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Biomedical subjects

M A Perazella

Publications and source records attributed to M A Perazella.

At least 37 records · Page 2Linked to original sources
PubMed1999

Trimethoprim-sulfamethoxazole therapy in outpatients: is hyperkalemia a significant problem?

A prospective, randomized clinical study was undertaken to determine the effect of standard-dose trimethoprim-sulfamethoxazole combination treatment on serum potassium concentrations in outpatients treated in an ambulatory clinic. Ninety-seven patients were treated with oral antibiotics for a variety of infections. Fifty-one patients treated with trimethoprim-sulfamethoxazole (trimethoprim, 320 mg/day; sulfamethoxazole, 1,600 mg/day) constituted the treatment group, while 46 patients treated with other antibiotics served as controls. Serum potassium, sodium, and chloride concentrations, serum carbon dioxide content, blood urea nitrogen level, serum creatinine level, and serum glucose concentration were measured. The baseline serum potassium concentration in the treatment group was 4.30 +/- (SD) 0.36 mmol/l, and it increased significantly (p < 0.001) to 4.66 +/- 0.45 mmol/l on day 5 of therapy. Subgroup analysis of mean serum potassium concentration on day 5 of therapy failed to detect clinically relevant hyperkalemia. In patients with a serum creatinine level equal to or greater than 1.1 mg/dl (K+, 4.83 +/- 0.48 mmol/l), a nonsignificant difference (p = 0.3) in the potassium concentration was noted on day 5 as compared with patients with a serum creatinine level <1.1 mg/dl (K+, 4.63 +/- 0.44 mmol/l). Although diabetics had a higher serum potassium concentration (K+, 4.91 +/- 0.44 mmol/l) than nondiabetics (K+, 4.61 +/- 0.44 mmol/l), the difference was not statistically significant (p = 0.055). Patients aged >/=50 years (K+, 4.82 +/- 0.59 mmol/l) had a significantly different (p = 0.046) serum potassium concentration on day 5 than patients aged <50 years (K+, 4.55 +/- 0.28 mmol/l). In contrast, the baseline serum potassium concentration in the control group was 4.37 +/- 0.45 mmol/l, and it decreased (p = 0.1) to 4.22 +/- 0.4 mmol/l on 5 days of drug therapy. Trimethoprim-sulfamethoxazole therapy, when used to treat a variety of infections, leads to an increase in serum potassium concentration in most patients. After 5 days of therapy with this drug, the treatment group developed a statistically significant rise in the serum potassium concentration as compared with the control group. However, severe hyperkalemia (K+ >/=5.5 mmol/l) occurred in only 3 patients (6%) treated with trimethoprim-sulfamethoxazole. In addition, none of the subgroups of treated patients developed clinically important hyperkalemia. This suggests that outpatients, in contrast to acquired immunodeficiency syndrome patients and hospitalized patients with mild renal insufficiency, develop severe or life-threatening hyperkalemia less commonly when treated with this antimicrobial regimen. However, outpatients having risk factors which may predispose to the development of hyperkalemia should be carefully monitored when treated with trimethoprim-sulfamethoxazole.

Ambulatory Care↗
PubMed1998

Reduction in arteriovenous graft impairment: results of a vascular access surveillance protocol.

Impairment of hemodialysis (HD) vascular access, remains a frustrating problem for both the patient who possesses an arteriovenous graft (AVG) and the nephrologist who cares for the patient. We instituted a vascular access surveillance protocol intended to detect and correct evolving stenosis in patients with AVGs. The principal screen was the observation of dynamic venous pressure (VP) at a blood flow rate of 200 mL/min during the first 5 minutes of each HD session. If VP at a blood flow rate of 200 mL/min was 140 mm Hg or greater in three of six consecutive readings, recirculation greater than 15% on two observations, graft-arm swelling observed, or prolonged bleeding postdialysis observed, then the patient was referred for angiography and then angioplasty or surgery if a vascular stenosis of greater than 50% was documented. Sixty-four patients with a synthetic AVG comprised the study group. Seventy-two episodes of AVG impairment (56 with stenosis > or = 50% on angiography, 16 with thrombosis) occurred in these patients during the study period. In 63 of 72 impairment episodes, the preceding vascular access screening test was positive. The calculated sensitivity and specificity of the vascular access protocol was 88% and 81%, respectively. Calculation of the sensitivity and specificity for the VP alone was 81% and 85%, respectively. Comparison of the study group with a similar historical control group (55 patients) showed a significantly lower thrombosis rate (P = 0.03; 95% confidence interval [CI], 0.025 to 0.375) in the study group (0.29 thrombotic episodes/graft-year at risk) versus the historical control group (0.49 thrombotic episodes/graft-year at risk). In summary, a vascular access surveillance protocol is a useful tool to predict patients at risk for AVG venous stenosis and/or thrombosis. A dynamic VP of 140 mm Hg or greater appears to be the optimal threshold pressure. A decrease in synthetic AVG thrombosis rate resulted from the use of this surveillance protocol.

Adult↗
PubMed1998

Acute renal failure and intravenous immune globulin: sucrose nephropathy in disguise?

Intravenous immune globulin (IVIG) therapy has been used more commonly to treat a number of clinical disorders. During the past 10 years, IVIG infusion has been associated with a variety of complications. Acute renal failure, which was not described in the initial drug trials, was recognized as an adverse effect of IVIG therapy in 1987. Since the original report, a number of cases have been described in the literature. Older age and preexisting renal impairment appear to predispose to the development of acute renal failure. Acute renal insufficiency develops within days and resolves over several days to weeks. However, in some cases, recovery is delayed and initiation of renal replacement therapy is required. Chronic renal insufficiency requiring maintenance dialysis is extremely rare. The precise cause of IVIG-associated acute renal failure is unknown but may be attributable to either the direct effects of the immunoglobulin or the stabilizing agent used in the IVIG preparation.

Acute Kidney Injury↗
PubMed1998

Midodrine is effective and safe therapy for intradialytic hypotension over 8 months of follow-up.

Intradialytic hypotension (IDH) is a common and frustrating complication of hemodialysis. Certain end stage renal disease (ESRD) patients recurrently manifest this disabling condition. Both patient-specific factors (autonomic insufficiency, cardiac disease) and dialysis treatment-related factors (ultrafiltration, increased core body temperature) are thought to have significant causative roles. Most therapeutic interventions to date have been either unsuccessful or poorly tolerated. However, recent studies have shown that midodrine, an oral peripheral alpha-1 adrenergic agonist, is an effective and safe therapy for symptomatic IDH in the short-term. We report our experience with the predialysis use of midodrine for IDH in 13 hemodialysis (HD) patients over a 5 to 8 month period. Thirteen patients (8 male, 5 female, mean age 63.9 yrs) with recurrent symptomatic IDH were given midodrine 10 mg orally 30 min before each HD session. Blood pressures (pre-HD BP, lowest intradialytic [ID] BP, post-HD BP) and body weights were tracked for each HD treatment. Values for 10 HD sessions prior to midodrine therapy (Baseline) were compared to values (10 HD sessions each) during the 1st, 5th and 8th month of midodrine therapy. Data were analyzed using ANOVA for repeated measures and paired t-tests, with each patient serving as his/her own control. Patients were monitored for 5 months (n = 13) and 8 months (n = 8), respectively. All lowest intradialytic BPs, post-HD SBPs, and MAPs were significantly improved (p <0.05) on midodrine therapy. This effect was maintained during all periods of follow-up. There was no significant difference in mean albumin, hematocrit, Kt/V, calcium, and sodium between baseline and all periods of follow-up. Mean ultrafiltration volume per HD session was not significantly different than baseline over the course of study. A subjective improvement in hypotensive symptoms was also noted. Importantly, there were no adverse reactions to midodrine in all periods of follow-up. Midodrine appears to be an effective and safe treatment for HD patients with symptomatic IDH, and remains beneficial when used for an extended period of time.

Adrenergic alpha-Agonists↗
PubMed1998

Indinavir nephropathy in an AIDS patient with renal insufficiency and pyuria.

Indinavir has been described to cause crystalluria and nephrolithiasis in a variable number of treated patients. Acute renal failure, often reversible with discontinuation of the medication, induction of a diuresis and correction of urinary obstruction if present, occurs in a smaller percent of patients. One recent report described renal biopsy findings, indinavir crystals within cellular casts in the collecting tubules, in a patient receiving this antiretroviral agent. We report a second case of a patient with mild renal insufficiency and pyuria following indinavir therapy and describe similar renal biopsy findings.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Intradialytic hypotension: is midodrine beneficial in symptomatic hemodialysis patients?

Symptomatic hypotension during hemodialysis is a disabling complication in end-stage renal disease (ESRD) patients, especially in certain groups of patients who are at higher risk for this problem. Autonomic dysfunction is thought to play a significant role. We evaluated the efficacy of midodrine, an oral agent with selective alpha-adrenergic agonist activity used in the treatment of neurogenic orthostatic hypotension, on 10 hemodialysis patients with persistent intradialytic hypotension. The patients were given a dose of midodrine (mean dose, 5.5 mg; range, 5 to 10 mg) 30 minutes before each hemodialysis session. We compared blood pressure, pulse, body weight, and laboratory values for 10 consecutive dialysis sessions off and on midodrine therapy. There was a statistically significant improvement in lowest intradialytic systolic blood pressure (from 96.6 to 114.7 mm Hg; P < 0.001), lowest intradialytic diastolic blood pressure (from 53.2 to 59.0 mm Hg; P = 0.002), lowest intradialytic mean arterial pressure (from 67.7 to 77.6 mm Hg; P < 0.001), posthemodialysis systolic blood pressure (from 116.5 to 127.1 mm Hg; P < 0.001), posthemodialysis diastolic blood pressure (from 66.6 to 69.7 mm Hg; P = 0.040), and posthemodialysis mean arterial pressure (from 83.2 to 88.8 mm Hg; P = 0.001) after patients were placed on midodrine. There also was a small but statistically significant decrease in intradialytic pulse rate (from 86.3 to 81 beats/min; P = 0.021) and posthemodialysis pulse rate (from 87.4 to 81.7 beats/min; P = 0.024) after initiation of midodrine therapy. There was no significant difference in any of the prehemodialysis blood pressure measurements or pulse rate off or on midodrine therapy. The improvements in intradialytic and posthemodialysis blood pressure were associated with a uniform subjective improvement in symptoms associated with dialysis hypotension, such as cramps, fatigue, dizziness, and weakness. Other than scalp paresthesia in one patient, no adverse effects were noted. Our results suggest that the administration of a single dose of midodrine before hemodialysis is an effective therapy for intradialytic hypotension. A prospective trial with adequate patient numbers and long-term follow-up would be useful to evaluate this drug's efficacy and safety profile in patients with ESRD.

Administration, Oral↗
PubMed1997

Biochemical aberrations in a dialysis patient following parathyroidectomy.

Renal osteodystrophy is a common problem in patients with end-stage renal disease. Severe secondary hyperparathyroidism unresponsive to an intensive regimen of diet, phosphate binders, and calcitriol therapy is an indication for surgical parathyroidectomy. Certain unique postoperative electrolyte aberrations are seen after parathyroidectomy, including severe hypocalcemia and hypophosphatemia (hungry bone syndrome), as well as hyperkalemia. Identifying the patient at high risk for developing these electrolyte abnormalities will facilitate perioperative and postoperative management.

Adult↗
PubMed1997

Hyperkalemia in the elderly: drugs exacerbate impaired potassium homeostasis.

OBJECTIVE: To review the pathophysiology underlying the predisposition to hyperkalemia in the elderly; the medications that disrupt potassium balance and promote the development of hyperkalemia in the elderly; the prevention of hyperkalemia in elderly patients treated with potassium-altering medications; and the appropriate management of hyperkalemia when it develops. METHODS AND MAIN RESULTS: A MEDLINE search of the literature (1966-1996) using the terms hyperkalemia, drugs, elderly, and treatment was conducted and pertinent review articles, textbooks, and personal files were consulted. Elderly subjects appear to be predisposed to the development of hyperkalemia on the basis of both innate disturbances in potassium homeostasis and comorbid disease processes that impair potassium handling. Hyperkalemia in the elderly is most often precipitated by medications that impair cellular uptake or renal disposal of potassium. This electrolyte disorder is best prevented by recognition of at-risk physiology in the aged, avoidance of therapy with certain high-risk medications, and monitoring of plasma potassium concentration and renal function at intervals appropriate for the medication prescribed. Management of hyperkalemia entails identification of the clinical manifestations of severe hyperkalemia, stabilization of cardiac tissue, promotion of cellular potassium uptake, and ultimately removal of potassium from the body. CONCLUSIONS: Geriatric patients should be considered at risk of developing hyperkalemia, especially when they are prescribed certain medications. Potassium levels should be monitored at appropriate intervals when these patients are treated with potassium-altering medications. Appropriate management of hyperkalemia in the elderly can avoid life-threatening neuromuscular and cardiac complications.

Aged↗
PubMed1997

Renal insufficiency after intravenous immune globulin therapy: a report of two cases and an analysis of the literature.

Over the past decade, intravenous immune globulin therapy (IVIG) has gained widespread use for a variety of clinical disorders. IVIG treatment is associated with a number of complications, including acute renal failure (ARF). Although the cause of IVIG-associated ARF is unknown, it may be related to the stabilizing agent used in the IVIG preparation. The development and resolution of ARF is typically rapid, but is some cases recovery may be delayed and require renal replacement therapy. In such patients, recurrence of ARF may be avoided by selection of a preparation with a different stabilizing agent. Two cases of IVIG-induced ARF are described, and all reported cases are analyzed to assess the probable mechanism of renal injury.

Acute Kidney Injury↗
PubMed1997

Bone marrow transplant nephropathy: a case report and review of the literature.

Bone marrow transplantation can be complicated by renal failure resulting from a variety of causes. Early renal injury most often results from infection and its subsequent treatment with nephrotoxic medications. Late renal injury after bone marrow transplantation is characterized by a syndrome similar to the hemolytic uremic syndrome. This renal syndrome, called "bone marrow transplant nephropathy," is thought to evolve from the late effects of radiation therapy and cytotoxic chemotherapy on the kidney. In this article, a case of bone marrow transplant nephropathy and a review of the clinical and pathologic features are presented.

Adult↗