Hypertension occurs in nephritic syndrome due to increased inflammation at the glomerulus. This leads to hemodynamic changes that cause the over all GFR to decrease, and thus oliguria. It is the overall decreased ability to make urine, due to inflammatory damage, that causes hypertension. Also casts from inflammatory debris can cause blockage in the tubules leading to pathological overactivation of RAAS, by tricking the JG apparatus into thinking you're volume depleted.
Compare that to Nephrotic Syndrome, where albumin is lost due to effacement of foot proteins without inflammation. Only albumin is lost, leading to a decreased osmotic pressure in the vessels, causing edema. This decreased effective arterial volume activates RAAS also, however, in this case it is compensating for the decrease in systemic blood pressure from the edema, so the activation of RAAS just normalizes the previously low blood pressurel - thus no hypertension.
Sorry I am four years late 🙁