Pregnant lady may develop certain complications that may lead to AKI (acute kidney injury, acute kidney failure)
Acute kidney injury (acute renal failure) in pregnancy
Pregnant lady may develop certain complications that may lead to AKI (acute
kidney injury, acute kidney failure). Early period of pregnancy, pre-renal insult (dehydration) or ATN (acute tubular necrosis) may result from
hyperemesis gravidarum or due to septic abortion.
Late period of pregnancy, AKI may be developed
from pre-eclampsia, thrombotic micro-angiopathies
(TMA), acute fatty liver related to pregnancy, kidney cortical
necrosis, pyelonephritis (PN),
obstructed urinary tract or stone kidney (nephrolithiasis).
[1] Acute kidney injury
With associated thrombocytopenia and anemia may be due to either thrombotic thrombocytopenic purpura-hemolytic uremic
syndrome (TTP-HUS) or severe
preeclampsia that may associate the HELLP syndrome. Discrimination between these diseases can
be performed via a full-detailed history as well as the lab profile. Therapy of
preeclampsia
associated with the HELLP syndrome starts by induction of delivery.
Treatment
of TTP-HUS
Optimal approach for TTP-HUS treatment that develops within pregnancy includes induction
of labor, as differentiation from preeclampsia may be difficult. TTP-HUS
patients can be treated via plasma infusion with or with no plasmapheresis (exchange),
exactly simulating the protocol applied in the treatment of other types of
TTP-HUS.
Therapy of the HELLP variant of preeclampsia still uncertain. Induction of delivery is required,
and despite some of the laboratory profiles can deteriorate immediately post-partum,
they may be resolved though one week after delivery, with no specific intervention.
Steroids have been administrated in some centers, with some benefit; however, wide-scale
randomized clinical studies are currently lacking.
[2] Acute fatty liver
A rarely observed complication of pregnancy that may show many
clinical and lab features in common presentation with preeclampsia and
may induce AKI, hypoglycemia, hypo-fibrinogenemia,
hepatic profile alterations, and increased PTT. Treatment involves therapy of DIC and
immediate fetal delivery induction.
[3] Bilateral renal cortical necrosis
It can be seen as a complication of intense hypotension and/or DIC related
to abruptio placentae, symptomatizing placenta previa, neglected intrauterine fetal death, or amniotic fluid embolus. Patients with Bilateral renal cortical necrosis may present
with oliguria (low urine output) or complete anuria (no urine), frank
hematuria, loin pain, and low blood pressure. Accurate diagnosis can be achieved
by US or CT scan. There is no specific treatment for this disorder and many
patients will be commenced on dialysis. Some patients, however, may develop partial
recovery of kidney function.
[4] Acute pyelonephritis (PN)
PN may induce AKI in pregnant lady even with the lack of septicemia
or sever hypotension. Partial recovery after culture and sensitivity testing with
the proper antimicrobial medications may be occur owing to the presence of irreversible
lesions.
[5] Dilatation of the collecting
system
Owing to the impact of
gestational hormones and anatomical abnormalities associated with pregnancy, dilatation
of the collecting system can be developed, usually with no kidney dysfunction, sometimes
obstruction may be severe enough to induce kidney failure.
Recognition of this possibility can be defined via normalization of
kidney function in the lateral recumbent decubitus and reversal to kidney
dysfunction with the supine decubitus. However, certain cases may require ureteral
catheter placement or induction of delivery.
[6] Urinary tract obstruction
Can be developed due to obstructing kidney stones, despite that
many ladies may present with an acute loin pain with gross hematuria, instead
of a frank kidney failure. Diagnosis of nephrolithiasis (stone kidney) can be usually
recognized via a kidney U/S.
REFERENCES
§
Noris M, Remuzzi G.
Atypical hemolytic-uremic syndrome. N Engl J Med 2009; 361:1676.
§
Vesely SK, George
JN, Lämmle B, et al. ADAMTS13 activity in thrombotic thrombocytopenic
purpura-hemolytic uremic syndrome: relation to presenting features and clinical
outcomes in a prospective cohort of 142 patients. Blood 2003; 102:60.
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