Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Robert D. Lindeman is active.

Publication


Featured researches published by Robert D. Lindeman.


The American Journal of the Medical Sciences | 1976

Hypokalemia: causes, consequences and correction

Robert D. Lindeman

Hypokalemia poses a common diagnostic challenge with many potential etiologies. Multiple factors may contribute to this electrolyte deficiency in any given patient. Gastrointestinal potassium wasting usually is identifiable by an associated increase in fluid losses via biliary tract or bowel. A urinary potassium excretion of 20 mEq or more per day in the presence of a low serum potassium (less than 3.5 mEq/L) suggests inappropriate potassium wasting. Although diuretic therapy (loop diuretics, thiazides) undoubtedly is the most common cause of a potassium deficit, one also must consider abnormalities of the pituitary-adrenal axis, renal disorders including tumors, other drugs, and a variety of less well-defined entities. Potassium deficiency may produce both functional and structural defects in the kidneys, myocardium, skeletal muscle, central nervous system, and gastrointestinal tract. Treatment is aimed at replacing potassium intravenously or orally or preventing further potassium loss (spironolactone, triamterene); when associated with a metabolic alkalosis (chloride deficiency), the replacement should be potassium chloride.


Annals of Internal Medicine | 1978

Dysphagia and vertical nystagmus in magnesium deficiency.

Isam A. Hamed; Robert D. Lindeman

Excerpt Magnesium deficiency should be anticipated as a complication in patients with extensive intestinal resections (short-bowel syndrome) (1-2). In man, it produces neuromuscular hyperexcitabili...


Microvascular Research | 1977

An analysis of the relationship of malignant lesions of the kidney to hypertension.

Anil K. Mandal; Richard D. Bell; Donald E. Parker; John A. Nordquist; Robert D. Lindeman

Abstract This study, designed in a “blind” fashion, presents, for the first time, a relationship of the histopathology of the kidneys with mean arterial blood pressure (MAP) and age in hypertensive species. Kidneys from 46 spontaneously hypertensive rats (SHR) aged 8–104 weeks were studied using light and electron microscopy (LM and EM, respectively), and their findings were compared with those in age-matched 35 normotensive Wistar rats (NR) and 28 Wistar-Kyoto rats (WKY). A scoring system for the severity of the renal changes (index scores) was developed, and the grading of the renal changes was made without any knowledge of age, MAP, or strain of rat from which kidneys were obtained. The severe (or malignant) renal lesions were found only in old SHR (av: 91 weeks), in contrast to mild or moderate renal lesions (benign) in young SHR (52 weeks or less). The findings of highly significant ( P P


Annals of Internal Medicine | 1975

Therapy of Fluid and Electrolyte Disorders

Robert D. Lindeman; Solomon Papper

Abstract The accurate clinical assessment of the individual patients condition is the first, and often the most difficult, step in successful management of most electrolyte or acid-base disturbanc...


Annals of Internal Medicine | 1974

Membranous Glomerulonephritis: Virus-Like Inclusions in Glomerular Basement Membrane

Anil K. Mandal; Dennis R. Mask; John A. Nordquist; Katerina Chrysant; Robert D. Lindeman

Excerpt To the editor: Although numerous reports have been published on viral-like particles inside glomerular endothelial cells in collagen diseases (1-3), only rarely have such particles been fou...


The American Journal of the Medical Sciences | 1976

Case report. Severe hyperuricemia, hypokalemic alkalosis and tubulointersitial nephritis.

Sompong Kraikitpanitch; Robert D. Lindeman; Anil K. Mandal

A patient with severe idiopathic hyperuricemia and hypokalemic alkalosis was followed over a one-year period. A tubulointersitial nephritis consistent with hypokalemic nephropathy was found on biopsy. However, the possibility that the hyperuricemia contributed to the hypokalemia and renal lesion cannot be excluded. Inappropriate urinary loss of potassium could be prevented by administration of spironolactone or triameterene. Six months after initiation of allopurinol therapy with reduction of serum uric acid concentrations to normal concentrations, this potassium wasting was substantially decreased.


Life Sciences | 1977

The effect of renal vasodilation and hypotonic volume expansion on water excretion in dogs after anesthesia and surgery.

Steven G. Chrysant; Susan M. Townsend; Robert D. Lindeman; Edward David Frohlich

The possible effects of renal vasoconstriction from anesthesia and surgery on water excretion after hypotonic volume expansion (HVE) were studied in 18 well conditioned anesthetized dogs, with and without the infusion of phenoxybenzamine and acetylcholine into the renal artery of the cannulated kidney. In 6 dogs (Group 1 - Control) whose renal artery was infused with isosmotic saline, HVE resulted in a bilateral increase in GFR and UV (p < .05). ERPF, Cosm, CH2O, UNaV, UKV, RBF, RVR and MAP did not change significantly. In 6 other dogs (Group 2), whose cannulated kidney was infused with phenoxybenzamine 50 μg/min before and during HVE, GFR increased on the infused side while CH2O and UV increased bilaterally (p < .05). ERPF, Cosm, UNaV, UKV, RBF, RVR and MAP were not affected significantly. The addition of ADH, 2 mu/min into the phenoxybenzamine infusate, decreased ERPF, RBF and RVR bilaterally and CH2O on the infused side (p < .05). It had no effect upon GFR, Cosm, UNaV, UKV and MAP. In another 6 dogs, (Group 3), whose cannulated renal artery was infused with acetylcholine (20 μg/min) before and during HVE, CH2O, UV and RVR increased bilaterally (p < .05). ERPF and RBF decreased bilaterally (p < .05), whereas GFR, Cosm, UNaV and MAP were unaffected. UKV decreased on the infused side (p < .05). The addition of ADH (2 mu/min)_into the acetylcholine infusate, decreased CH2O bilaterally and increased Cosm and UKV on the control side (p < .05). It had no effect on ERPF, GFR, UV, UNaV, RBF, RVR and MAP. These observations suggest that anesthesia and surgery produce renal vasoconstriction and this together with increased ADH release, interfere with water excretion by the kidney. Previous renal vasodilation prevents these influences of anesthesia and surgery.


Journal of Laboratory and Clinical Medicine | 1972

Influence of acute tissue injury on zinc metabolism in man

Robert D. Lindeman; Robert G. Bottomley; Raymond L. Cornelison; Lawrence A. Jacobs


Journal of Laboratory and Clinical Medicine | 1973

Myocardial zinc metabolism in experimental myocardial infarction

Robert D. Lindeman; Aniece A. Yunice; Donald J. Baxter; Leonard R. Miller; John A. Nordquist


Journal of Laboratory and Clinical Medicine | 1978

Effects of acute and chronic splenectomy on experimental acute renal tubular lesions

Anil K. Mandal; Carl C. Haygood; Richard D. Bell; Thomas Sethney; Thomas M. James; John A. Nordquist; Aniece A. Yunice; Robert D. Lindeman

Collaboration


Dive into the Robert D. Lindeman's collaboration.

Top Co-Authors

Avatar

Aniece A. Yunice

United States Department of Veterans Affairs

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Donald J. Baxter

United States Department of Veterans Affairs

View shared research outputs
Top Co-Authors

Avatar

John A. Nordquist

United States Department of Veterans Affairs

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Richard D. Bell

United States Department of Veterans Affairs

View shared research outputs
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge