Electrolytes & Pregnancy

Amelia R. Bernasconi, CIN 2011

Hormonal and hemodynamic changes characterize the pregnant state Pregnancy is a condition of chronic volume overload This hyperdynamic state is associated with Haemodilution Decreased peripherial resistance
(from the very beginning )

PG NO
ERF Relaxin balance between

BP
Tx Et

To guarantee an adequate uterus and placental perfusion

TBW increases from 6 to 8. L

( 6 30 week)

Cardiac output 30-50%

GFR and RPF

Physiologic anemia
Vascular resistance

NA +
retention BP

Renal vasodilatation, decrease P and glomerular hyperfiltration without damage in renal function in normal women

The kidney in Normal Pregnancy

Anatomic changes
Kidney enlargement Increased renal vascular and interstitial volume Right side > Left Ureteral and renal pelvis dilatation
Mechanical compression by gravid uterus and ovarian venous plexus, smooth muscle relaxation by progesterone

Glomerular Changes
Pregnant woman is an interesting phenomenon, I do not know another method for increasing GFR by so prefaced periods. (Homer Smith,1956).

Renal perfusion increases during pregnancy as a function of the increased cardiac output
GFR and PF increase 40-60% Plasma volume and cardiac output Renal aferent and eferent vasodilatatiton (Relaxin plays an important role) Hyperfiltration without in GP ( P) Micropuncture studies in the rat suggest that the in single nephron GFR (SNGFR) results exclusively from in glomerular plasma flow (SNPF), due to balanced afferent and efferent vasodilation, and without changes in either the ultrafiltration coefficient (KF) or in glomerular capillary pressure (Ap) The rise in GFR that characterizes pregnancy translates to a fall in the different serum markers of renal clearance

BUN

P.Creatinine

Uric Acid

10 mg/dl

0.80 mg/dl

2.5 mg/dl

Tubular Changes

Filtered load of water and solutes

urinary excretion
Glucose: 1 - 10 g/d Aas y proteins: 150 - 300 mg/d Vitamins Calcium (hypercalciuria) Mg2+, citrate. Na+ Filtered Load (5000- 10000 meq/d)
Returns to normal by late third trimester

Na + Balance

SALT AND WATER METABOLISM

Plasma osmolality begins to decline by 2 weeks after conception
reduction in serum sodium and other accompanying anions

Sodium loss during pregnancy

50% rise in GFR/ Progesterone: natriuresis

Sodium homeostasis
Enhanced tubular reabsorption of Na+ secondary to aldosterone, estrogen and deoxycorticosterone -Na+ retention: 900 mEq but serum Na+ decreases: 3-4 mmol/l Plasma osmolarity decreseases 10 mOsm/Kg

Factors influencing Na+ balance in pregnancy

REABSORTION

Natriuresis GFR Progesterone Prostaglandins ANP

Aldosterone
Estrogens

Cortisol RAS

Mild Hyponatremia P osmol 10 mosmol/Kg

Angiotensin II and vascular reactivity

NORMAL PREGNANCY REFRACTARITY TO AII PREECLAMPTIC INCREASED SENSIBILITY TO AII

Agonist AT Ang II. (AT1 A)
Wallukat, J Clin Invest 1999; 103

Acid Base Balance Hyperventilation

Lung volume changes and altered compliance Progesterone stimulating the respiratory center

PCO2 drops 10 mmHg

(24-32 mmHg) / (pH 7.42 - 7.44) PO2

Chronic respiratory alkalosis

Acid base &Pregnancy

renal excretion of HCO318-22 mmol/l Typical ABGs in the Third Trimester pH: 7.43 pCO2: 33mmHg [HCO3]: 21mmHg pO2: 104 mmHg. 4 mmol/l

Compensated respiratory alcalosis

Adecuate control to acid balance for faetal metabolsim. No changes found in renal acidification during pregnancy.

Ketosis & Pregnancy

Pregnant woman is prone to develop elevated ketone levels

Insulin resistance increases as pregnancy progresses (placental hormones) Fasting during pregnancy hypoglycaemia and low insulin levels

Fasting ketosis develops in less than 16 hours.

Ketones cross the placenta and the foetus use them as an energy source. This fact is important in myelination in the developing central nervous system. (This mild ketosis that occurs with fasting does not seem to have any adverse effect on the mother or foetus). Ketoacidosis due to maternal diabetes : adverse effects on the foetus

What about Potassium& Pregnancy?

K + disorders & Pregnancy

Renal disease during pregnancy associated with:

Hypokalemia

Vomiting MCs excess Drugs (aminopenicillins) RTA I RTAII Diarrhoea DKA Bartter-Gitelman hKPP
RTA: renal tubular acidosis DKA: diabetic Ketoacidosis hKPP:hypokalemic periodic paralysis MCs: Mineralocorticoids

Case report

14 years, 15 weeks, nausea and intractable vomiting, weight loss, hypotention,

tachicardia.

Plasma
BUN mg/dL (18-50)
Creatinine

Hto

mg/dL (0.6-1.3)

Na+ mmol/L (135-145

K+ mmol/L (3-5)

Cl mmol/L (95-107)

HCO3mmol/L (21-23)

15

38

1.36

150

2.5

90

38

Urine input: 10 ml/hr. Osm= 504 mOsm/kg pH= 7.55 PCo2= 45 (severa metabolic alkalosis: UNa= 40meq/l urine =3+++ cetonuria Hyperemesis gravdae

gastric loss)

Nausea and vomiting occur commonly in the 1st trimester. Rarely:severe Vomiting can cause fluid loss and electrolyte disturbances. The acid-base result is typically a metabolic alkalosis. Ketosis may occur if oral intake is poor

The acid-base effect of vomiting depends on the mix of acidic gastric fluid

alkaline intestinal secretions found in the vomitus. Alkalosis does not always occur with prolonged vomiting.

Vomiting mechanism

unkown unique stimulus that causes vomiting.

Psychologic Factors
unwanted pregnany

Genetic factors monocigotic twins Placentary products HCG Estrogens

A prospective study of nausea and vomiting during pregnancy. British Journal of General Practice. 1993; 43: 245-248. Gadsby R, Barnie-Adshead AM, Jagger C.

Treatment: Always inpatient

Bedrest, no food,sedatives, fluid reposition!!!! Antihystaminics (direct action on vomiting center) (No fetal adverse effects) Vitamins B complex & Piridoxin Antiemetics
Ranitidine

metilprednisolone

Renal disease during pregnancy associated with:

Hyperkalemia

ESRD:
AKI ESRD MCs deficiency Drugs RTA IV (Hyperkalemic) HKPP

Pregnancy in patients suffering from renal disease Pregnancy in RRT (dialysis or tx)

AKI: acute Kidney injury RTA: renal tubular acidosis DKA: diabetic Ketoacidosis hKPP:hypokalemic periodic paralysis HKPP: hyperkalemic periodic paralysis MCs: Mineralocorticoids

1st Trimester
Fetal loss
Hyperemesis gravidarum
Ectopic pregnancy (rupture, haemorrhage , volume depletion)

Drugs (nefrotoxic). [cocaine, rhabdomiolisis]

3rd trimester
abruptio placentae
Pre-eclampsia, HELLP

Post partum hemorrage Puerperal sepsis

TMA HUS,TTP

AKI during pregnancy responds to the same etiologies that occur outside it. For didactic reasons they were grouped according to its frecuency Along pregnancy

Acute Fatty Liver Drugs.

HELLP:hemolisis, liver enzimes,low platelet. TMA:trombotic microangiopathy HUS Hemolityc uremic syndrome TTP:Trombotic trombombocitopenic purpura

CASE REPORT II
23 a, G1, P0,Ao

Pre -renal Oliguria 60 to 70 %

27 weeks HBP/ PCV 40% Proteinuria >3.5 g/24

oliguria

x
?

Plasma
Urea mg/dL (18-50) Crea mg/dL (0.6-1.3) Na mmol/L (135-145 K mmol/L (3-5) Cl mmol/L (95-107)
HCO3mmol/L (21-23)

Urine sample: Silent/ hialine casts

100

1.37

145

3.6

104

22
Na mmol/L Osmolality mOsm/Kg (400-900)

<10

529

FENa(%)

Preeclampsia

(UNa/PNa) (UCR/PCR)

x 100 =

<1%

Haemodinamic changes Preeclampsia endotelial injury

plasma volume tisular hypoperfusion
vascular resistance

RAS sensitivity

PF y del GFR 30-40% proteinuria BP , urate reabsortion

Vasocontraction Efective hypovolemia & glomerular hypofiltration Platelet activation

PRE-ECLAMPSIA RENAL PERSPECTIVE

Early hyperuricemia

Creatinine < 0.8 mg % unless Renal Failure Oliguria severe forms Silent urine sample (Principal cause of Nefrotic sindrome during pregnancy) Non selective Proteinuria (late) Hypocalciuria

Karumanchi A y col
Kidney Int., 1,51-64, 2005

Conclusion
Always promote medical consultation in young women Medicine is an art when diagnosis is correct, if and only if thought does represent in physicians mind the patients illnesss (paint the picture) A. Bernasconi