Effects of angiotensin II on NaPi-IIa co-transporter expression and activity in rat renal cortex

AbstractThe kidney plays a major role in reabsorption of phosphate with the majority occurring in the proximal tubule (PT). The type IIa sodium-phosphate co-transporter (NaPi-IIa) is the main player in PT. The purpose of current study was to determine the effect of angiotensin II (A-II) on membrane expression of NaPi-IIa in the rat renal cortex. A-II (500 ng/kg/min) was chronically infused into the Sprague–Dawley rats by miniosmotic pump for 7 days. The arterial pressure and circulating plasma A-II level along with urine output were markedly increased in A-II rats. There was diuresis but no natriuresis. The phosphate excretion increased sevenfold on day 4 and 5.7-fold on day 7. There was no change in Na-dependent Pi uptake in brush-border membrane (BBM) vesicles between A-II-treated group and control on day 4, however, there was a 43% increase on day 7. Western blot analysis of NaPi-IIa protein abundance showed a parallel pattern: no change after 4 days of treatment and a 48% increase after 7 days of treatment. However, Northern blot analysis of cortical RNA showed no change in NaPi-IIa mRNA abundance on day 7. A-II stimulation of Na/Pi co-transport activity is a result of increases in the expression of BBM NaPi-IIa protein level and that stimulation is most likely mediated by posttranscriptional mechanisms

Hyponatremic hypertensive syndrome (HHS) in an 18-month old-child presenting as malignant hypertension: a case report

BACKGROUND: The combination of hyponatremia and renovascular hypertension is called hyponatremic hypertensive syndrome (HHS). Malignant hypertension as a presentation has been reported in adults with HHS but is rare in children. CASE PRESENTATION: An eighteen month-old male presented with drowsiness, sudden onset status epilepticus and blood pressure of 210/160. The electrolytes on admission revealed sodium of 120 mEq/L and potassium of 2.1 mEq/L. The peripheral renin activity (PRA) was 172 ng/ml/min (normal 3–11 ng/ml/min) and serum aldosterone level was 91 ng/dl (normal 4 to 16 ng/dl). Patient underwent angioplasty with no success, followed by surgical correction. Two years since the diagnosis, the blood pressure is controlled with labetolol and amlodipine (at less than sixth of the pre-operative dosages). The PRA is 2.4 ng/ml/min and aldosterone 15.5 ng/dl. The child not only had three renal arteries on left but all of them were stenosed which to best of our knowledge has not been described. CONCLUSION: As uncommon as HHS with malignant hypertension may be in adults it is under-reported in children and purpose of the case report is to raise its awareness

Rescue Of Renal Function In A 3-Year-Old Girl With Goodpasture\u27S Syndrome With A Brief Review Of Literature

Goodpasture\u27s syndrome has been documented in only a handful of children under the age of four. We describe a 3-year-old girl presenting with anaemia and renal failure whose kidney biopsy showed anti-glomerular basement membrane (GBM) disease. She was treated aggressively with pulse steroids, plasmapheresis and monthly infusions of cyclophosphamide. After months of aggressive immunosuppression, her renal function normalized, and her anti-GBM antibody disappeared. A year after the onset, she underwent a second kidney biopsy for persistent proteinuria and hypertension that surprisingly showed focal sclerosing glomerulonephritis, an unreported finding at this age. The biopsy showed deposition of antibody on the GBM despite the fact that anti-GBM antibody had normalized in the serum 5 months earlier. Mycophenolate mofetil was added to the immunosuppression at that point. At her 3-year follow-up, creatinine clearance was 88.4 mL/min/1.73 m2, proteinuria was 408 mg/day and blood pressure was controlled with enalapril 0.2 mg/kg/day. She has not had a relapse or abnormal anti-GBM antibody for 30 months, but her renal prognosis remains guarded. To our knowledge, this is the youngest patient to have a successful rescue of renal function after isolated Goodpasture\u27s syndrome. © 2010 The Author. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved