Nephrology Hypertension

Acute Kidney Injury in Pregnancy

Does this patient have acute kidney injury in pregnancy?

How do you diagnose acute kidney injury in a pregnant patient?

Acute kidney injury (AKI) is defined as a marked decrease in glomerular filtration rate (GFR) that is inadequate to clear products of metabolism. Clinically can present as oliguria , increased creatinine, hyperkalemia , metabolic acidosis, or any uremic symptoms. AKI in pregnancy has a bimodal distribution with the first trimester peak secondary to septic abortion and the third trimester peak resulting from pregnancy complications; ie, pre-eclampsia.

A rapid increase in serum creatinine of at least 0.5mg/dl or greater is considered abnormal. Oliguria is defined as a urinary output of less than 0.5 cc/kg/hr or less than 400 cc in 24 hrs. Due to the physiologic increase in GFR during pregnancy, a normal serum creatinine level during pregnancy falls into the 0.4– 0.8mg/dl range. Determination of creatinine clearance via a 24-hr urine collection closely approximates GFR by inulin clearance in healthy pregnant women.

There is no published data on the accuracy of the Modification of Diet in Renal Disease (MDRD) formula in pregnant women with GFR < 60cc/min. The MDRD equation should not be applied to a pregnant woman to assess GFR given its inaccuracy; it has been reported to underestimate GFR by > 40 cc/min.

What tests to perform?

Laboratory studies are performed to assess hemoglobin, hematocrit, platelet count, coagulation profile, renal function, and urine sediment and dipstick. A 24-hour urine collection for total protein quantification and creatinine clearance should be considered as part of their work up especially in patients with pre-eclampsia.

A kidney ultrasound should be done in pregnant patients with AKI to rule out hydronephrosis.

What are the causes of acute kidney injury in pregnancy?

Prerenal causes of AKI during pregnancy

Any cause that causes hypoperfusion to the kidneys will cause AKI; ie, antepartum hemorrhage due to placenta previa, placenta accreta or abruptio placenta or post-partum hemorrhage due to atonic uterus, ruptured uterus, or retained products .

  • Excessive vomiting due to hyperemesis gravidarum

  • Excessive diuresis

  • Decreased cardiac output in the setting of valvular heart disease, pulmonary hypertension

  • Sepsis

  • Drugs such as non-steroidal anti-inflammatory drugs (NSAIDs), angiotensin converting enzyme inhibitors (ACEIs)

  • Other: Acute fatty liver of pregnancy

Intrarenal causes of AKI during pregnancy

  • Acute tubular necrosis (ATN) secondary to prolonged hypotension in the setting of antepartum or postpartum hemorrhage. Sepsis induced ATN

  • ATN secondary to HELLP syndrome, drugs (aminoglycosides, chemotherapy agents)

  • Glomerulonephritis: Lupus nephritis, IgA nephropathy, post-Infectious glomerulonephritis

  • Preeclampsia: the morphological changes of preeclamptic nephropathy begin to resolve 48 hrs following the delivery and complete resolution is common by 4-6 weeks post-partum

  • Other: Acute fatty liver of pregnancy, post partum hemolytic uremic syndrome

Post-renal causes of AKI during pregnancy

  • Renal pelvis obstruction: renal stones, papillary necrosis

  • Ureteric obstruction: renal stones, surgical ligation of ureters, cervical cancer

  • Urethral obstruction: blood clots, kinked urinary bladder catheter

  • Hydronephrosis of pregnancy is characterized by ureteral dilatation from progesterone-induced smooth muscle relaxation and mechanical pressure of the gravid uterus on the ureters. Risk factors for obstructive uropathy from ureteral compression include twin pregnancy, polyhydramnios, pyelonephritis, renal calculi, and ureteral narrowing.

How should patients with acute kidney injury in pregnancy be managed?

The cornerstone for management of established AKI in most cases remains supportive until kidney function recovers.

Restore intravascular volume, avoiding nephrotoxins; ie, IV contrast, aminoglycosides, NSAIDs, this should be the goal in all patients with AKI. Treat any reversible cause i.e. Obstruction due to Hydronephrosis secondary to a kidney stone. A Foley catheter placement is of vital importance to assess with accuracy urinary output in patients with AKI.

If a patient is diagnosed with acute tubular necrosis (ATN), there is no known therapy that modifies its outcome. Efforts should be directed towards maintaining adequate intravascular volume, removal of all nephrotoxins (ie, NSAIDS, aminoglycosides) or consider delivery depending on gestational age in cases of HELLP syndrome or pre-eclampsia.

Special attention should directed towards electrolyte disorders, especially hyperkalemia and hyponatremia, both of which, if severe, can be indications for dialysis support.

Loop diuretics ie furosemide, can be used judiciously in the treatment of hypervolemia during pregnancy.

Serum bicarbonate should be kept in the range of 18-22 meq/liter for a pregnant woman. If acidosis is due to AKI and is deemed to be severe and unresponsive to medical therapy, dialysis therapy should be initiated.

Consider starting dialysis support with following complications arise:

  • Pulmonary edema

  • Hyperkalemia

  • Metabolic acidosis

  • Hyponatremia

  • Hyperphosphatemia

  • Hypermagnesemia

  • Mental status changes i.e. confusion, coma

  • Bleeding disorder

  • Pericarditis

How to utilize team care?

Management of these patients should be in conjunction with the nephrology team.

Are there clinical practice guidelines to inform decision making?

Not available.

Other considerations

AKI due to obstetric causes has declined in incidence in developed countries in the last years with improvement in the management of obstetric complications and with liberalization of abortion laws allowing these procedures to be supervised by experienced health care providers.

AKI during pregnancy is rare; the overall incidence has declined from 1/3000 in the 1960’s to 1/15,000-1/20,000. Pre-eclampsia or eclampsia accounts for the majority of cases of AKI unique to pregnancy.

What is the evidence?

Maynard, SE, Thadhani, R. "Pregnancy and the kidney". J Am Soc Nephrol. vol. 20. 2009. pp. 14-22.

Mantel, GG. "Care of the critically ill parturient: oliguria and renal failure". Best Practice & Research Clinical Obstetrics and Gynecology. vol. 15. 2001. pp. 561-581.

Keller, F, Griesshammer, M, Haussler, U. "Pregnancy and renal failure". Drugs. vol. 61. 2001. pp. 1901-1920.

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