Urinary tract obstruction can cause pathophysiological changes in renal blood flow, glomerular filtration rate, and tubular function. Unilateral obstruction leads to an initial rise in renal blood flow followed by vasoconstriction and reduced GFR. Bilateral obstruction results in sustained reductions in renal blood flow and GFR. Tubular transport is impaired, reducing sodium reabsorption and concentrating ability. After relief of obstruction, post-obstructive diuresis may occur as the kidneys eliminate excess sodium, water, and urea retained during obstruction. Prolonged or excessive diuresis indicates pathological tubular dysfunction rather than physiological fluid restoration. Careful monitoring is needed to prevent electrolyte abnormalities.
Presentation delivered at a paediatric clinical meeting of the Federal Medical Center, Lokoja. Nigeria
This presentation doesn't serve as a substitute for texts and/or journals.
Diuretics are substances that increase the rate and flow of urine. Here we look at the various classes of diuretics, their actions and other pharmacological effects,
Presentation delivered at a paediatric clinical meeting of the Federal Medical Center, Lokoja. Nigeria
This presentation doesn't serve as a substitute for texts and/or journals.
Diuretics are substances that increase the rate and flow of urine. Here we look at the various classes of diuretics, their actions and other pharmacological effects,
We understand the unique challenges pickleball players face and are committed to helping you stay healthy and active. In this presentation, we’ll explore the three most common pickleball injuries and provide strategies for prevention and treatment.
Navigating Challenges: Mental Health, Legislation, and the Prison System in B...Guillermo Rivera
This conference will delve into the intricate intersections between mental health, legal frameworks, and the prison system in Bolivia. It aims to provide a comprehensive overview of the current challenges faced by mental health professionals working within the legislative and correctional landscapes. Topics of discussion will include the prevalence and impact of mental health issues among the incarcerated population, the effectiveness of existing mental health policies and legislation, and potential reforms to enhance the mental health support system within prisons.
Antibiotic Stewardship by Anushri Srivastava.pptxAnushriSrivastav
Stewardship is the act of taking good care of something.
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
WHO launched the Global Antimicrobial Resistance and Use Surveillance System (GLASS) in 2015 to fill knowledge gaps and inform strategies at all levels.
ACCORDING TO apic.org,
Antimicrobial stewardship is a coordinated program that promotes the appropriate use of antimicrobials (including antibiotics), improves patient outcomes, reduces microbial resistance, and decreases the spread of infections caused by multidrug-resistant organisms.
ACCORDING TO pewtrusts.org,
Antibiotic stewardship refers to efforts in doctors’ offices, hospitals, long term care facilities, and other health care settings to ensure that antibiotics are used only when necessary and appropriate
According to WHO,
Antimicrobial stewardship is a systematic approach to educate and support health care professionals to follow evidence-based guidelines for prescribing and administering antimicrobials
In 1996, John McGowan and Dale Gerding first applied the term antimicrobial stewardship, where they suggested a causal association between antimicrobial agent use and resistance. They also focused on the urgency of large-scale controlled trials of antimicrobial-use regulation employing sophisticated epidemiologic methods, molecular typing, and precise resistance mechanism analysis.
Antimicrobial Stewardship(AMS) refers to the optimal selection, dosing, and duration of antimicrobial treatment resulting in the best clinical outcome with minimal side effects to the patients and minimal impact on subsequent resistance.
According to the 2019 report, in the US, more than 2.8 million antibiotic-resistant infections occur each year, and more than 35000 people die. In addition to this, it also mentioned that 223,900 cases of Clostridoides difficile occurred in 2017, of which 12800 people died. The report did not include viruses or parasites
VISION
Being proactive
Supporting optimal animal and human health
Exploring ways to reduce overall use of antimicrobials
Using the drugs that prevent and treat disease by killing microscopic organisms in a responsible way
GOAL
to prevent the generation and spread of antimicrobial resistance (AMR). Doing so will preserve the effectiveness of these drugs in animals and humans for years to come.
being to preserve human and animal health and the effectiveness of antimicrobial medications.
to implement a multidisciplinary approach in assembling a stewardship team to include an infectious disease physician, a clinical pharmacist with infectious diseases training, infection preventionist, and a close collaboration with the staff in the clinical microbiology laboratory
to prevent antimicrobial overuse, misuse and abuse.
to minimize the developme
Medical Technology Tackles New Health Care Demand - Research Report - March 2...pchutichetpong
M Capital Group (“MCG”) predicts that with, against, despite, and even without the global pandemic, the medical technology (MedTech) industry shows signs of continuous healthy growth, driven by smaller, faster, and cheaper devices, growing demand for home-based applications, technological innovation, strategic acquisitions, investments, and SPAC listings. MCG predicts that this should reflects itself in annual growth of over 6%, well beyond 2028.
According to Chris Mouchabhani, Managing Partner at M Capital Group, “Despite all economic scenarios that one may consider, beyond overall economic shocks, medical technology should remain one of the most promising and robust sectors over the short to medium term and well beyond 2028.”
There is a movement towards home-based care for the elderly, next generation scanning and MRI devices, wearable technology, artificial intelligence incorporation, and online connectivity. Experts also see a focus on predictive, preventive, personalized, participatory, and precision medicine, with rising levels of integration of home care and technological innovation.
The average cost of treatment has been rising across the board, creating additional financial burdens to governments, healthcare providers and insurance companies. According to MCG, cost-per-inpatient-stay in the United States alone rose on average annually by over 13% between 2014 to 2021, leading MedTech to focus research efforts on optimized medical equipment at lower price points, whilst emphasizing portability and ease of use. Namely, 46% of the 1,008 medical technology companies in the 2021 MedTech Innovator (“MTI”) database are focusing on prevention, wellness, detection, or diagnosis, signaling a clear push for preventive care to also tackle costs.
In addition, there has also been a lasting impact on consumer and medical demand for home care, supported by the pandemic. Lockdowns, closure of care facilities, and healthcare systems subjected to capacity pressure, accelerated demand away from traditional inpatient care. Now, outpatient care solutions are driving industry production, with nearly 70% of recent diagnostics start-up companies producing products in areas such as ambulatory clinics, at-home care, and self-administered diagnostics.
One of the most developed cities of India, the city of Chennai is the capital of Tamilnadu and many people from different parts of India come here to earn their bread and butter. Being a metropolitan, the city is filled with towering building and beaches but the sad part as with almost every Indian city
Leading the Way in Nephrology: Dr. David Greene's Work with Stem Cells for Ki...Dr. David Greene Arizona
As we watch Dr. Greene's continued efforts and research in Arizona, it's clear that stem cell therapy holds a promising key to unlocking new doors in the treatment of kidney disease. With each study and trial, we step closer to a world where kidney disease is no longer a life sentence but a treatable condition, thanks to pioneers like Dr. David Greene.
QA Paediatric dentistry department, Hospital Melaka 2020Azreen Aj
QA study - To improve the 6th monthly recall rate post-comprehensive dental treatment under general anaesthesia in paediatric dentistry department, Hospital Melaka
Global launch of the Healthy Ageing and Prevention Index 2nd wave – alongside...ILC- UK
The Healthy Ageing and Prevention Index is an online tool created by ILC that ranks countries on six metrics including, life span, health span, work span, income, environmental performance, and happiness. The Index helps us understand how well countries have adapted to longevity and inform decision makers on what must be done to maximise the economic benefits that comes with living well for longer.
Alongside the 77th World Health Assembly in Geneva on 28 May 2024, we launched the second version of our Index, allowing us to track progress and give new insights into what needs to be done to keep populations healthier for longer.
The speakers included:
Professor Orazio Schillaci, Minister of Health, Italy
Dr Hans Groth, Chairman of the Board, World Demographic & Ageing Forum
Professor Ilona Kickbusch, Founder and Chair, Global Health Centre, Geneva Graduate Institute and co-chair, World Health Summit Council
Dr Natasha Azzopardi Muscat, Director, Country Health Policies and Systems Division, World Health Organisation EURO
Dr Marta Lomazzi, Executive Manager, World Federation of Public Health Associations
Dr Shyam Bishen, Head, Centre for Health and Healthcare and Member of the Executive Committee, World Economic Forum
Dr Karin Tegmark Wisell, Director General, Public Health Agency of Sweden
Struggling with intense fears that disrupt your life? At Renew Life Hypnosis, we offer specialized hypnosis to overcome fear. Phobias are exaggerated fears, often stemming from past traumas or learned behaviors. Hypnotherapy addresses these deep-seated fears by accessing the subconscious mind, helping you change your reactions to phobic triggers. Our expert therapists guide you into a state of deep relaxation, allowing you to transform your responses and reduce anxiety. Experience increased confidence and freedom from phobias with our personalized approach. Ready to live a fear-free life? Visit us at Renew Life Hypnosis..
8. Introduction
• Obstructive uropathy refers to the functional or anatomic obstruction of
urinary flow at any level of the urinary tract.
• Obstructive Nephropathy is present when the obstruction causes functional
or anatomic renal damage.
• Hydronephrosis is the dilatation of the renal pelvis or calyces.
It may or may not be associated with obstruction but may be present in the
absence of obstruction.
9. Urinary tract Obstruction
tubular pressure changes, renal blood flow, and glomerular filtration rate
affecting the excretion function and renal homeostasis
irreversible renal impairment
13. Symptoms
Depends on
• Acute / Chronic
• Unilateral / Bilateral
• Extrinsic vs Intrinsic cause of obstruction
• Complete vs Partial
• Presence or absence of infection
• Compliance of collecting system
16. A. RBF,GFR, and Ureteral Pressure
Pre-glomerular vasodilatation
Phase I (0-90 mins)
- Increased RBF in response to increased ureteral pressure.
- Due to preglomerular vasodilatation, a compensatory response intended to
increase capillary hydrostatic pressure and thus GFR.
- Vascular mediators thought to play major role:
Eicosanoids
Nitric Oxide
17. Post-glomerular vasoconstriction, then pre- and post-glomerular vasoconstriction
• Phase II (90 mins – 4/5 hours) characterised by a fall in RBF with a continued rise
in ureteral pressure. Due to post-glomerular vasoconstriction. Further attempt by
kidney to maintain GFR.
• Phase III (5 hours+) associated with concomitant falls in RBF and ureteral pressure.
Further fall in RBF due to pre-glomerular vasoconstriction. By 24 hours tubular
pressure and ureteral pressure fall to 30% and 50% of control values respectively.
• Vaso-constrictive mediators in Phase II and III:
-Eicosanoids
-Thromboxanes
-Renin/ Angiotensin II
-Endothelin
18. • Triphasic relationship between ipsilateral renal blood flow (RBF) and ureteral
pressure during 18 hours of Unilateral ureteral obstruction.
19. • Decreased GFR due to
o Reduced single-nephron renal blood flow
o Shunting of blood from outer to inner cortex, decreasing the total number
of perfused glomeruli. ? Mechanism of shunting. Increased production of renin
witnessed in outer vs. inner cortex.
• Fall in ureteral pressure due to
o Reduced GFR
o Pelvicalyceal dilatation
o Pyelolymphatic and pyelovenous backflow
21. B. Tubular Function in Unilateral Ureteric Obstruction
• GFR markedly reduced following release of obstruction, but total excretion from
post-obstructed kidney is normal/ slightly elevated, due to ineffective Na
reabsorption and water retention in the tubules, leading to impaired concentrating
ability.
• Active transport markedly impaired. Selective down-regulation of both transporter
activity and transporter protein synthesis after 24 hours of obstruction.
• Proximal tubule relatively spared, but marked failure of active transport mechanisms
from loop of Henle to collecting duct. Reduced reabsorption of sodium in ascending
limb, leads to a reduction in interstitial hypertonicity. Combined with insensitivity to
ADH in collecting duct, results in impaired concentrating ability.
• Potassium excretion falls proportionate to fall in GFR, due to defective distal tubular
secretion.
• Failed active transport also leads to an inability to acidify urine
22. • Urine
o Normal/ mildly elevated excretion of filtered load
o Low osmolality
o Normal/ high pH
o High sodium content (increased filtered fraction)
o Low potassium content
o Low phosphate content
24. A. Changes in RBF, GFR and Ureteric Pressure
• No triphasic patternBiphasic pattern
o Initial short-lived rise in RBF as in UUO, due to pre-glomerular vasodilatation
o Marked fall in RBF, associated with a persistently elevated ureteric pressure > 24
hours. Associated with post-glomerular vasoconstriction.
o NO pre-glomerular vasoconstriction seen in late-stage BUO. ? accumulation of a
‘substance’ which prevents preglomerular vasoconstriction.
GFR preservation, diuresis and natriuresis in UUO with contralateral nephrectomy,
and with contralateral urine perfusion of obstructed kidney, but not in UUO with
normal contrateral kidney. Substance believed to be Atrial Natriuretic Peptide
25. Atrial Natriuretic Peptide
• Released by cardiac atrium in response to increased intravascular volume
• Effects designed to maximise diuresis and natriuresis
o Increased GFR through pre-glomerular vasodilatation and postglomerular
vasoconstriction
o Increased glomerular capillary ultrafiltration co-efficient (leakier
membrane)
o Direct inhibition of tubuloglomerular feedback mechanism (renin/AII)
o Specific inhibition of NaCl co-transport in ascending limb of loop of Henle
o Blocks vasopressin-mediated osmotic water permeability
• Elevated in BUO but not in UUO in rats
27. B. Tubular Function in Bilateral Ureteric Obstruction
• Similar tubular defects as seen in UUO, but exacerbated due to activity of ANP
• Marked post-obstructive diuresis and natriuresis may be seen
• A marked increase in Na delivery to the distal nephron, combined with elevated serum
potassium, results in an increased filtration fraction of potassium
• Urine
o Significantly increased total excretion of filtered load
o Low osmolality (lower cf. UUO)
o Normal/ High pH
o High sodium content
o High potassium content
29. A. Unilateral Ureteric Obstruction
Different durations of acute UUO
o If reversed within 2 weeks = full recovery of function
o After 14 days ~ up to 70% return of function
o No functional recovery after 6 weeks
o Continued improvement up to 6 months following obstruction
o Anecdotal reports of total return to function after as long as 6 months
o ? due to multi-calyceal kidney or pyelolymphatic ‘escape’
30. B.Bilateral Ureteric Obstruction
• No clear relationship between the duration of obstruction and recoverability of
function. Furthermore no pre-release chemistry which can predict recoverability.
• 2 phases of recovery of function:
An initial ‘tubular’ phase associated with improvements in creatinine clearance
and fractional excretion of sodium.
A further ‘glomerular’ phase associated with a gradual improvement in GFR
over approximately 3 months.
31.
32. Effect of obstruction on tubular function
• Urinary Concentrating Ability
Normally it requires a hypertonic medullary interstitial gradient because of
– active salt reabsorption from the thick ascending limb of Henle,
– urea back flux from the inner medullary collecting duct,
– water permeability of the collecting duct mediated by vasopressin and aquaporin
water channels
Obstructive nephropathy can disrupt some or all of these mechanisms and lead to
deficits in urinary concentration
33. • Sodium Transport
- Active transport of Na+ across cell membranes requires apical entry through
selective Na+ transporters or channels and basolateral exit driven by Na+-K+-ATPase
and adequate ATP must be generated to drive these primary transport steps.
In obstruction there is reduced activity of the apical Na channel (ENaC) and also
decreased ATPase activity.
• Hydrogen Ion Transport and Urinary Acidification
- Major acidification defect is in the distal nephron, related to defective H+ secretion
in the distal tubule and collecting duct and/or decreased bicarbonate reabsorption in
the juxtamedullary nephron.
Obstruction causes a deficit in urinary acidification
• Insensitivity to ADH
- Dysregulation of aquaporin water channels in the proximal tubule, thin descending
loop, and collecting duct may contribute to the long-term polyuria and impaired
concentrating capacity caused by obstructive nephropathy.
34. • Obstruction has an effect on other cation transport as well
• In UUO, potassium secretion is decreased in proportion to the decrease in GFR
after release of a 24-hour period of UUO. (due to reduced delivery of sodium to the
distal nephron and a low flow state, along with intrinsic defect in potassium
secretion)
• In contrast, potassium excretion increases in parallel with sodium excretion after
relief of BUO, and it appears that proximal reabsorption of potassium remains
unchanged whereas its secretion in the collecting duct is increased after relief of
obstruction. (related to increased water and sodium delivery to the collecting duct
and to the presence of high levels of ANP that can stimulate potassium secretion in
the distal nephron.)
• Magnesium excretion is also markedly increased
• Effect on phosphate reabsorption,
• In BUO after relieving the obstruction , accumulated phosphate is
rapidly excreted in proportion to sodium,
• Whereas, in UUO a decrease in phosphate excretion and a net
retention occur with release.
36. Gross Pathologic Findings
Renal Pelvis Dilates
-Generally assumed to occur in the first few days after ureteral obstruction
-Extrarenal pelvis dilatation>>intrarenal dilatation.
-Increased intrarenal pelvic pressure results in papillary compression and
thinning, with eventual septation and production of a ‘rim’ of functioning
cortex.
Initial Increase in Mean Kidney Weight
-Oedema > atrophy in first three months.
Pigmentation, Focal Ischaemia and Necrosis
-Focal necrosis and haemorrhage of papilla and fornix in particular
37. Microscopic Pathologic Findings
Tubular Apoptosis
-Initial dilatation and thinning of epithelium
-Apoptosis within 30 mins in animal models
-Dysregulation of proliferation and apoptosis
-Disappearance of recognisable tubular subunits within 21 days.
Glomerular Sparing
-Slight thickening of GBM with loss of filtration slits.
-Hyalinisation reported but not until ~ 6-9 months following obstruction, and then
only in a relatively small number of glomeruli.
38. • Inflammatory Infiltrate.
- Influx of predominantly macrophages but a few T-cells after 3-4 hours
- Associated conversion of fibroblasts to myofibroblasts.
- Production of mediators (TXA2, PAF and TGFB), leading to tubuloinsterstitial
fibrosis (TGF beta major is determinant)
• Tubulointerstitial fibrosis
- Thought to be major determinant of deranged renal function and failed
recovery following release of obstruction
39. Tubulointerstitial fibrosis
• Inflammatory Cell Infiltration
• Fibroblasts and Extracellular Matrix Production
• Epithelial-to-Mesenchymal Transition
• Cytokines and Vasoactive Mediators of Fibrosis
Transforming Growth Factor-β
Tumor Necrosis Factor-α
Interleukin-18
Angiotensin II
Apoptosis
41. • After infiltration of the interstitial space by activated macrophages,
inflammatory mediators are released,
• TGF-β1, TNF-α, and IL-18 trigger renal tubular cell apoptosis, the
transformation of renal tubular cells into matrix-producing
fibroblasts, and further inflammatory cell infiltration.
• Additional fibroblasts are recruited from the bone marrow, and
resident fibroblasts in the interstitial space are stimulated to secrete
extracellular matrix.
• Angiotensin II is produced in response to the decreased RBF
associated with obstruction, and it further stimulates macrophage
infiltration and cytokine production (TNF-α and TGF-β1).
• The resulting imbalance in ECM deposition results in expansion of the
interstitial space and increasing tubulointerstitial fibrosis.
42. Clinical impact of Obstruction
• Hypertension
• Increased ANP levels and intravascular volume
• A volume-mediated mechanism for hypertension
• BUO>UUO
• Compensatory Renal Growth
• Contralateral renal growth is influenced by age and the degree and duration
of obstruction
• While the kidney enlarges, an increase in the number of nephrons or
glomeruli does not occur, indicating that the increase in renal volume is
primarily a consequence of cellular hypertrophy rather than hyperplasia.
44. • Post-obstructive diuresis refers to the polyuria that may be encountered after
release of urinary obstruction as the body attempts to restore fluid and solute
homeostasis.
• Definition: Urine production exceeding 200 mL per hour for 2 consecutive hours
or producing greater than 3 L of urine in 24 hours is diagnostic of POD
45. • Factors necessary are
- Accumulation of total body water, Sodium and urea
- Impairment of Tubular re-absorptive capabilities. (in pathological POD)
• Clinical scenarios with significant POD
> Prior bilateral
> Ureteral obstruction
> Unilateral obstruction of a solitary functioning kidney
>Uncommon following UUO due to compensation by normally functioning
contralateral kidney.
46. • PHYSIOLOGICAL POD: Self limiting, generally lasts 24 hours– As a response to
simple solute and water overload. Stops after return to euvolemic state
• PATHOLOGICAL POD: Generally lasts longer than 48 hours and can be
exacerbated with excessive intravenous fluid replacement. Inappropriate diuresis
of water beyond euvolemic state.
47. Contributing factors after the release of obstruction
➢ Physiological
1. Excess Na and water retention
2. Retention of urea and non reabsorbable solutes
3. Accumulation of ANP
➢ Pathological
1. Concentration defect
2. Decreased tubular reabsorption of Na
3. Insensitivity to ADH
4. Increased tubular flow reducing equilibration time for reabsorption of Na and
water
48. ETIOLOGY
• The location of obstruction: Anywhere from meatus to the PUJ
• Common situations resulting in POD :
1) Infravesical obstructions-BPH,
CAP, NB,BT,urethral
strictures, meatal stenosis,
phimosis, CA penis
2) Bilateral ureteric obstructions-
Calculi, papilla, strictures,
PUJ obstructions, IRPF, RP tumors,
Abdominal aortic aneurysm
3) Unilateral obstruction in solitary
kidney-
Calculi, papilla, strictures
49. CLINICAL FEATURES/MONITORING
• Depend on duration and severity of obstruction- Asymptomatic to critically ill
• In POD following acute obstructions- Rapid to start, short plateau and rapid
normalisation of urinary volumes. Usually physiological POD.
• In POD following chronic obstruction (CRF)- Slow to start, longer plateau and
slow normalisation. This is the extended time taken for the concentrating
mechanisms to repair themselves.-Pathological POD)
50. Clues to possible pathological diuresis:
1)High degree of derangement of renal parameters.
2)Painless B/L HDUN/ unilateral in solitary kidney-Chronic
3)Hematuria following catheterisation-
Chronic obstruction - decompression hematuria
Slow decompression no longer advised.
51. During POD- Watch for
-Urine output recorded every hour initially and vital signs checked every 6 to 8 hours.
- Serum electrolyte (especially potassium), magnesium, phosphate, urea, and
creatinine levels should be checked every 12 to 24 hours and corrected if necessary.
-The intensity of monitoring depends on presence of risk factors for POD and the
subject's mental status, renal function, and electrolyte status.
-A urine sample should be collected for urinary sodium and potassium levels and urine
osmolality to determine if it is a salt or urea type of diuresis.
Urea diuresis is generally self-limiting,
Salt diuresis can convert to pathologic POD and requires careful monitoring of serum
electrolyte levels and hydration status.
52. • A simple method to estimate urine osmolality, if an automated
method is not available, is to assess the urine specific gravity.
A specific gravity of 1.010 is iso-osmotic with serum osmolality, indicating that the
kidneys do not need to concentrate the urine. This is consistent with physiologic
POD and is generally self-limiting.
A specific gravity of 1.020 demonstrates that the kidneys are concentrating the urine
and POD has resolved or has nearly resolved.
However, a specific gravity of 1.000 is hypo-osmotic with serum osmolality, indicating
the kidneys’ inability to concentrate the urine. This is consistent with pathologic
salt-wasting POD and should alert the health care team to monitor the patient
closely
53. MANAGEMENT
• Physiological POD: Basic monitoring and oral fluids regulated by thirst.
• Pathological POD: -Sequential monitoring
- Oral fluids + IV replacement depending on
volume of diuresis and ability of the patient to
take adequate oral fluids
- If Sodium is high- 0.45% saline. If Normal- 0.9%
saline
- Slightly under-hydrate to avoid iatrogenic
propagation of the diuretic phase and allow ADH
mechanisms to act on the tubules. (50-70-%
replacement is generally accepted)
- Correct hypokalemia that can be threatening.
54. • In the first 24 hours, urine output should be checked hourly.
➢ If it is over 200 mL/hour, then 80% (50% at CMCH) of the hourly output should be
replaced intravenously with 0.45% saline. Alternatively the same volume of water
may be consumed orally.
• After 24 hours of persistent diuresis,
➢ total fluids infused should be about 1 L less (or <75%) than the previous day's
output, provided the patient is hemodynamically stable.
- Once the urine output </- 3 L per day, oral fluids should suffice.
- If there are signs of hypovolemia, then total fluids replaced should be about 0.5 L
less, instead of 1 L, than the last 24 hours' output.
55. Pharmacological treatments
• Aquaporin expression was improved by administration of COX2 inhibitors and
associated with reduced urine output in the acute phase of POD but not after
24hours.
• PDIE -5 inhibtors has been shown to induce aquaporin membrane insertion
• Some interventions focus on preventing the long term consequences of
obstruction, such as fibrosis. For example, in rodent UUO models treatment with
statins, erythropoietin or rotenone decreased renal fibrosis.
• However, definitive human data are lacking to support routine pharmacological
intervention for POD at this time.