weeks in 25 stable patients undergoing continuous ambulatory peritoneal dialysis (CAPD). After 2 weeks, the serum magnesium level decreased from 2.2 to 1.9 mg/dL (0.9 to 0.8 mmol/L) (P less than .02) and the peritoneal removal rate increased from 66 to 83 mg/d (2.8 to 3.5 mmol/d) (P less than .05), with both values remaining stable thereafter. There was a strong association between these parameters (r = -0.62, P less than .05), suggesting that the serum magnesium level decreased as a result of the initial increased peritoneal removal rate. For an additional 4-week period, a subgroup of nine patients received magnesium-containing, phosphate binding agents instead of those containing only aluminum. During this phase, serum inorganic phosphorus was well controlled. The serum magnesium level increased only from 1.8 to 2.5 mg/dL (0.7 to 1.0 mmol/L) (P less than .05), due in great part to the concomitant 41% rise in peritoneal magnesium removal from 91 to 128 mg/d (3.8 to 5.3 mmol/d) (P less than .05). No toxicity was noted during the entire 16-week study period, nor did serum calcium change. Thus, serum magnesium levels remained within an acceptable range as magnesium-containing phosphate binders were given through the use of magnesium-free peritoneal dialysate.(ABSTRACT TRUNCATED AT 250 WORDS)
Metabolism-clinical and Experimental | 1982
Robert L. Winer; M.Mashhoordin Rajudin; W. Ronald Skowsky; Lawrence N. Parker
A common endocrine defect in uremia is gonadal dysfunction with decreased testosterone production. Since gonadal and adrenal tissues share androgen biosynthetic pathways, we studied the stimulated adrenal androgen response in uremic patients. In contrast to the delayed or subnormal gonadal response to hCG reported by others, the adrenal response of androgens, as well as cortisol and aldosterone, to cosyntropin stimulation was unimpaired. In summary, the secretory reserve capacity of the adrenal gland for androgen, glucocorticoids and mineralocorticoids in uremia was studied with cosyntropin stimulation and found to be wall preserved.
The Journal of Urology | 1975
Raymond Fay; Robert L. Winer; Arthur M. Cohen; Stanley A. Brosman; Cleaves M. Bennett
The association of hypertension with congenital renal hypoplasia (Ask-Upmark kidney) has been well established. A case is presented that clearly demonstrates the distinctive clinical, roentgenographic and pathologic features. An abnormal production of renin by the affected kidney suggested that the renin-angiotensin-aldosterone axis was involved in the genesis of the hypertension. Hypertension was cured by unilateral nephrectomy.
American Journal of Kidney Diseases | 1986
Gaurang M. Shah; Robert L. Winer; Harvey C. Krasny
Acyclovir is an effective agent for the treatment of herpes virus infections, however, the pharmacokinetics of the drug are altered in renal failure. We studied this drug in a continuous ambulatory peritoneal dialysis (CAPD) patient who was immunocompromised and had cutaneous herpes infection. The elimination half-life (17.1 hours) was similar to that reported for end-stage renal disease (ESRD) patients, while the volume of the central compartment (29.6 L/1.73 m2), the steady state volume of distribution (68.1 L/1.73 m2), and the total body clearance (48.3 mL/min/1.73 m2) were greater. The mean CAPD clearance was only 4.4 mL/min, with less than 10% of an administered dose being recovered in the 24-hour dialysate. Further studies are needed to establish a dosing regimen for CAPD patients.
Archive | 1982
Joel D. Kopple; Charlotte E. Roberts; Gerald P. Grodstein; Gaurang M. Shah; Robert L. Winer; Warren D. Davidson; Dan A. Henry; Stanley S. Franklin
It is accepted that in patients with chronic renal failure, dietary control of salt and water balance and diuretics should be used to prevent depletion or excessive retention of salt and water.1 Similarly, there is little argument concerning the need to control dietary potassium, phosphorus, and magnesium intake, to provide calcium and vitamin supplements, and to use phosphate binders in such patients.1,2 Thus the controversy concerning the value of dietary therapy in chronic uremia relates to the management of protein intake to postpone dialysis therapy and optimize nutritional status.
JAMA | 1977
Khosrow S. Mirahmadi; Wellington Paul; Robert L. Winer; Nosratolah Dabir-Vaziri; Bill Byer; John T. Gorman; Stanley M. Rosen
JAMA | 1981
Khalid K.Muhalwas; Gaurang M. Shah; Robert L. Winer
American Journal of Nephrology | 1984
Michael A. Madden; Stephen W. Zimmerman; David P. Simpson; Donald Purcell; Dennis C. Dobyan; Antonia C. Novello; Richard N. Fine; Diane P. Haley; Arnold R. Eiser; Damasus Jayamanne; Chester Kokseng; Hung Che; Robert F. Slifkin; Martin S. Neff; Nancy G. Kutner; Diana D. Cardenas; Vito M. Campese; Warren R. Procci; Daniel Levitan; Mark S. Romoff; David Goldstein; Shaul G. Massry; A. Côté; S. O’Regan; Arnold J. Felsenfeld; Robert A. Gutman; Francisco Llach; John M. Harrelson; Robert L. Winer; Raymond B. Wuerher