It can occur following hemorrhage, shock, volume depletion, congestive heart failure, adrenal insufficiency, and narrowing of the renal artery among other things.
In turn, the decreased flow and pressure to the kidney will be sensed by baroreceptors in the Juxtaglomerular (JG) Cells of the afferent arteriole.
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.
Increased aldosterone levels results in salt and water absorption in the distal collecting tubule.
[4] A decrease in volume or pressure is a non-osmotic 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.
This generally leads to a BUN:Cr ratio greater than 20, a fractional excretion of Na of less than 1%, and an elevated urine osmolarity.
[citation needed] In cases of kidney disease, glomerular filtration rate decreases, so nothing gets filtered as well as it normally would.
Third-spacing of fluids, as in peritonitis, osmotic diuresis, or low aldosterone states such as Addison's disease all elevate urea.
[3] Persistent obstruction damages the tubular epithelium over time, and renal azotemia will result with a decreased BUN:Cr ratio.