Hypertension: Assadi F

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A digest of articles written 1999 and later, on the topic "Hypertension," originating from Planet Earth —» Assadi F.  Display:  All Citations ·  All Abstracts
1 Guideline Diagnosis of hypokalemia: a problem-solving approach to clinical cases. free! 2008

Assadi F. · Section of Pediatric Nephrology, Rush University Medical Center, Chicago, Illinois 60612, USA. · Iran J Kidney Dis. · Pubmed #19377223 links to  free full text

Abstract: In situations where the cause of hypokalemia is not obvious, measurement of urinary potassium excretion and blood pressure and assessment of acid-base balance are often helpful. A random urine potassium-creatinine ratio (K/C) less than 1.5 suggests poor intake, gastrointestinal losses, or a shift of potassium into cells. If hypokalemia is associated with paralysis, we should consider hyperthyroidism, familial or sporadic periodic paralysis. Metabolic acidosis with a urine K/C ratio less than 1.5 suggests lower gastrointestinal losses due to diarrhea or laxative abuse. Metabolic acidosis with K/C ratio of 1.5 higher is often due to diabetic ketoacidosis or type 1 or type 2 distal renal tubular acidosis. Metabolic alkalosis with a K/C ratio less than 1.5 and a normal blood pressure is often due to surreptitious vomiting. Metabolic alkalosis with a higher K/C ratio and a normal blood pressure suggests diuretic use, Bartter syndrome, or Gitelman syndrome. Metabolic alkalosis with a high urine K/C ratio and hypertension suggests primary hyperaldosteronism, Cushing syndrome, congenital adrenal hyperplasia, renal artery stenosis, apparent mineralocorticoid excess, or Liddle syndrome. Hypomagnesemia can lead to increased urinary potassium losses and hypokalemia. The differential rests upon measurement of blood magnesium, aldosterone and renin levels, diuretic screen in urine, response to spironolactone and amiloride, measurement of plasma cortisol level and the urinary cortisol-cortisone ratio, and genetic testing.

2 Clinical Conference Effect of microalbuminuria lowering on regression of left ventricular hypertrophy in children and adolescents with essential hypertension. 2007

Assadi F. · Rush Children's Hospital, 1725 West Harrison Street, Professional Building, Suite 710, Chicago, IL 60612, USA. · Pediatr Cardiol. · Pubmed #17308944 No free full text.

Abstract: Microalbuminuria (MA) is associated with increased cardiovascular risk in adult hypertensive patients, but no study has specifically examined the effects of MA lowering on regression of left ventricular hypertrophy (LVH) among pediatric patients with hypertension. Fifty-five patients with essential hypertension, 11-19 years old, were prospectively studied. All patients received concomitant therapy of hydrochlorothiazide and angiotensin-converting enzyme inhibitor. Five patients also required angiotensin receptor blocker to achieve the blood pressure goal. Baseline and 12-month follow-up measures of left ventricular mass index (LVMI), determined by echocardiography and urine microalbumin/creatinine ratio (MA/Cr), were collected. MA was defined as MA/Cr >30 microg/mg. LVH was defined as LVMI >38.6 g/m(2.7). The primary end points were reductions in MA and LVMI of 25% or more. Weight (r = 0.83), body surface area (r = 0.85), body mass index (BMI) (r = 0.86), systolic blood pressure (SBP) (r = 0.57), diastolic blood pressure (DBF) (r = 0.49), mean arterial pressure (r = 0.53) and MA (r= 0.87) were all univariate correlates of LVMI. In a multiple regression analysis, MA, BMI and SBP were significant correlates of LVMI. MA alone explained 76% of the variance of LVMI, whereas BMI and SBP explained only 1.6 and 0.4% of the variance, respectively. MA was the most significant correlate of follow-up LVMI after BMI and SBP were included in the overall multiple regression models. Thus, MA is a strong predictor of LVH in hypertensive children and adolescents. MA lowering halts the progression of LVH or induces its regression.

3 Article Childhood Henoch-Schonlein nephritis: a multivariate analysis of clinical features and renal morphology at disease onset. free! 2009

Assadi F. · Department of Pediatrics, Section of Nephrology, Rush University Medical Center, Chicago 60612, USA. · Iran J Kidney Dis. · Pubmed #19377254 links to  free full text

Abstract: INTRODUCTION: Risk factors of renal involvement in Henoch-Schonlein nephritis (HSN) have been extensively studied, but their relations with the severity of glomerular lesions at the disease onset are much less known. MATERIALS AND METHODS: Data were collected retrospectively on 45 patients (age range, 2 to 15 years) with HSN to identify the initial clinical and laboratory features that most accurately correlate with histological findings. Nephritic syndrome was defined as hypertension, proteinuria, hematuria, and a creatinine clearance of 60 mL/min/1.73 m2 or less. Kidney biopsy findings were graded according to the International Study of Kidney Disease in Children classification for HSN. RESULTS: Purpura was present in all the 45 children, arthritis in 73.3%, abdominal symptoms with or without bleeding in 68.6%, and a high serum IgA level in 24.4%. Hematuria was present in 88.6% of the patients, hematuria and proteinuria (not in nephrotic range) in 66.7%, nephrotic syndrome in 17.8%, acute nephritic syndrome in 8.9%, and nephritic-nephrotic syndrome in 13.3%. Grades II (33.3%) and III (22.2%) lesions were the most common pathologic findings on kidney biopsy followed by grades IV (17.8%), V (15.6%), and I (11.1%) lesions. Univariate analysis demonstrated that nephrotic syndrome, acute nephritic syndrome and a creatinine clearance less than 30 mL/min/1.73 m2 were all associated with a significantly increased risk of developing grades IV and/or V lesions. multivariate analysis showed nephritic-nephrotic syndrome as significant independent predictors of severity of glomerular disease at onset. CONCLUSIONS: The severity of renal symptoms at onset determines the intensity of glomerular lesions.

4 Article Vasoconstrictor-induced hypertension following multiple blood transfusions in children with congenital hemolytic anemia. free! 2008

Assadi F. · Department of Pediatrics, Section of Nephrology, Rush University Medical Center, Chicago, Illinois 60612, USA. · Iran J Kidney Dis. · Pubmed #19377226 links to  free full text

Abstract: INTRODUCTION: The mechanism by which blood transfusion increases blood pressure in a substantial proportion of patients with congenital hemolytic anemia is unknown. Vascular endothelium dysfunction and increased endogenous vasoactive substances have been postulated in the pathogenesis of hypertension following multiple blood transfusions. The present study was undertaken to test the hypothesis whether increased circulating vasoconstrictors following blood transfusions, if documented, is a potent modulator of hypertension in patients with congenital anemia. MATERIALS AND METHODS: Four children with congenital hemolytic anemia developed severe hypertension and convulsions 2 to 4 days after they received multiple blood transfusions. None had a history of prior hypertension, kidney disease or seizures before the blood transfusion. Baseline blood and urine samples were obtained for routine renal function studies. Blood samples were also drawn during and 2 weeks after the clinical events for determination of epinephrine, norepinephrine, dopamine, and plasma renin activity. RESULTS: Kidney function was normal in all the 4 patients. All had elevated plasma renin activity and increased blood epinephrine, norepinephrine, and dopamine concentrations during hypertensive crises. Hypertension responded to antihypertensive drugs with the patients remaining normotensive 3 to 6 days after commencing therapy. All recovered without further seizures. The elevated plasma renin activity, epinephrine, norepinephrine, and dopamine levels returned to reference levels 2 weeks after completion of the last blood transfusion. CONCLUSIONS: These data suggest that increased activity of vasoconstrictors in the recipient plasma may be responsible for the development of hypertension after multiple blood transfusions.

5 Article Relation of left ventricular hypertrophy to microalbuminuria and C-reactive protein in children and adolescents with essential hypertension. 2008

Assadi F. · Rush Children's Hospital, 1725 West Harrison Street, Suite 710, Chicago, IL 60612, USA. · Pediatr Cardiol. · Pubmed #18046596 No free full text.

Abstract: Microalbuminuria (MA) and C-reactive protein (CRP) levels are predictors of increased risk for left ventricular hypertrophy (LVH). Whether the strength of association between CRP and LVH is comparable to that of MA in hypertensive children is unknown. CRP and MA were measured in 64 children and adolescents with essential hypertension (HTN). In the entire population, CRP and MA showed positive relations with body mass index (BMI) (r = 0.30, p = 0.04 and r = 0.32, p = 0.04, respectively), systolic blood pressure (SBP) (r = 0.63, p = 0.03 and r = 0.58, p = 0.03, respectively), and LVH (r = 0.86, p < 0.001 and r = 0.81, p < 0.001, respectively). Patients with LVH (n = 23) had significantly higher BMI (p = 0.32), increased SBP (p = 0.031), and higher levels of CRP (p < 0.001) and MA (p < 0.001) compared with those without LVH. Multiple linear regression analysis demonstrated that CRP (r = 2.11, p < 0.001), MA (r = 1.94, p < 0.003), BMI (r = 0.53, p = 0.02), and SBP (r = 0.48, p = 0.04) were significantly associated with LVH. By analysis of covariance, CRP and MA were significantly different between patients who had LVH and those without LVH after adjustment for age, gender, BMI, SBP, SBP index, and diastolic blood pressure (p < 0.001 for the two markers). In conclusion, the strength of association between LVH and CRP is comparable to that of MA in children and adolescents with essential HTN.

6 Article C-reactive protein and incident left ventricular hypertrophy in essential hypertension. 2007

Assadi F. · Department of Pediatrics, Section of Nephrology, Rush University Medical Center, 1725 West Harrison Street, Professional Building, Suite 710, Chicago, IL 60612, USA. · Pediatr Cardiol. · Pubmed #17563829 No free full text.

Abstract: Elevated C-reactive protein (CRP) levels have been associated with increased cardiovascular risk in hypertensive adults. The aim of this study was to determine whether plasma CRP level is more predictive of left ventricular hypertrophy (LVH) than is ambulatory blood pressure (BP) in hypertensive children. Baseline and 12-month follow-up measures of BP, body mass index (BMI), low-density lipoprotein/high density lipoprotein cholesterol, left ventricular mass (LVM), and CRP data collected from 48 newly diagnosed, untreated hypertensive children were analyzed. CRP was measured by a highly sensitive nephelometric method. Left ventricular mass index (LVMI) was calculated as LVM/height2.7, and LVH was defined as LVMI>38.6 g/m2.7 being the cut-point for the 95th percentile found in healthy children. Average systolic BP (SBP), diastolic BP (DBP), SBP index, and DBP index were calculated. All patients received hydrochlorothiazide therapy in combination with angiotensin converting enzyme inhibitor treatment. Five patients also had angiotensin receptor blocker therapy to reach the target BP (<95th percentile corrected for age and gender). In a multiple regression analysis, LMVI was correlated with CRP, BMI, SBP, and SBP index. CRP alone explained 77% of the variance of LVMI, whereas BMI, SBP, and SBP index explained only 1.3, 0.3, and 0.4% of the variance, respectively. CRP was also the most significant correlate of follow-up LVH. In conclusion, elevated CRP level is significantly associated with LVH in children with essential hypertension. BP reduction with renin-angiotensin system blocker and hydrochlorothiazide therapy reduces LVH while lowering CRP level.

7 Article Autonomic dysreflexia manifested by severe hypertension. 2004

Assadi F, Czech K, Palmisano JL. · Department of Pediatrics, Section of Nephrology, Rush University Medical College, Chicago, IL 60612, USA. · Med Sci Monit. · Pubmed #15567988 No free full text.

Abstract: BACKGROUND: Autonomic dysreflexia (AD) is a sudden and exaggerated autonomic response to stimuli in patients with spinal cord injuries or dysfunction above the splanchnic sympathetic outflow (T5-T6). Hypertension is a relatively common manifestation of AD. CASE REPORT: We describe a case of a young man with T4-T6 spinal cord tumor who developed severe hypertension before any other clinical feature of AD, leading to a subsequent clinical evaluation and the correct diagnosis. Treatment with labetalol was only partially successful in controlling the elevated blood pressure. Hypertension resolved immediately after bladder decompression. CONCLUSIONS: AD manifested by severe hypertension is uncommon. Bladder decompression appears to be safe and effective for management of hypertension in patients with AD.

8 Article Bilateral pheochromocytomas and congenital anomalies associated with a de novo germline mutation in the von Hippel-Lindau gene. 2003

Assadi F, Brackbill EL. · Department of Pediatrics, Section of Nephrology, Rush Presbyterian St. Luke's Medical Center, Rush University Medical College, Chicago, IL, USA. · Am J Kidney Dis. · Pubmed #12500216 No free full text.

Abstract: A 12-year-old boy presented with severe hypertension, congenital microcephaly, severe hearing loss, developmental delay, cryptorchidism, and bilateral pheochromocytomas, without the phenotypic features of multiple endocrine neoplasia type II syndromes (MEN-2). Sequence analysis of the polymerase chain reaction (PCR)-amplified gnomic DNA identified a missense mutation at nucleotide 451 of the von Hippel-Lindau (VHL) gene (A451G) that changes a codon for serine (AGT) to one for glycine (GGT) at amino acid position 80 (S80G). The sequence DNA analysis of the parents did not show a mutation in the VHL gene that was previously identified in their affected son. The observed constellation of microcephaly, deafness, cryptorchidism, developmental delay, hypertension, and bilateral pheochromocytoma in association with a VHL mutation A451G in a patient with negative family history has not previously been described in the literature. Knowledge that VHL mutation plays a critical role in sporadic pheochromocytoma should aid in the future diagnosis and treatment of this tumor. Genetic testing in known pheochromocytoma families is indicated to identify genetically abnormal subjects that carry the MEN-2, VHL, and glomus tumor gene mutations.