Post-obstructive diuresis refers to high urine output that can occur after relief of urinary tract obstruction. It is caused by accumulation of water, sodium, and urea during the period of obstruction. There are two main types - physiological diuresis which is self-limiting as fluid balance returns to normal, and pathological diuresis where inappropriate water loss continues beyond normalization of volume status. Treatment involves careful fluid management to replace losses based on urine output and electrolyte monitoring, as most cases will resolve spontaneously once homeostasis is restored. However, those with risk factors like edema may require closer monitoring and intravenous fluids.

1. 19.09.14
Post Obstructive
Diuresis
Dr. Garima
Aggarwal
DM Nephrology Resident
Amrita Institute of Medical Sciences,
Kochi, India

2.  Refers to dramatic increase in urine output after the release of
Urinary tract Obstruction.
 Factors necessary are
- Accumulation of total body water, Sodium and urea ( or)
- Impairment of Tubular re-absorptive capabilities.
 True incidence of Post obstructive diuresis (POD) is not
known
 Clinically significant POD occurs only in the setting of prior
bilateral ureteral obstruction (BUO) or unilateral obstruction
of a solitary functioning kidney
 Appears uncommon following UUO due to compensation by
normally functioning contra-lateral kidney.

3. Postobstructive Diuresis
• Definition
– High urine output exceeding (>200ml/hr) 0.5-1 L
per hour after the obstruction is relieved.
• Patients with edema, hypertension, weight gain, and
azotemia are most likely to exhibit this condition.

4. Types

Post obstructive Diuresis is of 2 types:
- Physiological Diuresis
- Pathological Diuresis
- Urea Diuresis ( Uosm > 250)
- Sodium Diuresis ( Uosm > 250)
- Water Diuresis ( Uosm < 150)

5. Types
Physiological Diuresis - Self limiting – As
a response to solute and water overload. Stops after
return to euvolumeic state.

Pathological Diuresis - Inappropriate
diuresis of water beyond euvolemic state, due to
insensitivity of collecting tubule to ADH and other
defects in urinary concentrating ability of the
kidney and tubular reabsorption of solutes
– Self limiting and can be managed easily


6. • Urea diuresis
–Is the most common.
–It is self-limiting, lasting 24-48 hours.
–Monitor fluid balance and electrolytes.
–Unless otherwise contraindicated,
increased fluid intake should suffice.

7. • Sodium diuresis
–Second most common.
–It usually is self-limiting, potential for
longer duration (>72 h).
–Monitor fluid balance and electrolytes
more aggressively

8. • Water diuresis
–Rare and self-limiting.
–It is a temporary nephrogenic diabetes
insipidus, which occurs secondary to
impaired renal tubular response to ADH.

9. Pathophysiology
of
Post Obstructive Diuresis

10. After the release of obstruction
• Contributing factors are both physiological and pathological
 Physiological
1.Excess Na and water retention
2.Retention of urea and non reabsorbable solutes
3.Accumulation of ANP
 Pathological
1.Decreased tubular reabsorption of Na
2.Concentration defect
3.Increased tubular flow reducing equilibration time for
reabsorption of Na and water

11. Derangement of Urinary concentrating
ability
• Normal urine concentrating ability 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, and
– 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
• The onset of concentration defects may develop soon after
obstruction.

12. Insensitivity to ADH

13. Another aquaporin, AQUAPORIN 1 (AQP1) - renal proximal tubules, the thin
descending limb of Henle, and the descending vasa recta in the kidney.
It promotes urinary concentration through the countercurrent multiplier by
facilitating water transport from the descending limb of Henle into the interstitium

14. • Li and coworkers (2001) demonstrated that the polyuria
following the release of BUO correlates with a decreased
expression of the aquaporin water channels AQP1, AQP2, and
AQP3 in rats.
• Jensen and coworkers (2006) examined changes in water
channels after bilateral ureteral obstruction in rats. As
expected, post-obstructive polyuria with reduced urine
osmolality was accompanied by decreased expressions of
AQP1, AQP2, and AQP3 compared with control rats.
Thus 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.

15. Defects in Sodium Transport
• BUO- sodium and water excretions may be quite robust after
release of obstruction- FENa may be increased to as much as
20 times normal in this setting (Zeidel and Pirtskhalaishvili,
2004)
• In spite of differential quantitative responses between UUO
and BUO after release of the obstruction, the reabsorption
defects in segmental nephron Na+ transport are similar.
• Active transport of Na+ across cell membranes requires apical
entry through selective Na+ transporters or channels and
basolateral exit driven by sodium-potassium adenosine
triphosphatase (Na+,K+-ATPase) and adequate adenosine
triphosphate (ATP) must be generated to drive these primary
transport steps.

16. A marked decrease in amiloride-sensitive oxygen consumption
and Na+ entry in isolated cells from the inner medullary
collecting ducts of obstructed rabbit kidneys reflects reduced
activity of the apical Na channel (ENaC). In addition, ouabain-sensitive
transport as measured by oxygen consumption and
ATPase activity was shown to be reduced in cells from this
portion of the nephron harvested from obstructed kidneys
(Hwang et al, 1993a)

17. • When urine flow is obstructed, upstream Na+ delivery to
apical cell membranes slows so that the transmembrane
gradient is reduced. This could then serve as the signal for the
downregulation of transporter activity or expression resulting
in reduced active Na+ transport across the basolateral cell
membrane (Zeidel, 1993).
• Ischemia has also been proposed as a signal in this setting,
where ischemia that accompanies the reduced perfusion of the
kidney with obstruction can also be a mediator of reduced
transporter expression. (Kwon et al, 2000)
• *A number of investigators have shown that obstruction
markedly increases the endogenous production of PGE2 in the
renal medulla- supraphysiologic concentrations of PGE2 -
produce natriuresis (Strandhoy et al, 1974)

18. Accumulation of ANP
• An accumulation of vasoactive substances in BUO that could
contribute to significant post obstructive natriuresis.*
• ANP
– increases afferent arteriolar dilation
– efferent arteriolar vasoconstriction, thus increasing PGC
– decreases the sensitivity of tubuloglomerular feedback
– inhibits release of renin,
– increases Kf
– secreted ANP contributes to a profound diuresis and
natriuresis.

19. Treatment
of
Post Obstructive Diuresis

20. • Usually
– Sodium, urea, and free water are eliminated
and the diuresis subsides after solute and fluid
homeostasis is achieved.
–With the return of homeostasis, the period of
diuresis ends.
• However, a “pathologic” postobstructive
diuresis may ensue,
– characterized by inappropriate renal handling
of water or solutes, or both.

21. • Those who are susceptible to this phenomenon
– typically have signs of fluid overload including
edema, congestive heart failure, or hypertension.
– The most common clinical setting is release of
urinary retention.
• The intensity of monitoring
– depends on presence of risk factors for
postobstructive diuresis and the subject's
mental status, renal function, and electrolyte
status.

22. Fluid Management
• In the first 24 hours, urine output should be
checked hourly.
If it's over 200 mL/hour, then 80% of the hourly
output should be replaced intravenously with 0.45%
saline.
• 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.

23. • 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.
• Replacement of electrolytes, e.g. potassium and
magnesium, may be necessary and should be guided
by the levels. MP

24. Obstruction relieved
Risk factors
for POD
edema,
congestive
heart failure,
hypertension
azotemia
Absent, mentally alert, oral fluids
No POD
Discharge
POD
mentally alert,
oral fluids
Rfts, na, k daily till
diuresis subsides

25. Risk factors for POD, hypotension, poor cognition
Hypo-osmolar urine is indicative of a primary
water diuresis as opposed to a solute diuresis
Creat, Na, K, Mg, Urine osmo every 12 hrs
mentally alert, oral fluids
Hypovolemia,
dyselectrolytemia
poor cognitive function
I V below normal
maintenance
ICU care Majority self-limiting

26. • Ureteral obstruction
– induces expression of COX-2 in collecting duct
cells and downregulation of AQP2 receptors is
mediated by COX-2.
– COX-2 inhibitors prevented the
downregulation of AQP2 and significantly
diminished postobstructive diuresis in rats.

27. • In addition, with ureteral obstruction,
– cGMP pathway has been demonstrated in both
in vitro and in vivo models to allow membrane
insertion of AQP2.
– Sildenafil Citrate elevated intracellular cGMP
and facilitate collecting duct accumulation of
AQP2.
• Pharmacological manipulation
–beneficial or harmful - unclear

28. Thank you