Table 3.

Kidney involvement in pregnancy: pathologic findings.

Structure	Main Clinical Feature	Pathologic Findings	Long-Term Effects
Glomerular	Isolated proteinuria, PE, AKI	Glomerular endotheliosis (PE), focal-segmental glomerulosclerosis (FSGS); podocyte loss. Differential diagnosis with CKD	Endotheliosis is the hallmark of PE. It is considered reversible, and may also be found in normal pregnancies. FSGS is not reversible. Its frequency has been differently assessed, and the symptoms of severe endotheliosis may merge with it. Podocyte loss, with permanent damage to the basal membrane seems to be the unifying cellular lesion.
Tubular	AKI, severe PE, HELLP	Acute tubular necrosis, tubulitis, no alteration	AKI can be an outcome of ischemic, hypovolemic. septic or toxic (iatrogenic) damage. The long-term effects of AKI are not fully understood, but severe dialysis-requiring AKI even when reversible in the short term, is associated with CKD and ESRD later in life.
Vascular	Hypertensive disorders, PE, AKI	Vascular hypertrophy, up to “onion skin” lesions; ischemic or necrotic glomerular changes	Hypertensive crises in pregnancy may exhibit the features of “malignant” or accelerated hypertension. While onion-skin changes indicate a progressive onset, necrotic changes are the hallmark of the abrupt development of severe hypertension.
Global	AKI followed by CKD	Cortical necrosis	The irreversible loss of function associated with necrotic changes is often multifactorial (hypovolemic or haemorrhagic shock, sepsis, HELLP); can be diagnosed using magnetic resonance imaging.