The intensity of proteinuria is an important element to define the degree of chronic renal failure. As a clinician, what importance do you attribute to the type of protein (low/high molecular weight) detected?
The type of proteinuria is an important clue to establish renal disease, and to clarify indications for renal biopsy. If there is a glomerular type, is it selective or nonselective? If there is a tubular type of proteinuria than there is nonglomerular disease.
Dear Nicole Gillain-Martin,
I agree with Dr.Evers and Dr.Holt regarding the importance of type of proteinuria; glomerular vs. tubular proteinuria.
I would like to add its importance in kidney transplantation as well. Increased level of one of urine low MW tubular proteins, RBP could also predict a decline in allograft function in the early post-transplant period.
References
1. Amer H, Fidler ME, Myslak M, Morales P, Kremers WK, Larson TS et al. Proteinuria after kidney transplantation, relationship to allograft histology and survival. Am J Transplant 2007;7(12):2748-2756.
2. Hosaka B, Park SI, Felipe CR, Garcia RG, Machado PG, Pereira AB et al. Predictive value of urinary retinol binding protein for graft dysfunction after kidney transplantation. Transplant Proc 2003;35(4):1341-1343.
Best regards,
Wisit
Thanks for posting the Hosaka paper - interesting. However, outside of Dr Holt's mentioned situation of HIV disease, I find it hard to think of a clinical scenario in which RBP is clinically useful in native renal disease for diagnosis or prognostication. I would be interested to know of any.
The interpretation of proteinuria is based on amount (heavy indicates glomerular disease), type (glomerular disease primarily albumin; tubular disease b2 micro globulin, light chains etc), and transient/persistent. The former can be orthostatic (benign) and the latter more likely to indicate a disease state. It is a risk marker for progressive disease: the higher the value more likely the disease will progress. It is also used as a surrogate marker to assess treatment efficacy: angiotensin blocking agent dosage is titrated per proteinuria, with the largest of bringing it down to less than 1 g/day. There are issues around measurement of proteinuria as well (spot measurement vs 24 hr values vs ACR). A good source is the 2012 KDIGO CKD Guidelines (Free download: http://www.kdigo.org/clinical_practice_guidelines/pdf/CKD/KDIGO_2012_CKD_GL.pdf).
A big thank you for all the answers that confirm the importance I have always attributed to have reliable techniques to quantify or separate these proteins by electrophoresis. This opinion is not shared by all nephrologists some being especially attached to the quantitative aspect of proteinuria
About RBP: a study was conducted in the neonatal unit of my hospital. It revealed that this protein was the best marker of neonatal asphyxia. The analyzes were performed by nephelometry with reagents from Behring. Unfortunately, the technique on urine has not been "accredited" by the Behring. I have replaced it by cystatin C. New research with this molecule in neonatology has not been carried out.
About kidney problems of AIDS patients, monitoring can be easily realized on the basis of electrophoresis in SDS or determination of albumin and either low MW protein
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