PPD 1–2: urinary tract infections risk factors include multiple catheterization during labor, multiple vaginal examinations during labor, and untreated bacteriuria. PPD 2–3: endometritis ( the most common cause ) risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and multiple vaginal examinations during labor. PPD 4–5: wound infection risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and multiple vaginal examinations during labor. PPD 5–6: septic pelvic thrombophlebitis risk factors include emergency cesarean section, prolonged membrane rupture, prolonged labor, and diffuse difficult vaginal childbirth. PPD 7–21: mastitis risk factors include nipple trauma from breastfeeding. Diagnosis
Puerperal fever is diagnosed with:

A temperature rise above 38 °C (100.4 °F) maintained over 24 hours or recurring during the period from the end of the first to the end of the 10th day after childbirth or abortion. (ICD-10)
Oral temperature of 38 °C (100.4 °F) or more on any two of the first ten days postpartum. (USJCMW)Puerperal fever  (from the Latin puer, male child (boy)), is no longer favored as a diagnostic category. Instead, contemporary terminology specifies:
the specific target of infection: endometritis (inflammation of the inner lining of the uterus), metrophlebitis (inflammation of the veins of the uterus), and peritonitis (inflammation of the membrane lining of the abdomen). the severity of the infection: less serious infection (contained multiplication of microbes) or possibly life-threatening sepsis (uncontrolled and uncontained multiplication of microbes throughout the blood stream).Endometritis is a polymicrobial infection.
This, in turn, stimulates release of proteases and oxidants by the mesangial and epithelial cells, damaging the capillary walls and causing them to become "leaky". In addition, the epithelial cells also seem to secrete an unknown mediator that reduces nephrin synthesis and distribution.Within membranous glomerulonephritis, especially in cases caused by viral hepatitis, serum C3 levels are low.Similar to other causes of nephrotic syndrome (e.g., focal segmental glomerulosclerosis or minimal change disease), membranous nephropathy is known to predispose affected individuals to develop blood clots such as pulmonary emboli. Membranous nephropathy in particular is known to increase this risk more than other causes of nephrotic syndrome though the reason for this is not yet clear. Morphology
The defining point of MGN is the presence of subepithelial immunoglobulin-containing deposits along the glomerular basement membrane (GBM). By light microscopy, the basement membrane is observed to be diffusely thickened. Using Jones stain, the GBM appears to have a "spiked" or "holey" appearance. On electron microscopy, subepithelial deposits that nestle against the glomerular basement membrane seems to be the cause of the thickening. Also, the podocytes lose their foot processes. As the disease progresses, the deposits will eventually be cleared, leaving cavities in the basement membrane. These cavities will later be filled with basement membrane-like material, and if the disease continues even further, the glomeruli will become sclerosed and finally hyalinized. Immunofluorescence microscopy will reveal typical granular deposition of immunoglobulins and complement along the basement membrane.Although it usually affects the entire glomerulus, it can affect parts of the glomerulus in some cases.