The ‘gold standard method’ measurement of GFR by inulin clearance is invasive and cumbersome. Estimation of MG-132 research buy the GFR by the MDRD or Cockcroft and Gault formulae has been shown to be inaccurate and tends to underestimate the GFR.6 Thus, practically, the assessment of renal function in pregnancy is limited to the measurement
of serum creatinine and measured (24 h urine collection) creatinine clearance. Given the primary vasodilation of pregnancy,7 the normal ‘non-pregnant’ ranges for serum creatinine do not apply to pregnant patients. Thus, mean normal serum creatinines in the 1st, 2nd and 3rd trimesters are: 61, 55 and 47 µmol/L.8 The normal ‘pregnant’ measured creatinine clearances would be 125, learn more 122 and 118 mL/min for the 1st, 2nd and 3rd trimesters respectively9,10 Therefore, sequential serum creatinine measurements showing an increasing concentration above these limits may provide evidence of preeclampsia in the absence of other renal diagnoses. The definitive diagnosis occurs when the creatinine is >90 µmol/L in absolute terms. Renal involvement
in preeclampsia usually presents with an increase in urinary protein excretion defined as a urinary protein excretion of greater than 300 mg/24 h, or a spot urinary protein excretion of greater than 30 mg/mmol.1 Renal involvement is also defined by an acute absolute elevation of creatinine to >90 µmol/L and or oliguria. Any rise in the serum creatinine concentration from the sub ‘normal’ range even into the non-pregnant reference range is a cause for concern and should indicate the need for a careful assessment of foetal and maternal well-being to safely continue the pregnancy. The rise in creatinine concentration is not always associated
with proteinuria, although this is common. The rise in Dichloromethane dehalogenase serum creatinine indicates a reduction in GFR and is thus viewed as a potential early marker of impending renal failure due to widespread endothelial damage,11 intravascular coagulation and its attendant renal ischaemia; the natural history of which, at its extreme, is bilateral cortical necrosis and irreversible renal failure.12 The rate of acute dialysis for renal failure resultant from preeclampsia has drastically reduced in Australia in the last 50 years. Better blood pressure control and biochemical and haematological monitoring may in part explain the reduced requirement for peri-partum dialysis. The improved support for premature neonates has also been a factor, as this has allowed for more expeditious and early delivery.13 As the development of acute renal dysfunction in pregnancy represents a severe form of preeclampsia, renal dysfunction has been associated with other events more common in women with severe preeclampsia including placental abruption and foetal demise, incisional hematoma and cesarean hysterectomy, but rarely maternal mortality. In developed countries mothers are mostly discharged with intact renal function.