Search PubMed⌕ Search

Biomedical subjects

R A Bear

Publications and source records attributed to R A Bear.

At least 37 records · Page 2Linked to original sources
PubMed1985

A clinical approach to common electrolyte problems: 4. Hypomagnesemia.

Magnesium plays a critical role in many cell functions. Hypomagnesemia may occur because of decreased intake or absorption, internal redistribution or increased loss of this element through either renal or nonrenal routes. Manifestations of magnesium deficiency include alterations in calcium, phosphate and potassium homeostasis along with cardiac disorders such as malignant ventricular arrhythmias refractory to conventional therapy, enhanced sensitivity to digoxin and, possibly, coronary artery vasospasm and sudden death. Other features of magnesium deficiency include a host of neuromuscular and neuropsychiatric disorders. In this review we detail mechanisms that may lead to magnesium deficiency, summarize the clinical features of the deficiency and provide a clinical approach to the diagnosis and treatment of this electrolyte disorder.

Alcoholism↗
PubMed1985

Malakoplakia and immunosuppressive therapy. Reversal of clinical and leukocyte abnormalities after withdrawal of prednisone and azathioprine.

Malakoplakia is a chronic granulomatous inflammatory disorder. It is suspected clinically by the presence of chronic infection and diagnosed by histologic examination of affected tissues. Studies of 4 patients with malakoplakia--2 renal transplant recipients, 1 patient with systemic lupus erythematosus, and 1 patient with polymyositis--are reported. All patients were receiving prednisone and azathioprine at the time of diagnosis and had an infection caused by Escherichia coli. Leukocytes from all patients failed to kill Staphylococcus aureus and E coli normally in vitro. Cholinergic agonists had no apparent effect on bacterial killing in vitro or in vivo in the 2 patients examined. Clinically, malakoplakia improved significantly when immunosuppressive therapy was tapered or discontinued, and leukocyte function returned to normal in all 4 patients. The cases reported here and those documented previously suggest that the pathogenesis of malakoplakia and its treatment may not be the same for all patients. Malakoplakia may be more common than previously thought, particularly with the increased use of immunosuppressive therapy.

Abscess↗
PubMed1984

A clinical approach to common electrolyte problems: 3. Hypophosphatemia.

Hypophosphatemia is a common disorder caused by decreased intake, increased loss or transcellular shift of phosphorus. Symptoms of severe hypophosphatemia include reversible depression of myocardial function, acute respiratory failure, coma, rhabdomyolysis, osteomalacia, renal tubular acidosis and hemolysis. This paper discusses common clinical disorders associated with hypophosphatemia and presents an approach to diagnosis and treatment.

Acute Disease↗
PubMed1984

Dissecting aneurysm of renal artery. Reversible cause of high-renin hypertension.

A forty-two-year-old man was evaluated for malignant hypertension. Renal angiography demonstrated several aneurysmal dilatations and dissections involving the right renal artery. During a period of conservative medical management, hypertension was resolved; repeat renal angiography demonstrated marked spontaneous resolution of the lesion.

Adult↗
PubMed1983

Recurrent Goodpasture's syndrome.

Goodpasture's syndrome was diagnosed in a 17-year-old boy with glomerulonephritis and hemoptysis. He was successfully treated with cyclophosphamide, prednisone and courses of plasmapheresis. The syndrome recurred 3 1/2 years later and was again successfully treated.

Adolescent↗
PubMed1983

A clinical approach to common electrolyte problems: 2. Potassium imbalances.

A clinical approach to potassium imbalances is presented. Hypokalemia is rarely due solely to a reduced intake of potassium; instead, it usually results from a potassium flux into the cells or increased loss of the element, at times combined with a decreased intake. The clinician must seek the cause of the intracellular flux or the source of the gastrointestinal or renal loss. The causes of gastrointestinal losses are generally self evident. Renal potassium wasting, though, generally results from increased mineralocorticoid activity, an increased rate of urinary flow or of sodium delivery to the distal nephron, or both, hypomagnesemia or a combination of these factors. Hyperkalemia may be factitious, but usually it is caused by a flux of potassium from the cells or a decrease in the renal loss of potassium, the latter being mediated by a reduction in renal function, mineralocorticoid activity, or the rate of urinary flow or sodium delivery, or both. In both hypokalemia and hyperkalemia, treatment must be guided by the specific clinical circumstances.

Calcium↗
PubMed1983

A clinical approach to common electrolyte problems. 1. Hyponatremia.

The clinical approach to hyponatremia described in this paper involves identification of the hyponatremia as iso-osmolar (factitious), hyperosmolar (mediated by osmotically induced flux of water from cells) or hypo-osmolar. Hypo-osmolar hyponatremia results from decreased renal excretion of dilute urine. This may be caused by renal failure through decreased delivery of filtrate to or function of the ascending limb of the loop of Henle, where dilute urine is made, or through increased water reabsorption in the collecting duct, either independent of antidiuretic hormone or related to a physiologic, drug-induced or pathologic increase in the bioactivity of antidiuretic hormone. The treatment of hyponatremia must be individualized.

Absorption↗
PubMed1983

Ureteral obstruction of renal transplant due to ureteral candidiasis.

In a diabetic renal transplant recipient a nephrocutaneous fistula developed after percutaneous renal graft biopsy, and ureteral obstruction due to Candida albicans fungus balls was demonstrated. Local irrigation with amphotericin B, systemic antifungal therapy, and rigid blood sugar control led to rapid clearing of the fungal infections. This cause of renal transplant insufficiency should be considered prior to renal biopsy in diabetic patients with yeast forms in the urine.

Adult↗
PubMed1983

Localized amyloidosis of urethra.

A case of primary amyloidosis of the urethra is described. Although rare, this entity is important since its antecedent causes, clinical symptoms, and panendoscopic and radiographic appearance are similar to and must be differentiated from carcinoma of the urethra. The prognosis of this disorder is excellent, and aggressive therapy is not indicated.

Adult↗
PubMed1981

Amyloidosis and systemic lupus erythematosus.

A 59 year old man with systemic lupus erythematosus developed proteinuria and renal insufficiency. Renal biopsy revealed both crescentic glomerulonephritis and amyloid in glomeruli and blood vessels. The amyloid was characterized as secondary because of its sensitivity to potassium permanganate pretreatment of Congo red stained sections. Amyloidosis is very uncommon in systemic lupus erythematosus but may be a cause of steroid unresponsive proteinuria and renal insufficiency.

Amyloidosis↗
PubMed1981

Selected aspects of the pathophysiology of metabolic acidosis in diabetes mellitus.

Metabolic acidosis with a normal anion gap results from either bicarbonate loss or a urine acidification defect. The bicarbonate loss may be via the gastrointestinal tract or the urine, or may be indirect due to excretion of the sodium and potassium as opposed to the ammonium salts of ketone body anions. Defects in urine acidification in the diabetic have several etiologies: first, hydrogen ion secretion may be decreased because of an intrinsic defect in the hydrogen ion pump (i.e., diseases of the renal medulla); second, there may be a failure to augment hydrogen ion secretion by a favorable electrical gradient (e.g., reduced mineralocorticoids); and third, there may be a failure to generate a favorable chemical gradient to augment hydrogen ion secretion (e.g., reduced urine ammonia). Reduced levels of aldosterone associated with hyporeninemia has been termed type IV RTA, and these patients have specific therapeutic needs.

Anions↗
PubMed1981

Malakoplakia: evidence for an acquired disease secondary to immunosuppression.

A 44-year-old man was maintained on prednisone and azathioprine after renal transplantation. One and a half years after transplantation, he developed multiple perianal Escherichia coli abscesses. These became chronic and resisted antibiotic therapy. Histologically, the lesions were typical of malakoplakia. Peripheral blood neutrophils and monocytes had impaired killing of Staphylococcus aureus and E. coli in vitro. No abnormality of hexose monophosphate pathway activity, tetrazolium dye reduction, lysosomal degranulation, or cyclic nucleotides could be demonstrated in either neutrophils or monocytes. Cholinergic agonists in vitro and in vivo did not improve bacterial killing by these cells. The infection resolved rapidly and bacterial killing returned to normal when the dose of azathioprine was reduced. Our findings, when considered with previous reports, suggest that there are different causes of malakoplakia and malakoplakia may be more common than previously thought. The etiology of malakoplakia should be identified for each patient if appropriate treatment is to be given.

Adult↗