Some findings that may help in the clinical management of patients with P-TMA
| Findings to aid in management of patients with P-TMA . |
|---|
| 1. The context (PE/E, HELLP, severe delivery hemorrhage) in which TMA occurs is paramount. |
| 2. aHUS and TTP are rare disorders in general and during pregnancy.14,17,22,23 |
| 3. PE/E and HELLP syndrome are still the main cause of P-TMA.22,42 |
| 4. To date, there is no diagnostic test for aHUS and complement assays and results of genetic tests are not required for diagnosis at the acute phase |
| Normal complement assays do not rule out pregnancy-associated aHUS36,37 ; conversely, features of complement activation are not synonymous with pregnancy-associated aHUS (transient complement activation may be the consequence of endothelial damage). |
| 5. A pregnancy-associated aHUS or a TTP masquerading as HELLP is a very rare occurrence.26 |
| 6. Increased levels of serum liver enzymes are extremely rare in aHUS. |
| 7. The absence of thrombocytopenia does not rule out pregnancy-associated aHUS.23 |
| 8. HELLP syndrome is a TMA affecting mainly the liver and more rarely the kidney (the most frequent renal lesion is acute tubular necrosis).38,39 |
| 9. PE/E and HELLP syndrome are not predominantly complement-mediated TMA.41,109 |
| 10. Spontaneous evolution of renal/hematological parameters during the first 48 h after delivery is crucial in the management of P-TMA.42 |
| 11. Benefit of plasma exchanges is only proven in immune ADAMTS13-deficiency–related TTP. |
| 12. In case of anuria (particularly in context of postpartum hemorrhage), renal cortical necrosis (Doppler, magnetic resonance imaging) should be ruled out.40 |
| 13. A kidney biopsy, when feasible, may be helpful for the differential diagnosis between acute tubular necrosis, TMA, and other causes of AKI. |
| Findings to aid in management of patients with P-TMA . |
|---|
| 1. The context (PE/E, HELLP, severe delivery hemorrhage) in which TMA occurs is paramount. |
| 2. aHUS and TTP are rare disorders in general and during pregnancy.14,17,22,23 |
| 3. PE/E and HELLP syndrome are still the main cause of P-TMA.22,42 |
| 4. To date, there is no diagnostic test for aHUS and complement assays and results of genetic tests are not required for diagnosis at the acute phase |
| Normal complement assays do not rule out pregnancy-associated aHUS36,37 ; conversely, features of complement activation are not synonymous with pregnancy-associated aHUS (transient complement activation may be the consequence of endothelial damage). |
| 5. A pregnancy-associated aHUS or a TTP masquerading as HELLP is a very rare occurrence.26 |
| 6. Increased levels of serum liver enzymes are extremely rare in aHUS. |
| 7. The absence of thrombocytopenia does not rule out pregnancy-associated aHUS.23 |
| 8. HELLP syndrome is a TMA affecting mainly the liver and more rarely the kidney (the most frequent renal lesion is acute tubular necrosis).38,39 |
| 9. PE/E and HELLP syndrome are not predominantly complement-mediated TMA.41,109 |
| 10. Spontaneous evolution of renal/hematological parameters during the first 48 h after delivery is crucial in the management of P-TMA.42 |
| 11. Benefit of plasma exchanges is only proven in immune ADAMTS13-deficiency–related TTP. |
| 12. In case of anuria (particularly in context of postpartum hemorrhage), renal cortical necrosis (Doppler, magnetic resonance imaging) should be ruled out.40 |
| 13. A kidney biopsy, when feasible, may be helpful for the differential diagnosis between acute tubular necrosis, TMA, and other causes of AKI. |
P-TMA, pregnancy-associated TMA.