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Biomedical subjects

J E Hano

Publications and source records attributed to J E Hano.

At least 19 recordsLinked to original sources
PubMed1998

Using the hemodialysis prognostic nutrition index and urea reduction ratio to predict morbidity and mortality: a pilot study of the 1995 council on renal nutrition national research question.

OBJECTIVE: To validate the use of the hemodialysis prognostic nutrition index (HPNI) in an alternate hemodialysis population and to determine if use of urea reduction ratio would improve use in outcome prediction for morbidity and mortality. DESIGN: Prospective random cohort. SETTING: Hospital based non-for-profit outpatient dialysis unit. PATIENTS: Forty chronic hemodialysis patients, 50% men, 50% black, 16% diabetic, 67.2 mean months on hemodialysis, mean age 54.5 years. INTERVENTIONS: None; observational; tracking of routinely collected demographic, biochemical, and clinical data. MAIN OUTCOME MEASURES: Number of times and days hospitalized, mortality RESULTS: Plotting of HPNI against urea reduction ratio produced risk quadrants for hospitalization that were more predictive than HPNI alone. CONCLUSION: Application continues as a multicenter collaborative Council on Renal Nutrition National Research Question.

Adolescent↗
PubMed1990

Asymptomatic, nonketotic, severe hyperglycemia with hyponatremia.

We describe five patients with asymptomatic, nonketotic, severe hyperglycemia (serum glucose concentrations between 45.8 and 92 mmol/L) in the face of renal insufficiency are described. As opposed to most of the previously described patients with hyperglycemic, nonketotic, hyperosmolar coma, our patients were hyponatremic. The lack of symptoms in our patients may be related to the absence of cerebral cellular dehydration. Aggressive treatment of hyperglycemia in such patients is unnecessary. Attention to the serum sodium level as well as to the serum glucose concentration will allow recognition of this clinical entity.

Acute Kidney Injury↗
PubMed1989

Successful revascularization of an occluded renal artery after prolonged anuria.

Renal atherosclerosis and fibromuscular dysplasia are the most common causes of curable human renovascular hypertension and renal failure. Vascular reconstruction often preserves renal function, but renal failure is rarely reversed, especially after days of anuria. We report a case of a 23-year-old woman who as a child underwent a nephrectomy for congenital hydroureter and renal hypoplasia. She later experienced fibromuscular dysplasia of the remaining renal artery, which ultimately progressed to a complete occlusion and 31 days of total anuria. The patient was revascularized, and within 2 months renal function returned with a blood urea nitrogen and creatinine of 9.0 and 1.0 mg/dl, respectively. After a follow-up of 6 months the patient's blood pressure remained 120/80 to 130/80 mm Hg without administration of hypertension medication. In this report we emphasize that under selected circumstances a kidney can survive prolonged ischemia and that delayed revascularization may reestablish renal function.

Adult↗
PubMed1988

Effects of interleukin-2 immunotherapy on renal function.

Recombinant interleukin-2 (IL-2) infusions have recently been evaluated as a new form of immunotherapy for the treatment of malignancies. This form of therapy has been complicated by the development of fluid retention, azotemia, and hypophosphatemia. To evaluate the effects of IL-2 on renal function, we prospectively studied eight patients who received IL-2 (10(5) micron/kg every eight hours intravenously [IV]) for five days as the initial phase of a treatment protocol using IL-2 plus lymphokine activated killer (LAK) cells. Dopamine and fluids were used to maintain blood pressure and all patients received indomethacin (100 mg/d). IL-2 therapy produced a syndrome similar to endotoxemia with the development of respiratory alkalosis (pH = 7.44 +/- .2, pCO2 = 30 +/- 2) and hypotension (mean BP, 71.3 mm Hg). These changes were accompanied by marked sodium avidity, edema formation, and mild elevations of BUN and creatinine. Hypophosphatemia, hypocalcemia, and hypomagnesemia were commonly seen. No defects in renal calcium, magnesium, phosphorous, net acid excretion, or glycosuria were demonstrated. We conclude: (1) IL-2 induces an increase in vascular permeability causing the development of edema, sodium avidity, and prerenal azotemia as occurs during endotoxemia; (2) IL-2 therapy induces respiratory alkalosis with the subsequent intracellular shift of phosphorous accompanied by increased renal phosphorous reabsorption; and (3) there is no evidence of renal tubular dysfunction (renal tubular acidosis [RTA], renal leak of glucose, phosphorous, or magnesium).

Acid-Base Equilibrium↗
PubMed1987

Occurrence of renal tubular dysfunction in lupus nephritis.

We prospectively evaluated 30 patients who presented with active systemic lupus erythematosus (SLE) for the presence of tubular abnormalities. All patients fulfilled the American Rheumatology Association criteria for SLE. When appropriate, a renal biopsy was performed. Of the 30 patients studied, 12 had no abnormal tubular study results, whereas 18 patients had some form of defect in the handling of potassium, sodium, or hydrogen ions. Eight patients had distal renal tubular acidosis (dRTA) due to an isolated proton secretory defect. Five had dRTA of the gradient or acid back-leak type. Two had an unresponsive voltage-dependent form of dRTA; one had a responsive voltage-dependent form of dRTA. One individual had hyporeninemic hypoaldosteronism and one had dRTA plus hypoaldosteronism. Clinically, patients with the abnormal tubular study results more often presented with nephritis or nephrotic sediment, peripheral edema, or anemia. Renal biopsies failed to demonstrate any difference in glomerular histologic findings and calculated activity, chronicity, or interstitial indexes. We conclude that SLE may be associated with a variety of tubular defects.

Acidosis, Renal Tubular↗
PubMed1986

Myocardial infarction with normal results of coronary angiography following diltiazem withdrawal.

Abrupt withdrawal of calcium channel blocking agents has been associated with symptoms of ischemic heart disease, but acute myocardial infarction has not been noted. Herein is described a severely uremic patient who had an acute myocardial infarction shortly after discontinuance of diltiazem, although results of subsequent coronary arteriography were normal. It is postulated that myocardial damage occurred because of increased intracellular calcium flux, augmented myocardial contractility, and/or drug withdrawal-related coronary spasm.

Adult↗
PubMed1986

Systemic lupus erythematosus presenting with hyporeninemic hypoaldosteronism in a 10-year-old girl.

Hyperkalemia has been noted to occur spontaneously in patients with long-standing systemic lupus erythematosus who did not have advanced renal insufficiency. The patients previously described all had relatively normal renin-aldosterone systems, and the hyperkalemia was thus presumed to be secondary to a primary defect in renal tubular potassium secretion. We describe at 10-year-old girl with lupus nephritis, without significant renal insufficiency, who had hyperkalemia from hyporeninemic hypoaldosteronism postulated to be due to vasculitis involving the afferent/efferent arterioles and juxtaglomerular apparatus.

Aldosterone↗
PubMed1986

Hypertension, mineralocorticoid-resistant hyperkalemia, and hyperchloremic acidosis in an infant with obstructive uropathy.

An 8-week-old infant with hypertension, hyperkalemia, and hyperchloremic acidosis, presumably due to chloride shunt type of distal renal tubular acidosis, is described. The patient's renin-aldosterone axis was intact. The infant was also found to have an obstructed solitary kidney. Despite correction of the obstruction and improvement in the glomerular filtration rate accompanied by normal development, hyperkalemia and renal tubular acidosis persisted. The defect was still demonstrable 9 months following relief of the obstruction. We conclude that neonatal obstructive uropathy can result in renal tubular acidosis of the chloride shunt type. The reversibility of this defect is, as yet, unknown.

Acid-Base Equilibrium↗
PubMed1986

Transdermal clonidine in mild hypertension. A randomized, double-blind, placebo-controlled trial.

In 30 patients with mild essential hypertension, clonidine hydrochloride was delivered from a skin patch reservoir designed to release medication at a constant rate for seven days. After a four-week washout period, patients were randomized (double-blind) into a clonidine- or a placebo-treated group. Clonidine or placebo was then given for five weeks, followed by a two-week washout period to assess withdrawal from treatment. Blood pressure was controlled in 11 of 15 clonidine-treated patients but in only four of 15 placebo-treated patients. The clonidine-treated group evidenced larger decreases in both systolic and diastolic blood pressures. In the clonidine-treated group, blood pressures and plasma clonidine levels were stable throughout a representative seven-day period. Besides mild skin irritation with both clonidine and placebo patches, few side effects were observed. After discontinuation of clonidine administration, plasma levels declined in a non-log linear manner. There was no rebound hypertension. The results suggest that clonidine delivered transdermally is safe and effective for control of mild essential hypertension.

Administration, Cutaneous↗
PubMed1985

In vivo effects of acute changes in osmolality and sodium concentration on myocardial contractility.

Effects of acute changes in osmolality and sodium concentration (Na) on myocardial contractility (MC) were examined in anesthetized dogs. Using a carotid to left anterior descending bypass, 4 cc of NaCl and/or dextrose of varying osmolality as injected and the percentage of change in MC measured. At Na = O mEq/L, a positive inotropic response occurred, which varied inversely as osmolality increased from 300 (MC = 100 +/- 23%) to 700 mOsm/L (MC = 39 +/- 10%, p less than 0.01). Similar ranges of positive responses of lesser magnitude were noted at Na = 75 mEq/L. At Na = 150, 190, or 350 mEq/L, similar increments in osmolality caused an increasingly negative inotropic response. An inverse relationship between Na and MC was noted with osmolality held constant. Injections of the nonionic contrast agent, P297, in 5% dextrose or 0.9% NaCl, resulted in 28 +/- 3% or -17 +/- 4% (p less than 0.01) change in MC, respectively. Sodium concentration and osmolality have independent effects on MC. Hyperosmolality/hypernatremia causes a negative inotropic response while hyponatremia causes a positive one.

Animals↗
PubMed1985

Ultrafiltration hemodynamics in conscious, uremic dogs: effect of a decreasing plasma urea level.

The hemodynamic effects of a decreasing plasma urea level during hemodialysis were studied in acutely uremic, conscious dogs. Each dog was studied twice, during dialytic ultrafiltration against both a urea-free (U-) and a urea-supplemented (U+) dialysate. Plasma osmolality (-13 mosm/kg/H2O +/- 10 SD, p less than 0.01) and urea levels (-43 mg/dl +/- 20, p less than 0.01) decreased when using the (U-) dialysate, but were unchanged with the (U+) dialysate. At the end-point of volume depletion (MAP less than 80 mm Hg) total peripheral resistance index [U (+): 3,376 +/- 743 dyn . s X cm-5 X m2, U(-): 3,091 +/- 537, NS)] and blood volume [U(+): 62.7 +/- 7.4 ml/kg, U(-): 63.7 +/- 7.5, NS)] were comparable whether or not the plasma urea level had been allowed to decrease. The data suggest that an acutely decreasing plasma urea level during dialysis does not impair hemodynamic response to volume depletion in the model described.

Acid-Base Equilibrium↗
PubMed1984

Rapid access for emergency dialysis.

Vascular access for acute hemodialysis or ultrafiltration in critically ill patients frequently requires cannulation of large-caliber veins. Repeated cannulation of these vessels present a finite risk of hemorrhage or hematoma. A teflon catheter introducer sheath system (TIS) allows for repeated use of the central circulation, requires only one major vascular entry, and can be adapted for either hemodynamic monitoring or emergency hemodialysis. Forty-six acute hemodialysis have been performed in 25 critically ill patients who have had TIS in place for hemodynamic monitoring. Dialysis was performed by inserting a femoral dialysis catheter through the TIS in place of the Swan-Ganz catheter. We have had no complications using the approach for emergency hemodialysis, and adequate dialysis was accomplished.

Blood↗
PubMed1984

Hemodynamic response to volume depletion in acutely uremic dogs.

Hemodynamic response to volume depletion by isolated ultrafiltration was compared in uremic (U) and nonuremic (N) conscious dogs. Fluid was removed at a constant rate until mean arterial pressure (MAP) decreased to less than 80 mmHg. Initial MAP was higher in the uremic dogs [132 +/- 8.6 (SD) mmHg] than in nonuremic controls (106 +/- 12, P less than 0.001). Initial cardiac index [U 4.97 +/- 0.831 X min-1 X m-2, N 4.44 +/- 0.62] and total peripheral vascular resistance index [(TPRI) U 2,160 +/- 353 dyn X s X cm-5 X m-2, N 1,976 +/- 420] were slightly, but not significantly, higher in uremic animals. Initial central venous pressure, wedge pressure, and plasma norepinephrine level were greater in the uremic dogs. At the end point of volume depletion, both uremic and nonuremic animals had achieved similar levels of TPRI, despite greatly attenuated or absent increases in plasma renin activity in the uremic group. At end point, blood volumes and plasma norepinephrine levels were comparable. The increase in pulse rate was higher in the uremic animals (59 +/- 37 pulses/min) compared with controls (25 +/- 52, P less than 0.05). In an additional group of uremic dogs, cardiovascular responses to hemorrhage and isolated ultrafiltration were compared and found to be similar, after allowance for blood viscosity changes had been made. The data suggest that in acutely uremic conscious dogs, despite reduced renin-angiotensin responses, hemodynamic adaptation to rapid volume depletion is not impaired.

Animals↗