The document discusses post-obstructive diuresis (POD), which is a dramatic increase in urine output that can occur after relief of bilateral ureteral obstruction or obstruction of a solitary kidney. POD is a normal physiological response as the kidneys eliminate accumulated sodium, urea, and water. It is usually self-limiting as fluid and electrolyte homeostasis is regained. Pathological POD occurs if inappropriate fluid and solute excretion persists beyond the regained homeostasis state, requiring evaluation and management of fluid, electrolyte, and volume status.

1. Dr.Gaurav Nahar
DNB Urology(Std.) 1st
Year
M.M.H.R.C., Madurai
POST-OBSTRUCTIVE
DIURESIS

2.  Dramatic urine output that may occur following relief of
bilateral ureteral obstruction (BUO) or obstruction of a solitary
kidney.
 In clinical practice, a urine output >200 mL/hr over 12
consecutive hours constitutes POD.
 Uncommon event.
 A normal physiologic response to volume expansion & solute
accumulation occurring during obstruction.
 Sodium, urea, & free water are eliminated, and diuresis subsides
after solute and fluid homeostasis is achieved.
 With the return of homeostasis, the period of diuresis ends.
INTRODUCTION

3.  Factors necessary for its development:
1. an accumulation of total body water, sodium, & urea
or,
2. an impairment of tubular reabsorptive capabilities.
 Clinically significant POD is uncommon with a
normal contralateral kidney. This reflects the
continued maintenance of fluid and electrolyte
homeostasis by the contralateral kidney.

4.  Urinary obstruction may be:
1. anatomic or functional (e.g., neurogenic bladder) in
etiology &,
2. intrinsic or extrinsic in location.
 Common Causes:
1. Benign prostatic hyperplasia (BPH) or prostate
cancer in males.
2. cervical cancer or pregnancy in females.
ETIOLOGY

5. Obstructive nephropathy refers to functional and
pathologic damage sustained by renal parenchyma
during urinary obstruction.
Profound changes in renal hemodynamics &
glomerular filtration take place.
Within the first 2 hours of obstruction, GFR begins to
fall as a consequence of elevated tubular hydraulic
pressure (PT)  PT continues to rise &, renal blood
flow (RBF) falls dramatically as a result of intense
efferent arteriolar vasoconstriction caused by
angiotensin II, thromboxane A2, and neural input.
PATHOPHYSIOLOGY OF
OBSTRUCTIVE NEPHROPATHY

6.  End result profound reduction in single nephron
and whole kidney GFR by 24 hours.
 Secreted in response to intravascular volume
expansion, ANP improves RBF and GFR through the
following means:
1. Afferent arteriolar vasodilation
2. Tubulo-glomerular feedback inhibition
3. Renin-angiotensin system (vasoconstrictive)
inhibition
4. Glomerular filtration coefficient (Kf) increase.

7. contribute to diuresis, natriuresis & rapid return to
maximal renal function following relief of BUO.
Decreased Na+,K,+,2Cl− cotransporter type 2, collapse
of the inner medulla osmotic gradient, and
suppressed phosphorylated renal aquaporins (AQP2)
may be responsible for impaired urine-concentrating
capacity in the chronic postobstructive phase
following release of ureteral obstruction.
Together, glomerular and tubular dysfunction
manifest as profound natriuresis and diuresis
following the relief of BUO.

8. POD may involve a water diuresis, a solute diuresis or
a combination.
PHYSIOLOGIC POD: In most cases, POD represents
an appropriate and self-limited physiologic response
to volume and solute overload.
Occasionally, it may extend inappropriately beyond
euvolemic state, as a result of excessive free-water loss
caused by collecting duct insensitivity to ADH(i.e.,
nephrogenic DI). Similar to physiologic POD, this
form of diuresis is often self-limited and easily
managed.
MECHANISM

9.  TRUE PATHOLOGIC POD : inappropriate
excretion of both water & solute as reflected by a
urine osmolality >250 mOsm/kg water.
 inability to concentrate urine in pathologic POD
stems from defective generation and maintenance of
a medullary solute gradient. Reasons :
1. Decreased reabsorption of sodium chloride in the
loop of Henle
2. Decreased reabsorption of urea in the collecting
tubule
3. Medullary solute washout caused by increased
medullary blood flow
4. Increased tubular flow rate and solute concentration
in the distal tubule.

10. Uosm (mOsm/kg
water)
Uosm:Posm
1. Pure Water <150 <0.9
2. Solute ≥250 >0.9
3. Mixed ≥250 <0.9
Diuresis Subtype Based on Urine
and Plasma Osmolalities

11. Chronic BUO: Non-specific signs and symptoms.
Most patients with complete obstruction: describe
anuria or oliguria.
Some patients with partial obstruction: polyuria
secondary to impaired renal concentrating ability.
Volume expansion is common and may present as
weight gain, peripheral edema, or even shortness of
breath if CHF is a complicating factor.
PRESENTATION

12. Long-standing obstruction may present with uremic
symptoms including mental status change, tremor,
and gastrointestinal (GI) bleeding.
Volume expansion or azotemia in the setting of BUO
should raise suspicion for possible diuresis following
the relief of obstruction.

13. a thorough baseline evaluation: CBC and complete
metabolic profile. Elevations in Serum BUN and
creatinine; hyperkalemia and metabolic acidosis
which require correction.
Most cases represent Physiologic POD: diuresis is
allowed to proceed until euvolemic state is reached as
determined by clinical parameters such as orthostatic
vital signs, breath sounds, jugular venous distention,
and peripheral edema. During this time, serum
electrolytes should be evaluated every 6 to 12 hours
because electrolyte imbalance, particularly
hypokalemia and hypomagnesemia, may develop.
EVALUATION & MANAGEMENT

14. If the diuresis persists beyond the euvolemic state, a
Pathologic concentrating defect or salt wasting
nephropathy should be suspected. Urinary diagnostic
indices are to determine type of diuresis (water versus
solute versus mixed) & to guide fluid replacement.
 With excessive free water loss, plasma osmolality
will rise while urine osmolality remains
inappropriately low (<150 mOsm/kg water).
Most patients with an intact thirst mechanism and
free access to water can compensate for this defect.

15. Patients in whom oral replacement is not an option
because of mental status, nil per os (NPO) status, or
limited access to water require IV supplementation
with hypotonic saline solutions (0.45% NaCl).
Most recommendations: replacement of half the urine
output at 2 hourly intervals so as to not perpetuate
the diuresis.
Contraindications to excessive hydration: CHF and
hypertensive crisis.

16. Pathologic POD secondary to salt-wasting
nephropathy: Dehydration and electrolyte
imbalance (Na+
, K+
, magnesium [Mg2+
]) are common as
the persistent natriuresis promotes the loss of water,
potassium and magnesium.
Urine osmolality (≥250 mOsm/kg water) is often
slightly higher than that of plasma.
Careful hemodynamic monitoring, CVP, frequent
monitoring of both serum and urine electrolytes.

17. Sodium and volume replacement using normal saline
(0.9% NaCl) supplemented on occasion with
hypertonic saline (3% NaCl) if the sodium deficit is
profound.
Serum and urine electrolytes serve as a guide.
Volume replacement should match urine output in a
1:1 fashion until vital signs and renal function
stabilize.
Hypokalemia and hypomagnesemia are common and
require correction. Hyperkalemia and acidosis also
may occur, particularly in the event of profound
dehydration and consequent worsening of renal
function.

18. 1. Ureteral obstruction induces expression of COX-2 in
collecting duct cells  downregulation of AQP2
receptors.
Administration of COX-2 inhibitors may prevent the
downregulation of AQP2 and significantly
diminish postobstructive diuresis in BUO.
EXPERIMENTAL MODULATION

19.  With ureteral obstruction, there is blunted cAMP
generation in response to vasopressin. Vasopressin-
induced, cAMP-mediated pathways induce
phosphorylation and subsequent membrane insertion
of AQP2.
A cAMP independent, (cGMP) pathway has been
demonstrated in both in-vitro and in-vivo models to
allow membrane insertion of AQP2.
Phosphodiesterase type 5 inhibitor sildenafil citrate
may elevate intracellular cGMP to facilitate collecting
duct accumulation of AQP2.

20. POD is a normal physiologic response to the volume
expansion and solute accumulation occurring during
obstruction.
Occurs usually after relief of BUO or Obstruction in
solitary kidney. Very rare in the presence of a normal
contalateral kidney.
Self limiting; subsides after attaining euvolemic state.
Pathological only if inappropriate excretion continues
beyond this state of fluid & electrolyte homestasis.
Prompt evaluation & treatment.
TAKE HOME MESSAGE

21. Thank you!!!