Azotemia
| Azotemia | |
|---|---|
| Specialty | Nephrology |
Azotemia(azot,"nitrogen" +-emia,"blood condition" ) is a medical condition characterized by abnormally high levels ofnitrogen-containing compounds (such asurea,creatinine,various body waste compounds, and other nitrogen-rich compounds) in theblood.It is largely related to insufficient or dysfunctional filtering ofbloodby thekidneys.[1]It can lead touremiaandacute kidney injury(kidney failure) if not controlled.
Types[edit]
Azotemia has three classifications, depending on its causative origin: prerenal azotemia, renal azotemia, and postrenal azotemia.[2]
Measurements ofureaandcreatinine(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.[3]
Prerenal azotemia[edit]
Prerenal azotemia is caused by a decrease in blood flow (hypoperfusion) to the kidneys. However, there is no inherent kidney disease. It can occur followinghemorrhage,shock,volume depletion,congestive heart failure,adrenal insufficiency, and narrowing of the renal artery among other things.[1]
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 inGlomerular 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 inreninsecretion 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 convertangiotensinogento angiotensin I, which is converted byangiotensin converting enzyme,to angiotensin II, which, in turn, stimulates aldosterone release. Increasedaldosteronelevels results in salt and water absorption in the distal collecting tubule.[4]
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 theproximal tubulesof the kidney back into the blood. In contrast, creatinine is actually secreted in the proximal tubule. This generally leads to a BUN:Cr ratio > 20 and afractional excretion of Naof < 1% and an elevated urine osmolarity.[5]
Primary renal azotemia[edit]
Renal azotemia (acute kidney failure) typically leads touremia.It is an intrinsic disease of the kidney, generally the result of kidneyparenchymaldamage. Causes includekidney failure,glomerulonephritis,acute tubular necrosis,or otherkidney disease.[3]
The BUN:Cr in renal azotemia is less than 15.[citation needed]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 such asperitonitis,osmotic diuresis, orlow aldosterone statessuch asAddison's diseaseall elevate urea.[3]
Postrenal azotemia[edit]
Blockage of urine flowin an area below the kidneys results in postrenal azotemia. It can be caused bycongenital abnormalitiessuch asvesicoureteral reflux,blockage of theuretersbykidney stones,pregnancy,compression of the ureters bycancer,prostatic hyperplasia,or blockage of theurethraby kidney orbladder stones.[1]Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into the kidneys, leading tohydronephrosis.[3]
The BUN:Cr in postrenal azotemia is initially >15. The increasednephrontubular pressure (due to fluid back-up) causes increased reabsorption of urea, elevating it abnormally relative to creatinine.[3]Persistent obstruction damages the tubular epithelium over time, and renal azotemia will result with a decreased BUN:Cr ratio.[6]
Signs and symptoms[edit]
- 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 whenureaand urea derivatives are secreted through the skin in sweat, which evaporates away to leave solid uric compounds, resembling afrost.
Aurinalysiswill typically show a decreased urine sodium level, a high urinecreatinine-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.[citation needed]
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. Incongestive 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.[citation needed]
Treatment[edit]
Prompt treatment of some causes of azotemia can result in restoration of kidney function; delayed treatment may result in permanent loss of renal function. Treatment may includehemodialysisor peritonealdialysis,medications to increase cardiac output and increase blood pressure, and the treatment of the condition that caused the azotemia.[citation needed]
See also[edit]
References[edit]
- ^abcKumar, Vinay; Fausto, Nelson; Fausto, Nelso; Robbins, Stanley L.; Abbas, Abul K.; Cotran, Ramzi S. (2005).Robbins and Cotran Pathologic Basis of Disease(7th ed.). Philadelphia, Pa.: Elsevier Saunders. pp. 960, 1012.ISBN0-7216-0187-1.
- ^Tyagi, Alka; Aeddula, Narothama R. (2022),"Azotemia",StatPearls,Treasure Island (FL): StatPearls Publishing,PMID30844172,retrieved2023-03-02
- ^abcdeGoljan, Edward F. (2007).Rapid Review Pathology(2nd ed.). Mosby. pp. 396–398.ISBN978-0-323-04414-1.
- ^Blantz, Roland C. (1998-02-01)."Pathophysiology of pre-renal azotemia".Kidney International.53(2): 512–523.doi:10.1046/j.1523-1755.2003_t01-1-00784.x.ISSN0085-2538.PMID9461116.
- ^Tyagi, Alka; Aeddula, Narothama R. (2022),"Azotemia",StatPearls,Treasure Island (FL): StatPearls Publishing,PMID30844172,retrieved2022-06-15
- ^"Types of Azotemia".AyurvedicCure.Archived fromthe originalon 2016-03-16.Retrieved2010-10-20.
