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nephritic syndrome
Diffuse proliferative glomerulonephritis was found in 60% of patients with acute nephritic syndrome.
      
Renal disease presented as nephritic syndrome and/or acute renal failure.
      
A 6-year-old boy, presenting with a nephritic syndrome, was diagnosed as suffering from Gaucher's disease (GD) and mesangiocapillary glomerulonephritis (MCGN).
      
Renal symptoms at presentation were as follows: 3 had isolated proteinuria, 9 had nephritic syndrome, 2 had nephritic and nephrotic components, and 10 had renal failure with one of the above features.
      
The nephrotic syndrome was present in 9 (64%) and the nephritic syndrome in 8 children (57%).
      
Five children had both nephrotic and nephritic syndrome together (35%).
      
Nephrotic and/or nephritic syndrome were found to be an unfavorable predictor both for short and long-term outcome (P>amp;lt;0.05).
      
We report our experience in treating two children with nephrotic-nephritic syndrome from idiopathic membranoproliferative glomerulonephritis.
      
The detection of an NPHS2 mutation affects the treatment plan for children with nephritic syndrome (NS).
      
Children with acute nephritic syndrome recovered spontaneously.
      
Acute nephritic syndrome is clinically characterized by hematuria, proteinuria, oliguria, and volume overload with or without azotemia and histologically be acute proliferative glomerulonephritis.
      
Sch?nlein-Henoch nephritis (SHN) usually presents with micro-haematuria or mild proteinuria but can be associated with heavy proteinuria and nephrotic or acute nephritic syndrome.
      
Glomerulointerstitial events in rapidly progressive nephritic syndrome, with special reference to histologic grade and stage on
      
Nineteen years later, acute nephritic syndrome with hypocomplementemia and an increasing anti-streptolysin O (ASO) titer developed 2 weeks after the onset of an upper respiratory infection.
      
After 2 weeks of observation, blood pressure, C3 level, and ASO titer had returned to normal, although the persisting nephritic syndrome necessitated steroid therapy.
      
Six months after the onset of the acute nephritic syndrome, the patient remained asymptomatic, except for microhematuria.
      
Because laboratory findings revealed massive proteinuria and hypoproteinemia, he was diagnosed as having nephritic syndrome caused by minimal change disease.
      
A clinical regression is observed in 10-15% of patients with nephritic syndrome.
      
At hospitalization, he presented with nephritic syndrome and acute renal failure.
      
Clinically it ranges from isolated proteinuria to a frank nephritic syndrome.
      
 

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