The American Journal of Kidney Diseases published a fascinating letter this month from Jochen Reiser's group concerning the transmission of the suPAR from a mother to her newborn infant. The patient in question had a history of primary FSGS and after her baby was born, the infant had proteinuria which eventually resolved. At the time, this was published as a letter in the NEJM and was used as evidence for the existence of a soluble FSGS "factor" which had yet to be identified.
Now, more than 10 years later, they got their hands on blood from the mother and the infant. The level of suPAR in the mother was 4635pg/ml and in the child was 5225 pg/ml. This compares with a mean of 2884 pg/ml in controls. Unfortunately, the family moved away from the area so there were no follow-up samples. However, the patient's pediatrician reported that the baby's urine was negative for albumin at one year of age.
Although this does not definitively prove that suPAR is the causative agent in primary FSGS, and there is some debate about the true pathogenicity, this, along with recently published data in JASN, adds to the weight of evidence suggesting that this may be the elusive factor we were looking for. Interesting times indeed.
Now, more than 10 years later, they got their hands on blood from the mother and the infant. The level of suPAR in the mother was 4635pg/ml and in the child was 5225 pg/ml. This compares with a mean of 2884 pg/ml in controls. Unfortunately, the family moved away from the area so there were no follow-up samples. However, the patient's pediatrician reported that the baby's urine was negative for albumin at one year of age.
Although this does not definitively prove that suPAR is the causative agent in primary FSGS, and there is some debate about the true pathogenicity, this, along with recently published data in JASN, adds to the weight of evidence suggesting that this may be the elusive factor we were looking for. Interesting times indeed.
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