1. ACUTE RENAL FAILURE IN PREGNANCY
BASIC OUTLINE
Investigations
MANAGEMENT PRINCIPLES
Prerenal Vs ATN Vs ACN
ROLE OF Nutrition
Volume & metabolic control
Diuretics : helpful or harmful ??
Dopamine : helpful or harmful ??
Dialysis : when & which ??
Renal biopsy ??
Delivery
Conditions specific to pregnancy

2. DEFINITIONS OF ARF
The syndrome is characterised by a sudden in parenchymal function (UOP<400ml/d;30ml/hr) which is usually but not always reversible
This produces disturbance of water, electrolyte, acid base balance and nitrogenous waste products & blood pressure.

3. Normal Physiologic Alterations of Pregnancy

4. Physiological changes in normal gestation
Kidney weight and size increase
Dilation of renal calyces, pelves, and ureters
Urinary stasis
Glomerular filtration, effective renal plasma flow, fractional clearance of urate increase
Bicarbonate reabsorption threshold decreases

5. Clinical relevance
Concentrations of serum creatinine, urea N, and uric acid of 0.9, 14, and 5.6 mg/dl, normal in nonpregnant subjects, are already suspiciously high in gravid women.
Asymptomatic bacteriuria - frank pyelonephritis.
PP reduction in size should not be mistaken for parenchymal loss
Post renal failure difficult to diagnose
S.bicarb lower,PCO2 10 mmHg lower

6. Causes Early in Pregnancy
Most common cause is pre-renal failure due to hyperemesis gravidarum
ATN due to septic abortion

7. Causes - ARF Late in Pregnancy/Postpartum
Thrombotic microangiopathy
TTP-HUS
Severe preeclampsia usually with HELLP syndrome
Renal Cortical Necrosis
Placenta previa
Prolonged intrauterine fetal death
Amniotic fluid embolism
Intrinsic renal disease/autoimmune diseaes

8. ARF Late in Pregnancy/Postpartum
Acute pyelonephritis
ATN from septicemia or hypotension
ARF from microabscesses
Acute fatty liver of pregnancy
ARF in up to 60% of cases
Preeclampsia + hypoglycemia, hypofibrinogenemia, LFT abnormalities, prolonged PTT
Obstructive uropathy
Mild-moderate hydronephrosis is normal
Occasionally, degree of obstruction sufficient to cause ARF.
Nephrolithiasis if solitary functioning kidney

9. Causes - Severe Preeclampsia/HELLP
Typically develops late in 3rd trimester; a few percent of cases can happen up to 48 hours post-partum.
Preceded by hypertension, proteinuria, and severe edema
ARF not typical unless marked DIC

10. Severe Preeclampsia/HELLP
But, there are cases reported in which renal abnormalities begin post-partum WITHOUT prior proteinuria
Typically, spontaneous recovery 2-3 days post-partum; complete recovery typical by 8 weeks post-partum.
Corticosteroids have been utilized but no large randomized clinical trials

11. Causes - TTP-HUS
Thrombocytopenia + microangiopathic hemolytic anemia + ARF
Traditionally, TTP if neurologic symptoms are abundant; HUS if ARF is dominant. BUT, distinctions are often unclear and may not be important for management decisions

12. TTP-HUS Timing variable:
25% before mid-pregnancy
65% peri-partum
20% postpartum: may follow normal pregnancy or be preceded by findings indistinguishable from preeclampsia
Can relapse if TTP-HUS occurred once prior to pregnancy; can occasionally relapse in subsequent pregnancy

13. TTP-HUS Plasma infusion +/- plasma exchange (plasmapheresis)
In one series of 11 women:
2 died
4 with residual CKD
5 recovered completely
Prior to use of plasmapheresis, 90% mortality rate reported

14. Causes - Renal Cortical Necrosis
Bilateral cortical necrosis
Severe renal ischemia or DIC with resultant endothelial damage
Abruptio placenta, placenta previa, prolonged intrauterine death, amniotic fluid embolism
THEN, patient develops acute onset of oliguria or anuria, gross hematuria, flank pain, and hypotension
ANURIA, GROSS HEMATURIA, FLANK PAIN – triad that is unusual in other causes of renal failure

15. Renal Cortical Necrosis
US or CT can be suggestive
Biopsy can demonstrate necrosis
No specific therapy – many patients require dialysis but 20-40% have partial recovery with CrCl between 15 and 50 mL/min.

16. To summarise Causes
Bimodal distribution -peaks in the first trimester (related to unregulated and/or septic abortion,hyperemesis) and the late third trimester (related to obstetric complications APH,PPH,Preeclampsia, Chorioamnionitis,AFE etc).

17. THOMBOTIC MICROANGIOPATHIES
ATN
CORTICAL NECROSIS
THOMBOTIC MICROANGIOPATHIES

19. Loss (L) - Persistent ARF, complete loss of kidney function >4 wk
The RIFLE classification (ADQI group) of ARF:
Risk (R) - Increase in serum creatinine level X 1.5 or decrease in GFR by 25%, or UO <0.5 mL/kg/h for 6 hours
Injury (I) - Increase in serum creatinine level X 2.0 or decrease in GFR by 50%, or UO <0.5 mL/kg/h for 12 hours
Failure (F) - Increase in serum creatinine level X 3.0, decrease in GFR by 75%, or serum creatinine level > 4 mg/dL; UO <0.3 mL/kg/h for 24 hours, or anuria for 12 hours
Loss (L) - Persistent ARF, complete loss of kidney function >4 wk
End-stage kidney disease (E) - Loss of kidney function >3 months

20. PHASES
OLIGURIA
POLYURIA
RECOVERY

21. Investigations URINE sp.gravity osmolality electrolytes proteins
BLOOD
CBC
Urea,creatinine,uric acid
Electrolytes
LFT
S.proteins
Coagulation profile
ABG
RBS
Osmolality
URINE
sp.gravity
osmolality
electrolytes
proteins
pigment casts
c/s
ECG

22. Management Restore or maintain fluid balance
The maintenance of electrolytes and acid base balance
The maintenance of nutritional support
Prevention of infection
Avoid renal toxins (including NSAIDS)
Instigate renal replacement therapies

23. Prerenal failure Adequately replace blood & fluid losses,maintain BP.
Control continuing blood loss
Mannitol (100ml, 25%) trial to d/d b/w reversible prerenal failure & established ATN (provided oliguria <48 hrs & U:P osmolality > 1.05)
If diuresis (>50ml/hr or doubling) established within 3 hrs,maintain NS infusion acc to UOP & replace electrolytes acc to urinary loss estimations.
If unsuccessful –objective is to support the functionally anephric pt till kidneys recover.

24. Volume control IP/OP charting daily State of hydration-wt,hct,protein
Input = Output/24hrs + 500ml(nonfebrile)
+ 200 ml/ deg C of inc. in Tem
Balance : kg wt loss/d
Avoid overhydration : Rx diuretics,dialysis
CVP monitoring (b/w 10-15cm H2O)

25. Diuretics
Diuretics commonly have been given in an attempt to convert the oliguric state to a nonoliguric state. However, diuretics have not been shown to be beneficial, and they may worsen outcomes.
In the absence of compelling contradictory data from a randomized, blinded clinical trial, the widespread use of diuretics in critically ill patients with acute renal failure should be discouraged.
Useful only in management of fluid-overloaded patients
Cantarovich F, Rangoonwala B, Lorenz H, Verho M, Esnault VL. High-dose furosemide for established ARF: a prospective, randomized, double-blind, placebo-controlled, multicenter trial. Am J Kidney Dis 2004;44:402-9.
Kellum JA. Systematic review: The use of diuretics and dopamine in acute renal failure: a systematic review of the evidence. Critical Care1997;1(2):53–9.

26. DOPAMINE
Dopamine traditionally has been used to promote renal perfusion(1-5 mcg/kg/min )
However, systematic reviews of dopamine treatment in critically ill patients and in patients with sepsis do not support the use of dopamine to prevent renal insufficiency, morbidity, or mortality. In the majority of ARF studies, dopamine was associated only with an increase in urine output.
Kellum JA, Decker MJ. Use of dopamine in acute renal failure: a meta-analysis. Crit Care Med 2001;29:
Denton MD, Chertow GM, Brady HR. "Renal-dose" dopamine for the treatment of acute renal failure: scientific rationale, experimental studies and clinical trials. Kidney Int 1996;50:4-14.

27. Nutrition
INTAKE 1500 cal (protein free) Oral/parenteral If vol limitation-50%D via central vein Essential L-aminoacids: K,Mg,P:Improve wound healing, hasten recovery Protein intake of 0.6 g per kg per day

28. Electrolyte & acid-base correction
Hyperkalemia, which can be life-threatening, should be treated by
decreasing the intake of potassium,
delaying the absorption of potassium,
exchanging potassium across the gut lumen using potassium-binding resins,
controlling intracellular shifts
dialysis.
Acidosis- sodabicarb ,dialysis

29. Treat coagulopathy with FFP for a prolonged aPTT, cryoprecipitate for a fibrinogen level less than 100 mg/dL, and transfuse platelets for platelet counts less than 20,000/mm3
Timely identification of UTI, proper treatment & prevention using prophylactic antibiotics

30. Should we Initiate Dialysis in Pts w/Low Cr Clearance?
Hou, S., Pregnancy in Women on Hemodialysis, 1994, revealed better outcomes of pregnancy in women w/ significant residual renal function or who initiate pregnancy before they need dialysis.
May reduce incidence of polyhydramnios, lower urea and lowers water load, also reducing risk of dialysis-induced hypotension 30

31. Outcome statistically significant when >20 hr / week dialysis implemented. Leads to 70% improvement in outcome.
Hou, et al, 1998 31

32. Hou, et al, 1998 32

33. Hou, et al, 1998 33

34. Indications for Kidney Replacement Therapy
Acidosis unresponsive to medical therapy
Acute, severe, refractory electrolyte changes (e.g., hyperkalemia)
Encephalopathy
Significant azotemia (blood urea nitrogen level >100 mg per dL [36 mmol per L])
Significant bleeding
Uremic pericarditis
Volume overload

35. Early “Prophylactic” Dialysis
Allows more liberal fluid, protein & salt intake.
Prevent hyperkalemic emergencies.
infectious Cx.
Improves comfort & survival

36. Hemodialysis Vs Peritoneal dialysis
Limited usefulness if hypotension
C/I in actively bleeding pt.
Controlled anticoagulation reqd
Volume shifts-careful
Faster correction
Can be used in preg/PP pt.
Easily available
Simple,inexpensive
Lower Cx rate
Minimises rapid metabolic pertubations & fluid shifts
Insert cath high direct vision

37. Delivery
Development of ARF in obs pt is indication of delivery in majority cases.
Deliver if UOP<20 ml/>2hrs despite adequate vol expansion & immediate delivery not expected
Redistribution of CO – better renal perfusion.
Remove fetus from hostile environment.
Neonate urea –osmotis diuresis -dehydration

38. Renal biopsy Potentially v.risky in pregnancy
Defer until postpartum even if ACN( for prognostication).
Rare indication sudden renal failure before 32 wks with no obvious cause.

39. Preeclampsia
A decrease in the GFR occurs secondary to intrarenal vasospasm. This may manifest as a "prerenal" picture. Acute renal failure (ARF) may develop, and acute tubular necrosis (ATN) may ensue if this hypoperfusion persists.

40. Pre-eclampsia: Management Renal problems
Hyperuricaemia and proteinuria are NOT indications for delivery per se
Consider delivery for progressive renal impairment (creatinine >0.09 mmol/L)
Care with fluids (pulmonary oedema can kill!)
Kidney Function is Critical for Drug Elimination

41. Pre-eclampsia Invasive monitoring
CVP monitoring may NOT be helpful!
poor correlation between CVP and PCWP
PA catheters have risks!
rare indications:
pulmonary oedema resistant to diuretics
oliguric renal failure despite volume expansion

42. Idiopathic postpartum renal failure
Associated primarily with microangiopathic processes
Postpartum hemolytic-uremic syndrome.
These were often irreversible and were associated with substantial mortality.
Now improved outcome with plasma exchange,dialysis,prostacyclin infusion, correcting coagulopathy

43. ACUTE FATTY LIVER OF PREGNANCY
Associated with acute renal failure in up to 60 percent of cases.
The diagnosis should be suspected in a woman with preeclampsia who has jaundice,hypoglycemia, hypofibrinogenemia, and a prolonged PTT in the absence of abruptio placentae.

44. KEY RECOMMENDATIONS FOR PRACTICE
Identify & prevent at prerenal phase as early as possible
Dopamine should not be used to prevent
acute renal failure. (Evidence level A)
Diuretics should not be used to treat oliguria in patients with acute renal failure unless volume overload (Evidence level B)
Early prophylactic dialysis should be strongly considered.
The maintenance of electrolytes,acid base balance & nutritional support plays vital role.

45. THANK YOU