If the decrease in blood pressure is systemic (rather than occlusion of the renal artery) baroreceptors in the carotid sinus and aortic arch will be stimulated. This leads to sympathetic nerve activation, resulting in  renin secretion through β 1 -receptors. Constriction of the afferent arterioles causes a decrease in the intraglomerular pressure, reducing GFR proportionally. Renin is the main effector of the juxtaglomerular baroreceptors. Renin is secreted from granules in the JG cells, and once in the blood stream, it acts as a protease to convert angiotensinogen to angiotensin I, which is converted by angiotensin converting enzyme, to angiotensin II, which, in turn, stimulates aldosterone release. Increased aldosterone levels results in salt and water absorption in the distal collecting tubule.A decrease in volume or pressure is a nonosmotic stimulus for antidiuretic hormone production in the hypothalamus, which exerts its effect in the medullary collecting duct for water reabsorption. Through unknown mechanisms, activation of the sympathetic nervous system leads to enhanced proximal tubular reabsorption of salt and water, as well as urea (BUN), calcium, uric acid, and bicarbonate. The net result of these 4 mechanisms of salt and water retention is decreased output and decreased urinary excretion of sodium (< 20 mEq/L). The increased reabsorption of Na leads to increased water and urea reabsorption from the proximal tubules of the kidney back into the blood. In contrast, creatinine is actually secreted in the proximal tubule.
The increased nephron tubular pressure (due to fluid back-up) causes increased reabsorption of urea, elevating it abnormally relative to creatinine. Persistent obstruction damages the tubular epithelium over time, and renal azotemia will result with a decreased BUN:Cr ratio. Signs and symptoms
Oliguria or anuria (decreased or absent urine output)
Fatigue
Asterixis (flapping tremor)
Decreased alertness
Confusion
Pale skin
Tachycardia (rapid pulse)
Xerostomia (dry mouth)
Thirst
Edema, anasarca (swelling)
Orthostatic blood pressure (fluctuates depending on body position)
Uremic frost, a condition that occurs when urea and urea derivatives are secreted through the skin in sweat, which evaporates away to leave solid uric compounds, resembling a frost.A urinalysis will typically show a decreased urine sodium level, a high urine creatinine-to-serum creatinine ratio, a high urine urea-to-serum urea ratio, and concentrated urine (determined by osmolality and specific gravity). None of these is particularly useful in diagnosis.In pre-renal and post-renal azotemias, elevation of urea exceeds that of the creatinine (i.e., BUN>12*creatinine). This is because urea is readily reabsorbed by the kidneys while creatinine is not. In congestive heart failure (a cause of pre-renal azotemia) or any other condition that causes poor perfusion of kidneys, the sluggish flow of glomerular filtrate results in excessive absorption of urea and elevation of its value in blood. Creatinine, however, is not absorbable and therefore does not rise significantly. Stasis of urine in post-renal azotemia has the same effect. Treatment
Prompt treatment of some causes of azotemia can result in restoration of kidney function; delayed treatment may result in permanent loss of renal function.