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Biomedical subjects

Farahnak K Assadi

Publications and source records attributed to Farahnak K Assadi.

5 recordsLinked to original sources

Value of urinary excretion of microalbumin in predicting glomerular lesions in children with isolated microscopic hematuria.

Urinary microalbumin excretion was assessed in 76 children with asymptomatic microscopic hematuria in whom the presence of proteinuria, hypertension, reduced renal function, hypercalciuria, urinary tract infection or structural abnormality of the urinary tract had been excluded. All children underwent a percutaneous kidney biopsy to determine whether microalbumin excretion can be used as a marker to predict the source of hematuria. Microalbumin excretion was considered normal if the urinary ratio of microalbumin to creatinine (MA/Cr ug/mg) was < or =30. Twenty-two (29%) had microalbuminuria (MA/Cr 96+/-30 microg/mg) and 54 (71%) had normal albumin excretion (MA/Cr 13+/-2 microg/mg). Of those with normoalbuminuria, 38 (70%) had normal renal tissue, 15 (28%) thin glomerular basement membrane (TGBM) disease and 1 (2%) IgA nephropathy. In contrast, 20 (91%) of those with microalbuminuria had IgA nephropathy and 2 (9%) had TGBM disease. The mean urinary MA/Cr ratio for all IgA children was 89+/-32 microg/mg higher compared with a value for the children with TGBM disease (14 +/-3 microg/mg, P <0.001) or children whose renal biopsy appeared normal (11+/-2 microg/mg, P <0.001). Statistical analysis revealed no significant differences between the mean MA/Cr ug/mg ratio for children with TGBM disease and those with normal glomerular findings. Fourteen of the 20 children with IgA nephropathy who also had microalbuminuria were treated with an angiotensin-converting enzyme (ACE) inhibitor. Over a mean follow-up of 51 months, none developed overt proteinuia; hematuria resolved and microalbuminuria returned to normal in eight (57%) during therapy with the ACE-inhibitor. In contrast, hematuria persisted and prtoteinuria developed in the other untreated children. None of the children with TGBM disease developed overt proteinuria after a mean of 51 months. Hematuria was persistent in children with TGBM disease, but often resolved in those whose biopsies were completely normal. These data suggest that determination of urinary microalbumin excretion is warranted in the routine examination of children with isolated microscopic hematuria. Routine screening for microalbuminuria may help to identify a subgroup of patients with IgA nephropathy who are at high risk for progressive kidney disease and need more intensive therapy and closer follow-up.

Adolescent↗

IgG-associated mesangial glomerulonephritis in a patient with Down syndrome.

BACKGROUND: Patients with Down syndrome have a variety of urinary tract abnormalities including obstructive hydronephrosis, dysplasia, reflux nephropathy and glomerular lesions. However, primary glomerulonephritis with prominent IgG deposits has not been reported previously in this syndrome. CASE REPORT: A 17-year-old girl with Down syndrome presented with proteinuria and chronic renal insufficiency. A percutaneous renal biopsy revealed prominent IgG deposition without IgA or IgM deposits in the absence of an identifiable autoimmune disorder, or any other etiologic factors known to cause secondary IgG-associated glomerulonephritis. CONCLUSIONS: The glomerular lesion identified in the present case demonstrates a distinct entity that further expands the spectrum of renal disease known to occur in Down syndrome. Early detection of renal disorder in Down syndrome may prevent or slow down the progression.

Adolescent↗

Liddle syndrome in a newborn infant.

A 10-week-old female infant developed hypertension. The elevated blood pressure was associated with metabolic alkalosis and urinary chloride wastage. The family history was unremarkable. Her urinalysis, blood urea nitrogen (BUN), and serum creatinine concentrations were all normal. A renal ultrasound was normal. A technetium-99m diethylenetriaminopentoacetic acid (DTPA) renal scan with captopril showed normal blood flow bilaterally. The head ultrasound and echocardiogram were normal. Blood epinephrine, norepinephrine, catecholamines, thyroxine, and steroid levels were also normal. Treatment with various combinations of labetalol, hydralazine, captopril, methyldopa, nifedipine, and spironolactone, all at high doses, failed to control the elevated blood pressure. Serum aldosterone level and peripheral plasma renin activity were low. The lack of therapeutic response to spironolactone, with a good response to amiloride and recurrence of hypertension and metabolic alkalosis after amiloride cessation that was subsequently treated with amiloride, established the diagnosis of Liddle syndrome. To our knowledge, this is the youngest patient with Liddle syndrome that has been reported in the literature.

Alkalosis↗

Quantitation of microalbuminuria using random urine samples.

Microalbuminuria is a harbinger of progressive renal disease and cardiovascular complications in patients with diabetes mellitus. The method most commonly used to measure microalbuminuria relies on a timed urine collection, either a 24-h or overnight specimen, which is time-consuming, cumbersome, and often inaccurate. We compared microalbumin-creatinine ratio (U(MA)/U(Cr)) in a random urine sample obtained after the first voided morning specimen with the quantity of microalbumin in a 24-h collection to determine whether the U(MA)/U(Cr) correlates with the microalbumin content of 24-h urine collection. In a study of 124 urine samples from 97 pediatric patients with type I diabetes, daily microalbumin excretion varied from 7 to 108 mg/24-h with a mean of 55.7 +/- 18.2 mg and U(MA)/U(Cr) ranged from 5 to 59 microg/mg with a mean of 39.4 +/- 11.3. An excellent correlation was found between the microalbumin excretion measured in 24-h urine collections and the random urine U(MA)/U(Cr) specimens (r=0.89, P<0.001). All patients who excreted more than 30 mg microalbumin in the 24-h specimen also had a U(MA)/U(Cr) of more than 20 microg/mg in the randomly voided sample. Microalbuminuria was unlikely if the U(MA)/U(Cr) was below 20 microg/mg. The results of this study indicate that the measurement of U(MA)/U(Cr) in a second voided morning specimen is a simple and reliable method for monitoring microalbuminuria in diabetic patients and may replace the need to assess quantitative microalbumin excretion on 24-h urine collections.

Adolescent↗

Infantile cystinosis presenting as chronic constipation.

An infant presented with persistent constipation as the first clinical symptom of cystinosis before evidence of renal Fanconi's syndrome. The history of muscle weakness, failure to thrive, polydipsia, and polyuria prompted subsequent clinical and laboratory evaluations, leading to the correct diagnosis of cystinosis. Primary and persistent constipation as an initial manifestation of cystinosis has not been reported previously. Although rare, cystinosis should be considered in the differential diagnosis of constipation if other suggestive signs or symptoms are present.

Chronic Disease↗