OBSTETRICS

RENAL AND URINARY TRACT DISORDERS

RCJ-3

URINARY TRACT DILATATION

Kidneys become larger
Dilatation of structures and pelvis as well as ureter
o Before 14 weeks due to hormonal relaxation of
muscular layers of urinary tract
o Hormone responsible: PROGESTERONE
Marked dilatation is apparent beginning in midpregnancy
because of ureteral compression
o More prominent on the right
(+) vesicuureteral reflux
Increased risk of upper urinary infection
o Important consequence
Secondary to hormonal or mechanically obstructive factors
FUNCTIONAL RENAL HYPERTROPHY
o apparent soon after conception
o Glomeruli are larger, but the cell numbers do not
increase
o Pregnancy-induced intrarenal vasodilatation

both afferent and efferent resistance

decreasesleads to increased effective
renal plasma flow and glomerular filtration
o at 12 weeks gestation\
o GFR increased by 20 percent above
nonpregnant values
o plasma flow and glomerular filtration
increase by 40 and 65 percent, respectively
o serum concentrations of creatinine and urea decrease
substantively across pregnancy
o Other alterations include those related to
o maintaining normal acid-base homeostasis
o osmoregulation
o fluid and electrolyte retention
ASSESSMENT OF RENAL DISEASE IN PREGNANCY
URINALYSIS
st
o Recommended as early as 1 TRIMESTER to assess
any signs of infection
o unchanged during pregnancy, except for occasional
glucosuria
o protein excretion normally is increased
o IDIOPATHIC HEMATURIA (3%)

1+ or greater blood on urine dipstick when

screened before 20 weeks

2x risk of preeclampsia
o PROTEINURIA

>300 mg/day

considered abnormal

500 mg/day

important
with
gestational
hypertension
SERUM CREATININE
o If > 0.9 mg/dl (75 mol/l)

Intrinsic renal disease should be suspected

ULTRASOUND
o imaging of renal size, relative consistency, and
elements of obstruction
IV PYELOGRAPHY
o Not done routinely

injection of contrast media with one or two

abdominal radiographs may be indicated by the
clinical situation
Cystoscopy
Renal Biopsy (usually postponed until pregnancy is completed)
URINARY TRACT INFECTION
Most common infection encountered during pregnancy
o Asymptomatic bacteriuria (most common)
o Systemic cystitis
o Pyelonephritis

Involves renal calyces, pelvis & parenchyma

Organisms that cause urinary infection
o Those from normal perineal flora about 90% of
strains are E. Coli

cause nonobstructive pyelonephritis

o (+)adhesions (P- and S-fimbriae)

cell-surface protein structures that enhance

bacterial adherence and thereby, virulence

adhesins promote binding to vaginal and

uroepithelial cells through expression of the
PapG gene that encodes the P-fimbriae tip
pregnant women have more severe sequelae from urosepsis
maternal deaths have been attributed to E coli bearing Dr+ and
P adhesins
Predisposing factors:
o urinary stasis
o vesicoureteral reflux
o diabetes
In the puerperium, risk factors that predispose a woman to
urinary infections.
o Bladder sensitivity to intravesical fluid tension is
decreased as a consequence of labor trauma or
conduction analgesia
o Sensation of bladder distention can also be diminished
by discomfort caused by an episiotomy, periurethral
lacerations, or vaginal wall hematomas
o Normal postpartum diuresis may worsen bladder
overdistention
o catheterization to relieve retention commonly leads to
urinary infection
DIAGNOSIS
o Urinalysis most cost effective
o Urine culture gold standard for asymptomatic
bacteriuria
ASYMPTOMATIC BACTERIURIA
Persistent, actively multiplying bacteria within urinary tract in
women who have no symptoms
typically present at the first prenatal visit
st
o recommened screening during 1 prenatal visit
highest incidence in African-American multiparas with sickle-cell
trait & lowest incidence in affluent white women of low parity
covert bacteriuria has been associated with preterm or lowbirthweight infants
INCIDENCE
o Varies from 2-7%
o Depends on parity, race and socioeconomic status

TRANSCOM|CLINGY,MD

OBSTETRICS

RENAL AND URINARY TRACT DISORDERS

RCJ-3
DIAGNOSIS
o Clean-voided
specimen
containing
>100,000
organisms per mL

Diagnostic

considered as evidenced of infection

o Importance of correct diagnosis if untreated can
lead to: acute pyelonephritis and symptomatic UTI
o Esterase-nitrite dipstick

Dipstick culture technique

excellent positive & negative predictive

values
Most common organism still E.coli
Urine culture not requested routinely
TREATMENT
o 3-day course
o May be treated empirically by antimicrobial agents
like: (please refer to the table)

Nitrofurantoin ideal, most sensitive

Quinolones reserved to prevent resistance

of microorganisms

CYSTITIS AND URETHRITIS

Cystitis dysuria, urgency and frequency
o Few associated systemic findings
Usually there is pyuria as well as bacteriuria
Microscopic hematuria common
Gross hematuria occasionally from hemorrhagic cystitis
Usually uncomplicated, involvement of upper urinary tract by
ascending infection
Mucupurulent cervicitis usually coexists
C. trachomatis common pathogen of gastrourinary tract
o Can cause lower urinary tract symptoms with pyuria
accompanied by a sterile urine culture may be from
urethritis
DIAGNOSIS
o Frequency, urgency, dysuria and pyuria accompanied
by urine culture with no growth
TREATMENT:
o Erythromycin therapy

safe in pregnancy, also DOC in PROM

NECROTIZING ENTEROCOLITIS
o complication of giving too much strong antibiotics

ACUTE PYELONEPHRITIS
Most common serious complication of pregnancy (renal infxn)
nd
o Which usually develops during 2 trimester (during
this period no workup performed in pt)
leading cause of septic shock during pregnancy
urosepsis is related to increased incidence of cerebral palsy in
preterm infants
no serious longterm maternal sequelae
ASSOCIATED RISK FACTORS:
o Nulliparity
o Young age
DIFFERENTIAL DIAGNOSIS
o Labor
o Chorioamnionitis
o Appendicitis
o Placental abruption
o Infected myoma
o Puerperium for metritis with pelvic cellulites
Almost all clinical findings are ultimately caused by
endotoxemia (bacteriuria -> endotoxemia -> urosepsis)
CLINICAL FINDINGS
o Pyelonephritis is unilateral (>1/2) and right-sided

Bilateral in a fourth
o Anorexia, nausea and vomiting
o abrupt onset of fever, shaking chills and aching pain
in one or both lumbar regions

Fever of variable degrees is always present,

can be as high s 40 degrees Celsius
o Tenderness usually can be elicited by percussion to
one or both costovertebral angle (kidney punch)
o Urinary sediment frequently contains many
leukocytes in clumps seen on urinalysis
o Bacteremia in 15 to 20% of women
o Organisms that are commonly isolated:

E coli (from urine or blood (70 to 80%)

Klebsiella pneumoniae (3 to 5%)

Enterobacter or Proteus species (3 to 5%)

gram-positive group B Streptococcus and S

aureus (up to 10%)
MANAGEMENT (IV hydration to ensure urinary output: corner stone)

MANAGEMENT FOR NON RESPONDERS

o Sonography

If there is no clinical improvement by 48-72

hrs

TRANSCOM|CLINGY,MD

OBSTETRICS

RENAL AND URINARY TRACT DISORDERS

RCJ-3

to look for urinary tract obstruction always

rule out if patient doesnt respond to
treatment

search is made for abnormal ureteral

pyocalyceal dilatation
OUTPATIENT MANAGEMENT
o for women w/uncomplicated pyelonephritis
o Women with pyelonephritis were given Ceftriaxone
IM two 1g doses 24hrs apart in the hospital

At this point only third were considered

candidates for outpatient therapy
Surveillance
o risk of recurrent infection (30-40%)

CHRONIC PYELONEPHRITIS
TYPES
Chronic Interstitial Nephritis
Nephrolitiasis

CHRONIC INTERSTITIAL NEPHRITIS

Frequently not symptomatic
Advance cases symptomatic, those of renal insufficiency
Obstruction promote chronicity
NEPHROLITIASIS
CALCIUM SALTS
o make up 80% of renal stones
o Half of affected women have polygenic familial
idiopathic hypercalciuria (most
common
predisposing factors)
STRUVITE STONES
o associated with Staghorn calculi; often seen with
Klebsiella
Kidney stones develop in 7% with an average age of onset
in the third decade
calcium oxalate stones in young nonpregnant women are
most common
most stones in pregnancy65 to 75%are calcium
phosphate or hydroxyapatite
a low-calcium diet promotes stone formation
Prevention of recurrences with hydration and a diet low in
sodium and protein
Thiazide diuretics also diminish stone formation
INDICATIONS OF STONE REMOVAL
o Obstruction
o Infection
o intractable pain
o heavy bleeding

Removal by a flexible basket via

cystoscopy

nonpregnant patients, stone

destruction by lithotripsy
COMMON PRESENTING SYMPTOM
o Infection -60%
o Flank and abdominal pain
o Hematuria
DIAGNOSIS
o More than 90% -present with pain

Gross hematuria presenting symptom in 23% of

pregnant patients

IMAGING
o Sonography

to visualize stones, many are not detected

because hydronephrosis
o one-shot pyelogram
o If there is abnormal dilatation without stone
visualization
o Transabdominal color Doppler sonography

to detect presence or absence of ureteral

jets of urine into the bladde
o Helical computed tomography (CT) scanning

the imaging method of choice for

nonpregnant individuals

avoided during pregnancy

o MR imaging

Recommended as the second-line test

following nondiagnosticsonography
MANAGEMENT
o Treatment depends on symptom and duration of
pregnancy (gestational age)
o IV hydration and analgesics are always given
o 2/3 symptomatic with conservative treatment and
stone usually passes spontaneously
o invasive procedure

ureteral stenting

ureteroscopy

percutaneous nephrostomy

transurethral laser lithotripsy

basket extraction
o persistent pyelonephritis should prompt a search for
obstruction due to nephrolithiasis
o fluoroscopy limits the utility of percutaneous
nephrolithotomy
o extracorporeal shock-wave lithotripsy is
contraindicated in pregnancy
o ureteroscopic removal is also safe in pregnancy.
GLOMERULAR

ACUTE GLUMERULONEPHRITIS
Abrupt onset of hematuria and proteinuria associated with
varying degrees of renal insufficiency and salt and water
retention
CAN CAUSE:
o Edema
o Hypertension

TRANSCOM|CLINGY,MD

OBSTETRICS

RENAL AND URINARY TRACT DISORDERS

RCJ-3
o

Circulatory congestion symptoms of end spectrum

of disease (pulmonary congestion or pulmonary
edema)
Acute post streptococcal glumerulonephritis prototypical in
diagnosis
DIAGNOSIS
o Renal biopsy may be necessary in determining
etiology as well as direct management
DIFFERENTIAL DIAGNOSIS
o Severe preeclampsia

no hematuria

hypertension evident after 20 weeks

EFFECTS OF GLUMERULONEPHRITIS IN PREGNANCY
(Very Important!)
Most common lesions on biopsy
o Membranous Glumerulonephritis
o IgA GN
o Diffuse Mesangial GN
Acute GN profound effect on pregnancy outcome
Overall fetal loss was 25% and perinatal morbidity after 28
weeks was 80/1,000 live births
About half of these women developed hypertension and fourth
did so before 32 weeks (in preeclampsia hypertension develops
after 20wks)
Worst perinatal outcome
o Women w/ impaired renal function
o Early or severe HPN
o Nephrotic-range proteinuria
RAPIDLY PROGRESSIVE GLUMERULONEPHRITIS
If acute GN doesnt resolve and rapidly progressive GN leads to
end stage renal failure within weeks to months
Patient with this feature may have (+) test for antineutrophil
cytoplasmic antibody (ACA)
CHRONIC GLUMERULONEPHRITIS
Many cases with unknown cause
Characterized by progressive renal destruction over years or
decades eventually producing ESRD
Gradual decline in renal function
o Persistent proteinuria
o Hematuria
MICRO
o Renal lesion categorized as proliferative, sclerosing or
membranous
Some women with typical preeclampsia-eclampsia does not
resolve post partum and found to have Chronic GN
DIAGNOSIS
o Renal biopsy established prognosis
NEPHROTIC SYNDROME
CHARACTERIZED BY:
o Heavy proteinuria >3g/day (HALLMARK)
o Hypoalbuminema
o Hyperlipidemia
o Edema

Others:
o Hypertension
o
Albumin nephrotoxicity
o renal insufficiency
DIAGNOSIS
o 24hr urine collection

Proteinuria of 300 mg/dL (cut-off value) or

even 500 mg/dL (in Williams daw sabi ni
Doc)
serum creatinine level > 1.4 mg/dL
Defects of barrier are glomerular capillary wall that alters
excessive filtration of plasma protein are caused by:
o Primary glomerular disease
o Haematological or toxic injury
o Metabolic vascular disease
Differential diagnosis: Preeclampsia
MANAGEMENT
o Depends on etiology
o Edema managed cautiously during pregnancy
o Normal amounts of dietary protein of high biological
value are encouraged

POLYCYSTIC KIDNEY DISEASE

Usually autosomal dominant systemic disease that primarily
affects kidney
Usually uncommon
85% are due to PKD1 gene mutations on chromosome 16
15% to PKD2 mutations on chromosome 4
Prenatal diagnosis is available if the mutation has been
identified in a family member or if linkage has been established
in the family
Renal complications are more common in men than in women
Hypertension develops in 75%
progression to renal failure is a major problem
Symptoms usually appear during third or fourth decade
FINDINGS:
o Flank pain
o Hematuria
o Nocturia
o Proteinuria
o abdominal masses
o calculi
o infection
o
10% die due to ruptured of associated intracranial berry
aneurysm
Others have
o cardiac valvular lesions

TRANSCOM|CLINGY,MD

OBSTETRICS

RENAL AND URINARY TRACT DISORDERS

RCJ-3

mitral valve prolapsed

mitral, aortic, and
incompetence

tricuspid

valvular

Pregnancy Outcomes
The prognosis depends on the degree of associated
hypertension and renal insufficiency
Urinary tract infections are common
Pre-eclampsia

CHRONIC RENAL DISEASE

pathophysiological process that can progress to end-stage renal
disease
Subclinical loss of function
Mild impairment -<1 mg/dL
Moderate impairment defined as serum creatinine of 1.5 to 3.0
mg/dL
Severe renal insufficiency serum crea >3mg/dL
2
It progresses from stage 0GFR > 90 mL/min/1.73 m to stage
2
5GFR < 15mL/min/1.73 m
Diabetes and Hypertension
o Most common causes of ESRD
CATEGORIES OF RENAL FUNCTION
o normal or mild impairment
o serum creatinine < 1.5 mg/dL
o moderate impairment
o serum creatinine 1.5 to 3.0 mg/dL
o severe renal insufficiencydefined as a serum
creatinine > 3.0 mg/dL
MANAGEMENT
o Frequent prenatal visits to determine BP trends
o Screened and treated

Serial serum creatine

Protein excretin

Bacteriuria is treated to decrease risk of

pyelonephritis
o CHON restricted diet is not recommended
o Anemia d/t CRI responds to erythropoietin
o S/E: HPN

PREVENTION OF ACUTE TUBULAR NECROSIS BY:

Acute kidney injury in obstetrics is most often due to acute
blood loss, especially that associated with preeclampsia
o Prompt and vigorous replacement of blood in
instances of massive hemorrhage such as placental
abruption and placental previa (blood loss is a very
important predisposing factor in developing ARF)
o Avoidance of vasoconstrictors, treat hypertension
(Never give Methergine in pregnancy ->further
vasoconstriction)
o Termination of pregnancy complicated by severe
preeclampsia and eclampsia wth careful blood
replacement
o Preserve health status of mother
o Avoid potent diuretics
DIAGNOSIS AND MANAGEMENT
o An acute increase in serum creatinine is most often
due to renal ischemia
o obstetrical cases, both prerenal and intrarenal factors
are commonly operative
o evident azotemia and severe oliguria
o Early dialysis appears to reduce the mortality rate

ACUTE RENAL FAILURE

AKA: Acute kidney injury
sudden impairment of kidney function with retention of
nitrogenous and other waste products normally excreted by the
kidneys(sudden decrease in GFR

Most common associated with severe preeclampsia and

eclampsia
Accompanied by serum creatinine level of 10.7 mg/dL
Oliguria important sign of acute impaired renal function
CAUSES AND ASSOCIATED FACTORS
o Preeclampsia-eclampsia
o HELLP syndrome
o Obstetrical hemorrhage

Placental abruption

Postpartum

abruption
o Septicemia
o Acute fatty liver
o Hyperemesis gravidarum

IDIOPATHIC POSTPARTUM RENAL FAILURE

Believed to be a new syndrome of acute irreversible renal
failure that developed within first 6 weeks postpartum
Pathological changes identified by renal biopsy
o Necrosis and endothelial proliferation in glomeruli
o Plus necrosis, thrombosis and intimal thickening of
arterioles
MORPHOLOGY
o Erythrocytes consistent with microangiopathic
hemolysis and thrombocytopenia
Microangiopathic hemolysis will give very high level of lactate
dehydrogenase (>600 is significant), thrombocytopenia and also
decreased platelet count
SGPT is also elevated, >60 level
- Italicized- from book
- yung hindi, from ppt/lecture
-According to Doc, expect cases on platings and exams

Believe you can and youre halfway there. Believe God can and the race is
won.

TRANSCOM|CLINGY,MD