• 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
• 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 (
• 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
• 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.
• 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.
 EXPERIMENTAL MODULATION
• 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.
 TAKE HOME MESSAGE
• 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.