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Biomedical subjects

J A Mitas

Publications and source records attributed to J A Mitas.

At least 19 recordsLinked to original sources
PubMed1990

Torulopsis glabrata fungemia in a diabetic patient.

We have presented a case of a stable diabetic outpatient who had an acute illness that proved to be Torulopsis glabrata fungemia responsive to amphotericin B therapy. Her only apparent additional predisposition was a nonobstructing renal calculus. Fungemia with this organism in an outpatient is most unusual. T glabrata should be an additional consideration in outpatient as well as inpatient illnesses, especially in diabetic women.

Amphotericin B↗
PubMed1985

Exogenous protein as the cause of nephrotic-range proteinuria.

Hematuria and proteinuria developed in a young woman with waxing and waning symptoms suggestive of systemic lupus erythematosus. Quantitatively, the proteinuria was in the nephrotic range, but other manifestations of the nephrotic syndrome were absent. Serologic evaluation demonstrated normal results. The hematuria was subsequently found to be self-induced and related to foreign objects in the bladder. Urine protein electrophoresis confirmed severe proteinuria with a spike in the gamma region. Immunoelectrophoresis demonstrated that the proteinuria was not of human origin. Subsequent urinary protein values were normal. This case exhibits features compatible with Münchausen's syndrome and shows that severe proteinuria may be factitious.

Adult↗
PubMed1985

Ureteral involvement complicating eosinophilic cystitis.

A thirty-three-year-old woman was evaluated for eosinophilia, irritative bladder symptoms, and renal insufficiency. Eosinophilic cystitis was documented by bladder biopsy and glomerulonephritis by renal biopsy. As the glomerulonephritis and other symptoms resolved, unilateral ureteral obstruction developed with irreversible loss of right renal function. The distal ureter was found to have eosinophilic infiltration. This entity should be considered in the differential diagnosis of unilateral ureteral obstruction associated with cystitis.

Adult↗
PubMed1984

Nephrotic syndrome. Pathogenesis, clinical and therapeutic considerations.

The nephrotic syndrome is the result of a variety of immunologic mechanisms which damage the glomerular capillary wall and cause excessive protein loss. The great number of potential predisposing factors and clinical settings necessitates a thorough history and a careful examination that includes well-defined laboratory studies. Appropriate therapy covers a broad range, from doing nothing more than reducing additional insults, to the aggressive use of combined modalities, depending on the factors involved in the individual case.

Humans↗
PubMed1984

Remission and exacerbation of tumor-related nephrotic syndrome with treatment of the neoplasm.

A 61-year-old man presented with nephrotic syndrome in March 1978. Renal biopsy revealed mesangial and endocapillary proliferation with no underlying cause found. One year later, evaluation of back pain resulted in the finding of undifferentiated adenocarcinoma with compression fracture of the T-11 vertebra. Local irradiation relieved the pain and ameliorated the nephrotic syndrome. In 1981 the nephrotic syndrome recurred. Evaluation revealed metastases to the right pelvis and to the brain without an identifiable primary lesion. Irradiation of these lesions reduced protein excretion to 50 to 150 mg/day. A gastric carcinoma was later found. Exacerbation of nephrotic syndrome may herald exacerbation of tumor activity as occurs in Hodgkin's disease. Survival with tumor-related nephrotic syndrome is not invariably poor, and treatment of metastases may be worthwhile in similar patients in whom only partial tumor reduction is possible.

Adenocarcinoma↗
PubMed1983

Baroreflex dysfunction in patients with adult-onset diabetes and hypertension.

Ten patients with adult-onset diabetes in whom diabetes antedated the appearance of hypertension were evaluated. These patients had evidence of diabetic autonomic neuropathy, including significant orthostatic hypotension (four patients), impotence (three patients), and evidence of diabetic peripheral sensorimotor neuropathy (nine patients) in clinical testing and nerve conduction study results. Baroreflex function was evaluated by multiple hemodynamic tests, including inhalation of amyl nitrite and intravenous administration of phenylephrine, before and after parasympathetic blockade with atropine, and the cold pressor test; results were compared with results in normal control subjects, patients with essential hypertension, and two subgroups of uremic patients undergoing maintenance hemodialysis. Baroreflex function was significantly abnormal in the diabetic patients and was consistent with combined parasympathetic and sympathetic motor nerve (efferent) dysfunction in the baroreflex arc. There was a significant inverse correlation between the degree of orthostatic hypotension in the diabetic patients and their baroreflex response to phenylephrine (r = -0.680, p less than 0.05). There was no significant correlation between supine hypertension in the patients with diabetes and any of the hemodynamic or biochemical parameters examined. The results suggest that orthostatic hypotension in these patients is related to baroreflex dysfunction. However, baroreflex dysfunction does not appear to be a factor in the development of hypertension in these patients, although more studies with normotensive diabetic patients are needed to confirm this point.

Aged↗
PubMed1983

Determinants of serum 1,25(OH)2D levels in renal disease.

Serum 1,25(OH)2D and factors related to its production were studied in 39 patients with various degrees of renal insufficiency. Serum 1,25(OH)2D levels correlated positively with 1/serum creatinine values (r = 0.54, P less than 0.001) and negatively with serum phosphorus (r = -0.39, P less than 0.02) and age (r = -0.33, P less than 0.05). There was no significant correlation between 1,25(OH)2D levels and serum calcium or calcitonin or PTH, although the logarithm of PTH correlated inversely with 1,25(OH)2D levels (r = -0.47, P less than 0.01). Patients who had normal or supranormal 1,25(OH)2D levels despite low GFR tended to have low serum phosphorus values. Serum levels of bone Gla protein (BGP), a biochemical marker for bone metabolism, correlated negatively with 1/serum creatinine (r = -0.39, P less than 0.02) and positively with PTH (r = 0.57, P less than 0.001) and age (r = 0.33, P less than 0.05). Prophylaxis with 1,25(OH)2D should be considered in patients with significantly decreased serum 1,25(OH)2D levels, as seem to occur when serum creatinine is greater than 4.0 mg/dl. However, despite the statistically significant correlation between serum 1,25(OH)2D and 1/serum creatinine, direct measurement should be used to ascertain the serum concentration of 1,25(OH)2D in chronic renal insufficiency.

Adult↗
PubMed1983

Crescentic glomerulonephritis complicating idiopathic membranous glomerulonephropathy.

We describe the course of a patient with multiple rectal abscesses and progressive renal dysfunction. A renal biopsy demonstrated a membranous glomerulopathy associated with extensive crescent formation. No underlying cause for the glomerulonephritis could be identified and, specifically, the anti-GBM antibody present in other similar cases was not found. There appears to be a subset of patients with membranous glomerulopathy in whom crescents develop with rapid loss of renal function. Anti-GBM antibody is not necessary in the pathogenesis of this lesion.

Abscess↗
PubMed1983

Diabetic neuropathic pain: control by amitriptyline and fluphenazine in renal insufficiency.

Seven patients with diabetes of ten to 24 years' duration and renal insufficiency were treated with fluphenazine and amitriptyline in an attempt to control severe pain in the extremities. Six patients had relief of pain within five days of initiation of therapy. One patient had no pain relief despite mood alteration. The relief of pain persisted whether renal function was stable or declining. This form of therapy is safe and as effective in patients with neuropathic pain and mild to moderate renal insufficiency as in patients with normal renal function.

Adult↗
PubMed1981

Renal papillary necrosis in thyroid carcinoma.

A thirty-four-year-old man with progressive visual impairment was found to have thyromegaly and renal insufficiency at the time of admission. Subsequent evaluation demonstrated bilateral optic neuritis and a thyroid nodule which proved to be a follicular carcinoma. Nephrologic studies revealed bilateral papillary necrosis and chronic interstitial nephritis on biopsy. The patient's renal function stabilized and twenty-four-hour protein excretion diminished after hemithyroidectomy. Carcinoma-related protein production may have played a role in the development of the observed renal lesions. Carcinoma should be a consideration in patients with unexplained papillary necrosis.

Adenocarcinoma↗
PubMed1981

Renal hemodynamic changes during long-term antihypertensive therapy.

Studies of renal hemodynamics were carried out in 84 patients with essential hypertension during long-term antihypertensive therapy with a number of drugs. Renal perfusion was maintained or enhanced despite a fall in mean arterial pressure during therapy with hydrochlorothiazide, furosemide, clonidine, prazosin, and the combination of guanabenz and hydrochlorothiazide. Renal perfusion deteriorated during long-term treatment with propranolol. Renal hemodynamics may be enhanced, maintained, or adversely influenced depending on the choice of antihypertensive agent.

Antihypertensive Agents↗
PubMed1981

Recovery from rapidly progressive glomerulonephritis. Improvement after plasmapheresis and immunosuppression.

Two patients with rapidly advancing renal insufficiency underwent biopsy and were found to have crescentic glomerulonephritis. Patient 1 demonstrated findings compatible with Goodpasture's syndrome. Crescents were present in 100% of his glomeruli. Patient 2 had findings of immune complex-mediated glomerulonephritis and crescents in greater than 90% of his glomeruli. Both patients were treated with high-dose prednisone, cyclophosphamide, and plasmapheresis. Patient 2 additionally required hemodialysis for a brief period. Renal function improved in both patients and has not deteriorated after follow-up of 14 and 18 months, respectively. Repeated renal biopsies were performed in each patient. Our findings suggest that clinical improvement and histologic healing are possible in rapidly progressive glomerulonephritis despite the initial presence of crescents in every glomerulus.

Adult↗
PubMed1980

Hypernatremia in hepatic failure.

The presence of hypernatremia in patients with hepatic failure has not received major attention. We examined the records of 25 patients admitted to the hospital with decompensated liver disease (usually Laënnec's cirrhosis) and found hypernatremia in 15. Probable causes include increased insensible water losses, impairment of water intake due to encephalopathy, and the use of osmotic cathartics with hypotonic enteric losses. Patients in this series showing hypernatremia had a mortality of 87%. Mortality in those without hypernatremia was 60%. The presence of increased serum sodium concentrations in patients with decompensated liver disease is an ominous but correctable abnormality reflecting a disturbance in water balance.

Adult↗
PubMed1980

Hepatic coma after open heart surgery.

Fulminant hepatic failure has been reported in patients with chronic congestive heart failure. Two patients in whom jaundice and coma followed cardiac surgery were studied to find the possible etiology. Clinical, biochemical, and histologic evaluations revealed low cardiac output; elevated levels of bilirubin, lactic dehydrogenase, serum glutamic oxaloacetic transaminase, and alkaline phosphatase; prolonged prothrombin time; and centrizonal necrosis of hepatocytes with sinusoidal dilatation. No other possible causes of hapatic dysfunction and coma were identified. We conclude that acute postoperative congestive heart failure may cause fulminant hepatic failure and metabolic encephalopathy.

Acute Disease↗