Hydronephrosis pathophysiology: Difference between revisions

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__NOTOC__
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{{Hydronephrosis}}
{{Hydronephrosis}}
{{CMG}}; {{AE}}  
{{CMG}}; {{AE}}{{Vbe}}  


==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
[[Hydronephrosis]] can result from [[anatomic]] or [[functional]] processes interrupting the flow of [[urine]]. This interruption can occur anywhere along the [[Urinary tract neoplasm|urinary tract]] from the [[kidneys]] to the [[urethral]] meatus. The rise in [[ureteral]] pressure leads to marked changes in [[glomerular filtration]], tubular function, and [[renal blood flow]]. The [[glomerular]] filtration rate (GFR) declines significantly within hours following acute [[obstruction]]. This significant decline of GFR can persist for [[weeks]] after relief of [[obstruction]]. In addition, [[renal]] [[tubular]] ability to transport [[sodium]], [[potassium]], and [[protons]] and concentrate and to dilute the [[urine]] is severely impaired.


OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
==Pathophysiology==
==Pathophysiology==


The obstruction may be either partial or complete and can occur anywhere from the [[urinary meatus|urethral meatus]] to the  [[Minor calyx| calyces]] of the [[renal pelvis]].  
*[[Hydronephrosis]] can result from [[anatomic]] or [[functional]] processes interrupting the flow of [[urine]].
*This interruption can occur anywhere along the [[urinary tract]] from the [[kidneys]] to the [[urethral meatus]]. The rise in [[ureteral]] pressure leads to marked changes in [[glomerular filtration]], [[tubular]] function, and [[renal blood flow]].
*The [[glomerular filtration rate]] (GFR) declines significantly within hours following acute [[obstruction]]. This significant decline of [[GFR]] can persist for weeks after relief of [[obstruction]]. In addition, renal tubular ability to transport sodium, potassium, and protons and concentrate and to dilute the urine is severely impaired.


The obstruction may arise from either inside or outside the [[urinary tract]] or may come from the wall of the urinary tract itself. Intrinsic obstructions (those that occur within the tract) include blood clots, stones, sloughed papilla along with tumours of the kidney, ureter and bladder. Extrinsic obstructions (those that are caused by factors outside of the urinary tract) include pelvic or abdominal tumours or masses, retroperitoneal fibrosis or [[neurological]] deficits. Strictures of the ureters (congenital or acquired), neuromuscular dysfunctions or schistosomiasis are other causes which originate from the wall of the urinary tract.
*The obstruction may be either partial or complete and can occur anywhere from the [[urinary meatus|urethral meatus]] to the [[Minor calyx| calyces]] of the [[renal pelvis]].
==Pathophysiology==
===Physiology===
The normal physiology of [name of process] can be understood as follows:


===Pathogenesis===
*The obstruction may arise from either inside or outside the [[urinary tract]] or may come from the wall of the urinary tract itself.
*The exact pathogenesis of [disease name] is not fully understood.
*Intrinsic obstructions (those that occur within the tract) include blood clots, stones, sloughed papilla along with tumours of the kidney, ureter and bladder. Extrinsic obstructions (those that are caused by factors outside of the urinary tract) include pelvic or abdominal tumours or masses, retroperitoneal fibrosis or [[neurological]] deficits.  
OR
*Strictures of the ureters (congenital or acquired), neuromuscular dysfunctions or [[schistosomiasis]] are other causes which originate from the wall of the urinary tract.<ref name="pmid29068584">{{cite journal |vauthors=Krajewski W, Wojciechowska J, Dembowski J, Zdrojowy R, Szydełko T |title=Hydronephrosis in the course of ureteropelvic junction obstruction: An underestimated problem? Current opinions on the pathogenesis, diagnosis and treatment |journal=Adv Clin Exp Med |volume=26 |issue=5 |pages=857–864 |date=August 2017 |pmid=29068584 |doi= |url=}}</ref><ref name="pmid29202965">{{cite journal |vauthors=Vercellini P, Buggio L, Somigliana E |title=Role of medical therapy in the management of deep rectovaginal endometriosis |journal=Fertil. Steril. |volume=108 |issue=6 |pages=913–930 |date=December 2017 |pmid=29202965 |doi=10.1016/j.fertnstert.2017.08.038 |url=}}</ref>
*It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
*The progression to [disease name] usually involves the [molecular pathway].
*The pathophysiology of [disease/malignancy] depends on the histological subtype.


==Genetics==
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*[[Hydronephrosis]] is transmitted in [[autosomal dominant]] pattern.<ref name="pmid1634233">{{cite journal |vauthors=Izquierdo L, Porteous M, Paramo PG, Connor JM |title=Evidence for genetic heterogeneity in hereditary hydronephrosis caused by pelvi-ureteric junction obstruction, with one locus assigned to chromosome 6p |journal=Hum. Genet. |volume=89 |issue=5 |pages=557–60 |date=July 1992 |pmid=1634233 |doi= |url=}}</ref>
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
*Evidence for [[genetic]] heterogeneity in hereditary [[hydronephrosis]] caused by pelvic-ureteric junction obstruction with one locus assigned to chromosome 6p has been found.<ref name="pmid8357406">{{cite journal |vauthors=Fryns JP, Kleczkowska A, Moerman P, Vandenberghe K |title=Hereditary hydronephrosis and the short arm of chromosome 6 |journal=Hum. Genet. |volume=91 |issue=5 |pages=514–5 |date=June 1993 |pmid=8357406 |doi= |url=}}</ref><ref name="pmid14564156">{{cite journal |vauthors=Neas KR, Chia N, Clarke M, Peters G, Adès LC |title=A case of partial trisomy 4p syndrome presenting as severe hydronephrosis in utero |journal=Clin. Dysmorphol. |volume=12 |issue=3 |pages=179–81 |date=July 2003 |pmid=14564156 |doi=10.1097/01.mcd.0000072162.33788.8d |url=}}</ref>
*The development of [disease name] is the result of multiple genetic mutations.


==Associated Conditions==
==Associated Conditions==
* [[Nephrolithiasis]]<ref name="pmid29775451">{{cite journal |vauthors=Wojciechowska M, Bieniaś B, Sobieszczańska-Droździel A, Wieczorkiewicz-Płaza A, Beń-Skowronek I, Sikora P |title=[Recurrent urolithiasis as a symptom of primary hyperparathyroidism in a 16-year-old boy] |language=Polish |journal=Pol. Merkur. Lekarski |volume=44 |issue=262 |pages=208–210 |date=April 2018 |pmid=29775451 |doi= |url=}}</ref>
* [[Urinary tract infection]]<ref name="pmid29576374">{{cite journal |vauthors=Hong IK, Chung MH, Bin JH, Lee KY, Kim JS, Kim CH, Suh JS |title=Prediction of vesicoureteral reflux in children with febrile urinary tract infection using relative uptake and cortical defect in DMSA scan |journal=Pediatr Neonatol |volume= |issue= |pages= |date=March 2018 |pmid=29576374 |doi=10.1016/j.pedneo.2018.03.001 |url=}}</ref>
*[[Congenital malformation]]<ref name="pmid29775448">{{cite journal |vauthors=Dudek-Warchoł T, Warchoł S, Bombiński P, Toth K, Szmigielska A, Krzemień G |title=Pyonephrosis as the first symptom of congenital hydronephrosis in a 6-year old girl |journal=Pol. Merkur. Lekarski |volume=44 |issue=262 |pages=196–200 |date=April 2018 |pmid=29775448 |doi= |url=}}</ref><ref name="pmid29621304">{{cite journal |vauthors=Morris JK, Springett AL, Greenlees R, Loane M, Addor MC, Arriola L, Barisic I, Bergman JEH, Csaky-Szunyogh M, Dias C, Draper ES, Garne E, Gatt M, Khoshnood B, Klungsoyr K, Lynch C, McDonnell R, Nelen V, Neville AJ, O'Mahony M, Pierini A, Queisser-Luft A, Randrianaivo H, Rankin J, Rissmann A, Kurinczuk J, Tucker D, Verellen-Dumoulin C, Wellesley D, Dolk H |title=Trends in congenital anomalies in Europe from 1980 to 2012 |journal=PLoS ONE |volume=13 |issue=4 |pages=e0194986 |date=2018 |pmid=29621304 |pmc=5886482 |doi=10.1371/journal.pone.0194986 |url=}}</ref>
*[[Tumor]]<ref name="pmid29875948">{{cite journal |vauthors=Rachidi SA, Zeriouel A |title=[Renal tumor or pseudotumoral xanthogranulomatous pyelonephritis] |language=French |journal=Pan Afr Med J |volume=29 |issue= |pages=67 |date=2018 |pmid=29875948 |pmc=5987130 |doi=10.11604/pamj.2018.29.67.14611 |url=}}</ref>
*[[Pregnancy]]
* [[Scarring of tissues]]( From injury or previous surgery)<ref name="pmid29879068">{{cite journal |vauthors=Yumoto T, Kondo Y, Kumon K, Masaoka Y, Hiraki T, Yamada T, Naito H, Nakao A |title=Delayed hydronephrosis due to retroperitoneal hematoma after a seatbelt injury: A case report |journal=Medicine (Baltimore) |volume=97 |issue=23 |pages=e11022 |date=June 2018 |pmid=29879068 |pmc=5999472 |doi=10.1097/MD.0000000000011022 |url=}}</ref>


==Gross Pathology==
==Gross Pathology==
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*On [[gross]]  [[pathology]], the [[following]] features may be see in [[hydronephrosis]].
**Renal papillary compression
 
[[Image:Hydronephrosis.jpg||400px|center|thumb|Specimen of a kidney that has undergone extensive dilation due to hydronephrosis. Note the extensive atrophy and thinning of the renal cortex]].


==Microscopic Pathology==
==Microscopic Pathology==
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
On microscopic histopathological analysis,findings of hydronephrosis include:
*Degenerative changes in the glomeruli and tubules of the renal cortex.
*Dilated lumen of distal tubules and collecting ducts
*Necrosis


==References==
==References==

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]

Overview

Hydronephrosis can result from anatomic or functional processes interrupting the flow of urine. This interruption can occur anywhere along the urinary tract from the kidneys to the urethral meatus. The rise in ureteral pressure leads to marked changes in glomerular filtration, tubular function, and renal blood flow. The glomerular filtration rate (GFR) declines significantly within hours following acute obstruction. This significant decline of GFR can persist for weeks after relief of obstruction. In addition, renal tubular ability to transport sodium, potassium, and protons and concentrate and to dilute the urine is severely impaired.

Pathophysiology

  • The obstruction may arise from either inside or outside the urinary tract or may come from the wall of the urinary tract itself.
  • Intrinsic obstructions (those that occur within the tract) include blood clots, stones, sloughed papilla along with tumours of the kidney, ureter and bladder. Extrinsic obstructions (those that are caused by factors outside of the urinary tract) include pelvic or abdominal tumours or masses, retroperitoneal fibrosis or neurological deficits.
  • Strictures of the ureters (congenital or acquired), neuromuscular dysfunctions or schistosomiasis are other causes which originate from the wall of the urinary tract.[1][2]

Genetics

Associated Conditions

Gross Pathology

Specimen of a kidney that has undergone extensive dilation due to hydronephrosis. Note the extensive atrophy and thinning of the renal cortex
.

Microscopic Pathology

On microscopic histopathological analysis,findings of hydronephrosis include:

  • Degenerative changes in the glomeruli and tubules of the renal cortex.
  • Dilated lumen of distal tubules and collecting ducts
  • Necrosis

References

  1. ↑ Krajewski W, Wojciechowska J, Dembowski J, Zdrojowy R, Szydełko T (August 2017). "Hydronephrosis in the course of ureteropelvic junction obstruction: An underestimated problem? Current opinions on the pathogenesis, diagnosis and treatment". Adv Clin Exp Med. 26 (5): 857–864. PMID 29068584.
  2. ↑ Vercellini P, Buggio L, Somigliana E (December 2017). "Role of medical therapy in the management of deep rectovaginal endometriosis". Fertil. Steril. 108 (6): 913–930. doi:10.1016/j.fertnstert.2017.08.038. PMID 29202965.
  3. ↑ Izquierdo L, Porteous M, Paramo PG, Connor JM (July 1992). "Evidence for genetic heterogeneity in hereditary hydronephrosis caused by pelvi-ureteric junction obstruction, with one locus assigned to chromosome 6p". Hum. Genet. 89 (5): 557–60. PMID 1634233.
  4. ↑ Fryns JP, Kleczkowska A, Moerman P, Vandenberghe K (June 1993). "Hereditary hydronephrosis and the short arm of chromosome 6". Hum. Genet. 91 (5): 514–5. PMID 8357406.
  5. ↑ Neas KR, Chia N, Clarke M, Peters G, Adès LC (July 2003). "A case of partial trisomy 4p syndrome presenting as severe hydronephrosis in utero". Clin. Dysmorphol. 12 (3): 179–81. doi:10.1097/01.mcd.0000072162.33788.8d. PMID 14564156.
  6. ↑ Wojciechowska M, Bieniaś B, Sobieszczańska-Droździel A, Wieczorkiewicz-Płaza A, Beń-Skowronek I, Sikora P (April 2018). "[Recurrent urolithiasis as a symptom of primary hyperparathyroidism in a 16-year-old boy]". Pol. Merkur. Lekarski (in Polish). 44 (262): 208–210. PMID 29775451.
  7. ↑ Hong IK, Chung MH, Bin JH, Lee KY, Kim JS, Kim CH, Suh JS (March 2018). "Prediction of vesicoureteral reflux in children with febrile urinary tract infection using relative uptake and cortical defect in DMSA scan". Pediatr Neonatol. doi:10.1016/j.pedneo.2018.03.001. PMID 29576374.
  8. ↑ Dudek-Warchoł T, Warchoł S, Bombiński P, Toth K, Szmigielska A, Krzemień G (April 2018). "Pyonephrosis as the first symptom of congenital hydronephrosis in a 6-year old girl". Pol. Merkur. Lekarski. 44 (262): 196–200. PMID 29775448.
  9. ↑ Morris JK, Springett AL, Greenlees R, Loane M, Addor MC, Arriola L, Barisic I, Bergman J, Csaky-Szunyogh M, Dias C, Draper ES, Garne E, Gatt M, Khoshnood B, Klungsoyr K, Lynch C, McDonnell R, Nelen V, Neville AJ, O'Mahony M, Pierini A, Queisser-Luft A, Randrianaivo H, Rankin J, Rissmann A, Kurinczuk J, Tucker D, Verellen-Dumoulin C, Wellesley D, Dolk H (2018). "Trends in congenital anomalies in Europe from 1980 to 2012". PLoS ONE. 13 (4): e0194986. doi:10.1371/journal.pone.0194986. PMC 5886482. PMID 29621304. Vancouver style error: initials (help)
  10. ↑ Rachidi SA, Zeriouel A (2018). "[Renal tumor or pseudotumoral xanthogranulomatous pyelonephritis]". Pan Afr Med J (in French). 29: 67. doi:10.11604/pamj.2018.29.67.14611. PMC 5987130. PMID 29875948.
  11. ↑ Yumoto T, Kondo Y, Kumon K, Masaoka Y, Hiraki T, Yamada T, Naito H, Nakao A (June 2018). "Delayed hydronephrosis due to retroperitoneal hematoma after a seatbelt injury: A case report". Medicine (Baltimore). 97 (23): e11022. doi:10.1097/MD.0000000000011022. PMC 5999472. PMID 29879068.

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