Editing Azotemia (section)

==Types==
Azotemia has three classifications, depending on its causative origin: prerenal azotemia, renal azotemia, and postrenal azotemia.<ref>{{Citation |last=Tyagi |first=Alka |title=Azotemia |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK538145/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30844172 |access-date=2023-03-02 |last2=Aeddula |first2=Narothama R.}}</ref>

Measurements of [[urea]] and [[creatinine]] (Cr) in the blood are used to assess renal function. For historical reasons, the lab test measuring urea is known as "[[blood urea nitrogen]]" (BUN) in the US. The BUN:Cr ratio is a useful measure in determining the type of azotemia and will be discussed in each section below. A normal BUN:Cr is equal to 15.<ref name=goljanpath>{{Cite book | author=Goljan, Edward F. | title=Rapid Review Pathology | year=2007 | publisher=Mosby | edition=2nd | isbn=978-0-323-04414-1 | pages=396–398}}</ref>

===Prerenal azotemia===
Prerenal azotemia is caused by a decrease in blood flow ([[hypoperfusion]]) to the kidneys. However, there is no inherent kidney disease. It can occur following [[hemorrhage]], [[shock (circulatory)|shock]], [[volume depletion]], [[congestive heart failure]], adrenal insufficiency, and narrowing of the renal artery among other things.<ref name=robbins7 />

The BUN:Cr in prerenal azotemia is greater than 20. The reason for this lies in the mechanism of filtration of urea and creatinine. Renal Plasma Flow (RPF) is decreased due to hypoperfusion which results in a proportional decrease in [[Glomerular filtration rate|Glomerular Filtration Rate]] (GFR). 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. This leads to sympathetic nerve activation, resulting in <!--renal afferent arteriolar vasoconstriction (in hypovolemic states vasodilation predominates due to autoregulatory mechanisms) > alpha1 vasoconstriction--> [[renin]] secretion through [[Beta-1 adrenergic receptor|β<sub>1</sub> receptor]]s. 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 [[angiotensin]]ogen to angiotensin I, which is converted by [[Angiotensin-converting enzyme|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.<ref>{{Cite journal |last=Blantz |first=Roland C. |date=1998-02-01 |title=Pathophysiology of pre-renal azotemia |journal=Kidney International |language=en |volume=53 |issue=2 |pages=512–523 |doi=10.1046/j.1523-1755.2003_t01-1-00784.x |pmid=9461116 |issn=0085-2538|doi-access=free }}</ref>

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. The net result of these 4 mechanisms of salt and water retention is decreased output and decreased urinary excretion of sodium (< 20mEq/L). The increased reabsorption of Na leads to increased water and urea reabsorption from the [[proximal tubule]]s of the kidney back into the blood. In contrast, creatinine is actually secreted in the proximal tubule. This generally leads to a BUN:Cr ratio greater than 20, a [[Fractional sodium excretion|fractional excretion of Na]] of less than 1%, and an elevated urine osmolarity.<ref>{{Citation |last1=Tyagi |first1=Alka |title=Azotemia |date=2022 |url=http://www.ncbi.nlm.nih.gov/books/NBK538145/ |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30844172 |access-date=2022-06-15 |last2=Aeddula |first2=Narothama R.}}</ref>

=== Primary renal azotemia ===
Renal azotemia (acute kidney failure) typically leads to [[uremia]]. It is an intrinsic disease of the kidney, generally the result of kidney [[parenchyma]]l damage. Causes include [[kidney failure]], [[glomerulonephritis]], [[acute tubular necrosis]], or other [[kidney disease]].<ref name=goljanpath />

The BUN:Cr in renal azotemia is less than 15.{{Citation needed|date=July 2009}} In cases of kidney disease, glomerular filtration rate decreases, so nothing gets filtered as well as it normally would. However, in addition to not being normally filtered, what urea does get filtered is not reabsorbed by the proximal tubule as it normally would be. This results in lower levels of urea in the blood and higher levels of urea in the urine as compared to creatinine. Creatinine filtration decreases, leading to a higher amount of creatinine in the blood. Third-spacing of fluids, as in [[peritonitis]], osmotic diuresis, or [[Hypoaldosteronism|low aldosterone states]] such as [[Addison's disease]] all elevate urea.<ref name=goljanpath />

===Postrenal azotemia===
[[hydronephrosis|Blockage of urine flow]] in an area below the kidneys results in postrenal azotemia. It can be caused by [[congenital abnormalities]] such as [[vesicoureteral reflux]], blockage of the [[ureter]]s by [[kidney stone]]s, [[pregnancy]], compression of the ureters by [[cancer]], [[prostatic hyperplasia]], or blockage of the [[urethra]] by kidney or [[bladder stone]]s.<ref name=robbins7 /> Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into the kidneys, leading to [[hydronephrosis]].<ref name=goljanpath />

The BUN:Cr in postrenal azotemia is initially >15. The increased [[nephron]] tubular pressure (due to fluid back-up) causes increased reabsorption of urea, elevating it abnormally relative to creatinine.<ref name="goljanpath" /> Persistent obstruction damages the tubular epithelium over time, and renal azotemia will result with a decreased BUN:Cr ratio.<ref>{{cite web|url=http://www.consultation.ayurvediccure.com/types-of-azotemia/|title=Types of Azotemia|website=AyurvedicCure.com|access-date=2010-10-20|archive-url=https://web.archive.org/web/20160316004603/http://www.consultation.ayurvediccure.com/types-of-azotemia/|archive-date=2016-03-16|url-status=dead}}</ref>