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Biomedical subjects

J Venkatesan

Publications and source records attributed to J Venkatesan.

13 recordsLinked to original sources
PubMed2000

Renal artery angioplasty and stent placement: predictors of a favorable outcome.

BACKGROUND: Renal artery stenosis is a common disorder and is an established cause of hypertension and renal insufficiency. Although treatment with renal artery stents has been shown to improve blood pressure and renal function for some patients, the patient population most likely to benefit is unknown. The current study was designed to determine which factors are predictive of improved blood pressure and renal function when patients with renal artery stenosis are treated with renal artery angioplasty and stent placement. METHODS: In a prospective evaluation 127 consecutively enrolled patients with renal artery stenosis in 171 vessels were treated with angioplasty and intravascular stents. Blood pressure and serum creatinine concentration were measured before stent placement and during the follow-up period. RESULTS: The mean length of the follow-up period was 15 +/- 14 months. Mean systolic blood pressure improved among patients with hypertension (from 177 +/- 26 mm Hg before stent placement to 151 +/- 24 mm Hg 6 months after stent placement (P <.001). The greatest improvement occurred among those with the highest baseline systolic blood pressure. This beneficial effect on blood pressure was sustained for 3 years. Sex, age, diastolic blood pressure, number of vessels into which stents were placed, serum creatinine concentration, presence of bilateral disease, race, and severity of stenosis were not predictive of improved blood pressure. Mean creatinine concentration was not significantly changed for the group as a whole. A significant decrease in serum creatinine concentration occurred among 43% of patients with baseline renal insufficiency. None of the examined variables was predictive of improvement. CONCLUSIONS: Renal artery angioplasty and stent placement produced a significantly greater reduction in systolic blood pressure among patients with the highest baseline systolic blood pressure. Other examined variables were not predictive of a significant improvement in blood pressure. No examined variable was predictive of improved renal function. We concluded that management of renal artery stenosis with renal artery angioplasty and stent placement is most likely to result in significant improvement in systolic blood pressure among patients with the highest baseline systolic blood pressure.

Aged↗
PubMed1998

Effect of sertraline hydrochloride on dialysis hypotension.

Hemodialysis hypotension (HH) is a very common disorder and has a multifactorial etiology. Autonomic dysfunction occurs in up to 50% of patients with end-stage renal disease (ESRD) and plays a key role in HH in some patients. Sertraline hydrochloride, a central nervous system serotonin reuptake inhibitor, has been shown to be an effective treatment of hypotension caused by autonomic dysfunction in disorders such as neurocardiogenic syncope and idiopathic orthostatic hypotension. This study sought to determine whether sertraline was effective in ameliorating HH. A retrospective chart analysis was performed that included nine consecutive patients (aged > or = 54 years, time on hemodialysis > or = 2.2 years) placed on sertraline (50 to 100 mg/d) for depression who also had HH (defined as prehemodialysis systolic blood pressure [SBP] < or = 100 mm Hg, > or = 40 mm Hg decrease in SBP during hemodialysis, SBP <90 mm Hg, any diastolic blood pressure <40 mm Hg, or a decrease in blood pressure-causing symptoms) before treatment with sertraline. The data from a 6-week pre-sertraline period were compared with the data from a 6-week sertraline period (defined as 6 weeks after drug begun). Blood pressure medications were unchanged during the trial period of sertraline. However, nadir mean arterial pressure recorded during a given dialysis session in the pre-sertraline period (55+/-4 mm Hg) was significantly lower than that recorded in the sertraline period (68+/-5 mm Hg; P < 0.05). In addition, the number of hypotensive episodes (same definition as HH) per dialysis session during the sertraline period was significantly lower than that during the pre-sertraline period (mean, 0.6+/-0.2 episodes per session v 1.4+/-0.3 episodes per session; P < 0.005). The number of therapeutic interventions required for hypotension during the sertraline period was also significantly less than that during the pre-sertraline period (mean, 1.7+/-0.8 interventions v 11.0+/-3.0 interventions; P < 0.005). The urea reduction ratio (62.7%+/-4.7% v 63.1%+/-9.3%; P = NS) and hematocrit (28.9%+/-0.8% v 29.5%+/-1.0%; P = NS) did not change significantly. It is concluded that the short-term (6 weeks) use of sertraline hydrochloride reduces HH in some patients with ESRD. A possible mechanism for this effect is sertraline-induced attenuation of the paradoxical sympathetic withdrawal that may underlie HH in some patients with ESRD.

1-Naphthylamine↗
PubMed1997

Cardiac disease in chronic uremia: management.

Heart disease is a common cause of morbidity in end-stage renal disease (ESRD) patients. The management of heart disease in these patients requires a multidimensional approach to the management of heart failure, coronary disease, and arrhythmias, and to risk factors such as hypertension, anemia, secondary hyperparathyroidism, and electrolyte/acid-base disturbances. Coronary artery disease management includes use of antianginal drugs and revascularization of coronary arteries with angioplasty +/- stent placement or coronary artery bypass grafting. The long-term outcomes of these procedures need to be assessed and improved. Hypertension occupies a major role in the pathogenesis of heart disease in ESRD, and early and adequate control of hypertension is likely to have a major impact on the progression of cardiac disease. This entails the achievement of optimal volume status, combined with the appropriate use of antihypertensive agents such as calcium channel blockers, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, vasodilators, alpha-blockers, and central sympatholytic drugs. In ESRD patients, specific dialysis-related complications such as intradialytic hypotension and pericardial effusion may have additional effects on cardiac function and require attention. The choice of dialysate composition and membrane may influence clinical outcomes with specific effects on cardiac performance.

Chronic Disease↗
PubMed1997

Anemia, hypertension, and myocardial dysfunction in end-stage renal disease.

Cardiovascular disease remains the major cause of mortality in patients with end stage renal disease (ESRD). The pathophysiology of cardiac dysfunction in ESRD is complex and not fully understood. However, it appears that the two major determinants of left ventricular (LV) hypertrophy and dysfunction are anemia and hypertension, both of which are very common in ESRD patients. Early and aggressive correction of anemia and hypertension may have a significant impact on cardiac disease in ESRD patients. This article presents a discussion on the management of anemia and hypertension, and the current information available on the pathogenesis and management of LV dysfunction in ESRD.

Anemia↗
PubMed1993

Plasma natriuretic factor(s) in patients with intracranial disease, renal salt wasting and hyperuricosuria.

To test our hypothesis that a circulating factor(s) may be causing the renal salt and urate wasting in patients (pts) with intracranial diseases, we exposed rats to the plasma of these patients and studied sodium and lithium transport. We selected 21 neurosurgical pts, 13 of whom had increased fractional excretion (FE) of urate, and 14 age and sex-matched controls. Plasma from pts and controls were injected IP (0.5 mL) and infused, 0.2 ml prime and 1.8 mL at 0.01 mL/min, to Sprague Dawley rats anesthetized with Inactin. Renal transport of sodium (Na), lithium (Li) and potassium (K) was determined. There were higher mean +/- SEM for FENa, 0.59 +/- 0.07% vs 0.29 +/- 0.05%, P < 0.01, FELi, 36.6 +/- 1.9% vs 24.0 +/- 1.6%, P < 0.001 and K excretion rates, 1.69 +/- 0.13 vs 1.31 +/- 0.09 mumol/min, p < 0.02, in rats infused with plasma of pts as compared to controls, respectively. FENa decreased with increasing dilution of plasma of 2 pts with ICD. There was no difference in mean weight of rats, blood pressure, urine flow rate or insulin clearance between pts and controls. These data suggest that pts with ICD have a plasma factor(s) which decreases net Na, Li and K reabsorption.

Adult↗
PubMed1992

Abnormal urate transport in patients with intracranial disease.

Based on our demonstration of a high incidence of hypouricemia, tubular urate transport abnormality, and cerebral atrophy in patients with acquired immunodeficiency syndrome (AIDS), we performed prospective renal clearance studies in 29 consecutive neurosurgical patients with intracranial diseases of multiple etiologies to test our hypothesis that patients with intracranial disorders had defective tubular urate transport. Similar studies were performed in 21 age-matched controls. None of the subjects had serum creatinine greater than 123.8 mumol/L (1.4 mg/dL), sickle cell or liver diseases, or received intravenous fluid or uricosuric drugs at the time of study. Seven patients had no surgical procedures, 12 were studied after a neurosurgical procedure, and 10 had preoperative and postoperative studies. Ten had more than one postoperative study. Twelve had 24-hour urine collections. We found that 18 of 29 patients had elevated fractional excretion (FE) of urate greater than 10%. There was no difference in preoperative and postoperative FE urate by nonpaired t test for all patients and by paired t test in the 10 patients who had preoperative and postoperative studies performed. Seven patients had hypouricemia, defined as serum urate less than or equal to 0.18 mmol/L (3 mg/dL). Only one had hyponatremia (serum sodium less than 130 mmol/L). Urate excretion averaged 3.6 +/- 0.32 mmol (603 +/- 52.7 mg)/24 h, suggesting that the hypouricemia was not due to decreased urate production. None of the medications or surgical procedures could be considered to have caused the urate transport abnormality, nor was it associated with any specific intracranial location or type of disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Biological Transport↗
PubMed1991

Hypokalemia and rhabdomyolysis.

Since the occurrence of rhabdomyolysis may elevate the serum concentration of potassium, hypokalemia as a cause of rhabdomyolysis often goes unrecognized in many instances. We undertook this study to evaluate the occurrence and determinants of rhabdomyolysis in the hypokalemic state. To identify patients with a hypokalemic state, we reviewed medical admissions for the period January 1988 through December 1989. A total of 120 patients (42 men and 78 women) were included in the present study. Thirty-eight hypokalemic patients showed biochemical evidence of rhabdomyolysis (serum creatine phosphokinase greater than 244 IU/l). The clinical and biochemical characteristics of the patients with rhabdomyolysis (group I) and the hypokalemic patients without rhabdomyolysis (82 patients, group II) were compared. There was no difference in age, sex and race of the patients of group I vs. group II. The mean serum values for potassium, bicarbonate, chloride, blood urea nitrogen, glucose, lactate dehydrogenase and uric acid were also not different between the two groups. The mean serum osmolality was higher (p less than 0.001) in patients with rhabdomyolysis (297.6 +/- 4.3 mosm/kg) than in those without rhabdomyolysis (283.5 +/- 5.0 mosm/kg). The levels of serum glutamic-oxaloacetic transaminase were elevated (p less than 0.001) in group-I patients (69.6 +/- 8.4 IU/l) but not in group-II patients (36.7 +/- 3.5 IU/l). The concentrations of serum creatinine were also higher (p less than 0.05) in patients with rhabdomyolysis (1.4 +/- 0.2 mg/dl) than in those without rhabdomyolysis (1.0 +/- 0.1 mg/dl). The mean values for serum sodium were higher (p less than 0.02) in group-I patients when compared to group-II patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatine Kinase↗
PubMed1990

Rhabdomyolysis in the hyperosmolal state.

PURPOSE: We undertook this study to determine the occurrence of rhabdomyolysis in the hyperosmolal state. PATIENTS AND METHODS: We reviewed 130 hospital admissions due to diabetic ketoacidosis or hyperosmolal coma, or both. Thirty-one patients (12 men and 19 women) were found to be in the hyperosmolal state. Sixteen of 31 patients showed biochemical evidence of rhabdomyolysis. The clinical and biochemical features of the patients with rhabdomyolysis (Group I) and the patients without rhabdomyolysis (Group II) were compared. RESULTS: Patients in Group I showed a 100-fold increase (7,156 +/- 2,820 IU/L) in serum creatine phosphokinase (CPK) when compared to the patients in Group II (61 +/- 11 IU/L). The mean serum osmolality was much higher (p less than 0.001) in patients with rhabdomyolysis (381 +/- 12 mOsm/kg) than in those without rhabdomyolysis (324 +/- 4 mOsm/kg). The serum sodium level was elevated (p less than 0.001) in Group I patients (151 +/- 4 mEq/L) but not in Group II patients (133 +/- 2 mEq/L). There was a linear association between serum CPK versus serum sodium (r = 0.62, p less than 0.05) and serum CPK versus serum osmolality (r = 0.05, p less than 0.05). The mean serum potassium level was lower (p less than 0.01) in Group I than in Group II. Only two patients (12%) in Group I and almost half the patients (seven of 15) in Group II were hyperkalemic. The mean serum phosphorus level was lower in Group II than in Group I. Four patients in Group I and one patient in Group II developed acute renal failure. CONCLUSION: Subclinical rhabdomyolysis is a common finding in the hyperosmolal state. Absence of hyperkalemia in the presence of muscle injury, hyperosmolality, hyperglycemia, and acidosis suggested pre-existing total-body potassium deficiency in many of these patients. In addition to hypokalemia, the hyperosmolal state predisposes to the development of rhabdomyolysis.

Adult↗
PubMed1990

Hyponatremia and hypouricemia: differentiation from SIADH.

Hypouricemia in coexistence with hyponatremia often differentiates the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from most other causes of hyponatremia. We report clearance studies in 5 cases of hyponatremia and hypouricemia that were not due to SIADH. One had metastatic pancreatic carcinoma with ascites, edema, hypoalbuminemia and hypophosphatemia. Two had adenocarcinoma of the lung with metastasis to the brain in 1, 1 had disseminated cryptococcus and 1 had Hodgkin's disease. None received radiation or known nephrotoxins at least 4 months prior to study. None had serum creatinine greater than 106.1 mumol/l (1.2 mg/dl). Two had postural hypotension and hyponatremia that responded to saline therapy. Fluid restriction corrected the hyponatremia in all patients, but the hypouricemia, high fractional excretion (FE) of urate, and high urine sodium concentration persisted. In 2 patients studied, ADH was appropriately suppressed after volume repletion but there was a defect in free water clearance due to high renal solute excretion. In contrast to patients with SIADH who correct their defect in renal urate transport with correction of hyponatremia by water restriction, our patients appear to have a persistent renal urate transport defect and abnormality in sodium conservation. Elevated FE urate of greater than 10% after correction of hyponatremia can thus differentiate these patients from SIADH. The diametrically opposing goals of fluid therapy emphasize the importance of differentiating one group from the other.

Adult↗
PubMed1989

Hypersensitivity angiitis associated with naproxen.

A 52-year-old male developed cutaneous necrotizing vasculitis, renal failure, massive proteinuria, and elevated serum IgE levels following oral naproxen therapy. Renal biopsy specimen revealed cellular crescents in more than 40% of the glomeruli and a rare arteriole displayed thickening and eosinophilia of intima. Electron microscopic examination showed fusion of epithelial foot processes. Discontinuation of naproxen therapy was associated with disappearance of cutaneous lesions and improvement of renal function.

Drug Hypersensitivity↗