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Published byGwendolyn Stewart Modified over 9 years ago
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Nephrology 1 Pathophysiology of upper tract obstruction
Euan Green Mr Brough
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40 yr old man Referred by GP Vague abdominal pain
USS shows solitary left kidney with hydronephrosis Seen in clinic and asymptomatic Wants to know “What’s up doc?”
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Does this mean my kidney is blocked?
No! Hydronephrosis = dilatation of renal pelvis or calyces with or without obstruction Hydroureteronephrosis = above + dilated ureter Obstruction = obstruction to the flow of urine
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What’s the cause? Congenital or acquired
Intra-luminal, in the lumen wall or extraluminal Complete or incomplete
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Site Cause Kidney Ureter Lower urinary tract Stone TCC RCC Renal cysts
PUJO Extrinsic mass Ureter Stone Tumour Retroperitoneal fibrosis Stricture Extrinsic compression Blood clot Sloughed papilla Ureterocoele Retrocaval ureter Endometriosis Ureteric atresia Surgical ligation Pregnancy Trauma Lower urinary tract BPH (HPCR) Stones Urethral stricture Procidentia Posterior urethral valves Hydrocolpos Meatal stenosis Phimosis Tumour
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What do you do next? U&E? CT? Renogram? Na+ 140 K+ 4.2 Urea 5.0
Creat 70
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What do you do next? U&E? CT? Renogram?
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What is the diagnosis? Extrarenal pelvis
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25 yr old woman Sudden onset severe right loin pain Colicky Vomiting
Dipstick haematuria Comes to A&E Seen by SHO who arranges a CT Urogram
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Followed by a renogram
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Your SHO asks you “what will happen
Your SHO asks you “what will happen? Will the kidney just fill up and then burst?” Triphasic response to upper tract obstruction Different for unilateral and bilateral obstruction
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Unilateral obstruction
Renal blood flow Collecting system pressure Comment 1 0 – 90 min (6.5 to 70 mmHg) Afferent arteriolar vasodilation 2 90 min – 5h (by 40 – 70%) (remains elevated) Afferent and Efferent arteriolar vasoconstriction 3 5 – 18h (continued decrease) (towards resting) Collecting system dilatation Pyelotubular reflux Pyelovenous reflux Pyelolymphatic reflux
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Unilateral obstruction
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The contralateral kidney
Compensatory Growth Response proportional to degree of injury Initial vasoconstriction, subsequent vasodilation Hypertrophy Increased blood flow and GFR Compensatory growth is age dependent The number of nephrons remains constant Increase in proximal tubular length due to increase in cell size
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75 yr old man Previously completely well
Nocturnal enuresis for the last 6 weeks Tired Pitting ankle oedema BP 180/100 Large abdominal mass
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What is the likely diagnosis? Initial management?
High pressure Chronic retention of urine Initial management? U&E Creatinine 1500, Urea 43, K+ 6.8 Admit as an emergency Catheterise 3.5 Litre residual ECG & Treat K+ CaGluconate, insulin dextrose, fluids, salbutamol If K+ still high with ECG changes? Dialysis USS urinary tract
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The patient wants to know:
What has happened to his kidneys What to expect over the next few days Whether his kidney function will recover
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Bilateral obstruction
Similar to unilateral upper tract obstruction Less pronounced rise in blood flow initially Less afferent vasodilation Lasts 90 mins More substantial decline in blood flow after Greater vasoconstriction (thought to be due to no renal clearance of vasoconstricters from other kidney) Renal pelvic and ureteric pressures remain raised for longer, approaching pre-obstruction pressure at 24 hrs No other side to compensate
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Macroscopic effects on kidney
Dilatation of pelvis/calyxes – hydronephrosis Dilation of ureter Flattened papillae (42hrs) Parenchymal oedema (7 days) Cortical parenchymal thinning (21 days)
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Microscopic effects 42 hrs – lymphatic dilatation, interstitial oedema
7 days – collecting duct, tubular dilation, widening of Bowman’s space, tubular basement membrane thickening 9 days – papillary tip necrosis and inflammatory cell infiltrate 16 days – interstitial fibrosis 3 weeks – tubular loss, fibroblast growth, collagen deposition 6 weeks – Widespread tubular atrophy and fibrosis Apoptosis is the principle mechanism of cell loss
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Effect on tubular function
Down-regulation of aquaporin channels impairs concentrating ability Some down-regulation of active sodium transporters. In addition fluid overload stimulates ANP secretion encouraging natriuresis Reduction in GFR and down-regulation of Na+/K+ ATPase transporters reduces K+ excretion Down-regulation of active H+ transporters results in a relative failure of H+ ion excretion In unilateral obstruction the other kidney can compensate
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Post-obstructive diuresis
Rare after relief of unilateral obstruction Typically a physiological response to retained solutes (urea, sodium) and water Pathological component due to tubular defects as mentioned, in particular the downregulation of aquaporin channels resulting in reduced sensitivity to ADH and the obliteration of the concentration gradient around the loop of Henle Can be due to excess fluid replacement Some patients develop hyponatraemia and hyperkalaemia due to tubular resistance to aldosterone
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Post-obstructive diuresis
Those at increased risk: Hypertension Oedema CCF Long standing obstruction Clinical uraemia 20% have a urine output >4L in 24hrs 5-10% require IV fluids ~1% develop long term salt loss/diuresis
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Return of renal function
Degree function return difficult to predict, relates to degree of obstruction, duration and prior function Dog experiments have been carried out: 7 days: full functional recovery 14 days: 70% recovery 28days: 30% recovery 6 weeks: no functional recovery In humans return of function has been noted after 150 days Difficult to predict 2 phases of recovery: First 2 weeks – recovery in tubular function Next 10 weeks – recovery in GFR
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21 year old woman comes to the haematuria clinic
Left sided loin pain after nights out in the pub Occasional haematuria Otherwise fit and well Flexible cystoscopy normal Young so she gets an MRI rather than a CT
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She wants to know what the diagnosis is?
Left PUJ obstruction 1: 50% present in adult life, 50% as a child Male 2:1 Female, Left > Right Associated with other abnormalities in 50% 10% bilateral VUR Horseshoe/renal duplication/ectopia Due to crossing vessel/poor canalisation during formation/abnormal insertion into renal pelvis/ smooth muscle mal-development causing atonic segment
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What are you going to do next?
Right – 18% Left – 82% What are you going to do next? Confirm obstruction and assess function in that kidney. i.e. do a renogram She wants to know: “how can this be treated?” Conservative Stent Endopyelotomy Pyeloplasty
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Treatment options in PUJO
Conservative Mx Suitable if asymptomatic and >40% relative function and unilateral Need monitoring Asymptomatic, non-functioning units Stent Palliation for the unfit Management of the acute presentation ?Diagnostic role
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Treatment options in PUJO
Endopyelotomy Ureteroscopy + laser/knife (60-85% success) Acucise Device (Retrograde balloon catheter + cutting wire) (65-80% success) Percutaneous endopyelotomy (80% success) See NICE guidance Dec 2009 Various definitions of success – all relatively short term success
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Treatment options in PUJO
Pyeloplasty (>90% success) Open Laparoscopic Robotic Aim of surgery is to restore normal urine flow Anastomosis has to be watertight and funnelled into the ureter
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Anderson-Hynes Pyeloplasty
Excise PUJ Spatulate the ureter Narrow pelvis defect if large Anastomose spatulated ureter to pelvis Usually over a stent
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Culp-DeWeerd Spiral flap
Suited to those with a long stricture Open a spiral flap of renal pelvis Rotate down and use flap to augment the width of the stenosed ureter
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Foley V-Y Pyeloplasty Useful for high ureteric insertion into pelvis
V-shaped flap from renal pelvis Inserted into Y-shaped defect opened over stricture
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Ureterocalicostomy Suitable for revision surgery or renal abnormalities that prevent other options Anastomose ureter to a lower pole calyx Requires lower pole partial nephrectomy to reduce risk of stenosis
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Treatment options in PUJO
Most now managed with laparoscopic pyeloplasty Poorly functioning kidneys <15-20% Can consider nephrectomy
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50 yr old man Presents with loin pain Intermittent Can be severe GP arranges USS which shows hydronephrosis A medical student in clinic asks “What types of imaging can be used to demonstrate obstruction?”
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Imaging for obstruction
USS Can show dilatation (ie hydronephrosis) False +ve Excess flow eg Diuresis Anatomy eg Extrarenal pelvis, Cysts False –ve Too little flow eg dehydration Operator dependant Can use doppler renal resistive index >0.7 suggests obstruction, ~0.6 normal (Peak systolic velocity-peak diastolic velocity) / Peak systolic velocity
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Imaging for obstruction
IVU Dynamic test Functional information Complete vs partial Level of obstruction Time consuming in obstructed patients
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Imaging for obstruction
CT with or without contrast Cheap Quick Good at identifying causes both intrinsic and extrinsic Comparatively high radiation dose
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Imaging for obstruction
MRI Can identify hydronephrosis Can’t detect stones No radiation Useful in the pregnant patient
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Imaging for obstruction
Renogram A study of the uptake, transit and elimination by the kidney of an intravenous dose of a radionucleotide Gives drainage and relative function Limited anatomical information Use of diuretic improves discrimination between obstructed and non-obstructed
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Renography 3 phases Vascular phase, represents uptake
Transit phase, represents transit through kidney Elimination phase, excretion from the kidney and expulsion down the ureter TIME (minutes) DOSE % 4 8 12 10 20 30 Bladder Renal
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O’Reilly Curves F+20 renogram
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Back to the patient What does this show? What next?
F-15 Renogram What if it’s still equivocal? Whittaker’s test
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Whittaker’s test A test to help differentiate in those with equivocal obstruction or poor function where renogram unhelpful Quite invasive Nephrostomy in affected kidney Catheterise Patient prone in fluoroscopy Infuse contrast/saline via nephrostomy at 10mls/min Measure pressure in kidney and bladder and subtract to get the difference <15 cm H20 – unobstructed 15-22 cm H20 – equivocal >22 cm H20 - obstructed
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MCQ 1 Which is not an agent that has been used in renography
99mTc-MAG-3 123I-Hippuran 99mTc- DTPA 99mTc-DMSA 131I-Hippuran
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131I-Hippuran 123I-Hippuran Used in the 1960s
Hippuran is an excellent renography agent very rapidly cleared by tubular secretion and some filtration 131I emits around 90% of its radiation as beta decay, which damages local tissue but doesn’t penetrate far enough to be detected 123I-Hippuran All gamma decay Half life of 13 hrs and needs a cyclotron to produce Very expensive
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99mTc- DTPA 99mTc-MAG-3 99mTc-DMSA Cleared by filtration
Slow rate of clearance High background signal 99mTc produced from a Mo-99 generator 99mTc-MAG-3 Rapidly cleared by tubular secretion and some filtration (although 60% slower than Hippuran) Low background signal 99mTc-DMSA Used for renal scans for scars Fixes in tubules – function, not drainage
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MCQ 2 In post-obstructive diuresis which one is true?
All patients require IV fluids The catheter should be clamped after each litre of urine output to discourage diuresis It only occurs in those with bilateral obstruction 10% will develop hyperkalaemia 1% develop a long term diuresis
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Only those with symptomatic hypovolaemia should be given IV fluids
Clamping catheters has no effect on diuresis Although much less likely to occur diuresis can occur following relief of unilateral obstruction – typically due to pathological changes rather than solute load <1% develop hyperkalaemia due to aldosterone insensitivity
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MCQ 3 Which is the most common cause of upper tract obstruction?
Urolithiasis Ureteric stricture Retroperitoneal fibrosis Iatrogenic Bladder outflow obstruction
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MCQ 4 Regarding upper tract obstruction:
Whittaker’s test is the investigation of choice In association with sepsis it should always be treated as an emergency Is always caused by urinary tract pathology Will result in a non-functioning kidney unless relieved within 72 hours Is always present where there is hydronephrosis
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Extrinsic, non-urological causes can easily result in obstruction
Whilst the Whittaker’s test is good at identifying obstructed from non-obstructed it is an invasive test and should be used in cases of ambiguity Obstruction and sepsis should always be regarded as a urological emergency Extrinsic, non-urological causes can easily result in obstruction The return in function is proportional to the degree of obstruction and the duration. 7 days: full functional recovery 14 days: 70% recovery 28days: 30% recovery 6 weeks: no functional recovery Data from dogs however. Not all patients with hydronephrosis are obstructed.
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EMQ A. urethral catheter E. Culp DeWeerd pyeloplasty
B. Nephrostomy F. Endopyelotomy C. Nephrectomy G. Observation D. Anderson-Hynes pyeloplasty H. Retrograde pyelogram Which of the above would be the most appropriate management for: 28 year old woman with a left PUJO, a history of recurrent pyelonephritis and 12% function in her left kidney 28 year old woman with a left PUJO, a history of recurrent pyelonephritis and 32% function in her left kidney with a crossing vessel on CT 75 year old man with new renal failure and bilateral hydroureteronephrosis and a distended bladder on ultrasound
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EMQ A. urethral catheter E. Culp DeWeerd pyeloplasty
B. Nephrostomy F. Endopyelotomy C. Nephrectomy G. Observation D. Anderson-Hynes pyeloplasty H. Retrograde pyelogram Which of the above would be the most appropriate management for: 28 year old woman with a left PUJO, a history of recurrent pyelonephritis and a relative function of 12% in her left kidney C 28 year old woman with a left PUJO, a history of recurrent pyelonephritis and a relative function of 32% in her left kidney with a crossing vessel on CT D 75 year old man with new renal failure and bilateral hydroureteronephrosis and a distended bladder on ultrasound A
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Suggested reading Comprehensive Urology Campbell-Walsh
Scientific Basis of Urology
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Any Questions?
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