PMID- 1558152
OWN - NLM
STAT- MEDLINE
DCOM- 19920504
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 262
IP  - 3 Pt 2
DP  - 1992 Mar
TI  - Plasma IgG pool is not defended from urinary loss in nephrotic syndrome.
PG  - F333-7
AB  - In the nephrotic syndrome, the plasma level of some proteins of hepatic origin is 
      partially defended by an increase in their synthetic rate. The plasma levels of 
      several liver-derived proteins, as well as immunoglobulin G (IgG) are increased 
      in one condition where plasma albumin concentration and oncotic pressure (II) are 
      reduced, i.e., hereditary analbuminemia. To determine whether the urinary loss of 
      IgG, a protein derived from the immune system, is compensated for by an increased 
      synthetic rate, we measured IgG synthesis in normal Sprague-Dawley rats (SD); two 
      models of the nephrotic syndrome: Heymann nephritis (HN) and Adriamycin 
      treatment; and in Nagase analbuminemic rats (NAR), a model of decreased II 
      without urinary protein loss. Plasma IgG and total IgG mass were significantly 
      reduced in both HN and Adriamycin, yet IgG synthesis was nearly identical in HN, 
      Adriamycin, and SD. In contrast, plasma and total IgG and IgG synthesis were all 
      markedly increased in NAR. We derived a pathogen-free colony of NAR by Caesarean 
      section and found that plasma IgG was not increased in pathogen-free NAR, despite 
      reduced II. Thus, unlike proteins of hepatic origin (e.g., albumin) where 
      synthesis increases following urinary loss, no compensatory increase in IgG 
      synthesis occurs. Increased plasma IgG as well as IgG synthesis in the NAR is not 
      a compensatory response to the absence of albumin or reduction in II, but rather 
      is due to subclinical infection. Profound hypogammaglobulinemia of nephrotic 
      syndrome occurs in part because no compensatory synthetic mechanisms balance 
      urinary loss, and alteration in plasma II does not modulate IgG synthesis.
FAU - al-Bander, H A
AU  - al-Bander HA
AD  - Department of Medicine, Veterans Affairs Medical Center, Martinez, California 
      94553.
FAU - Martin, V I
AU  - Martin VI
FAU - Kaysen, G A
AU  - Kaysen GA
LA  - eng
GR  - DK-42297-01/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Immunoglobulin M)
RN  - 0 (Serum Albumin)
RN  - 80168379AG (Doxorubicin)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - Doxorubicin/toxicity
MH  - Glomerulonephritis/*blood/immunology/urine
MH  - Homeostasis
MH  - Immunoglobulin M/*metabolism/urine
MH  - Male
MH  - Nephrotic Syndrome/*blood/immunology/urine
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Reference Values
MH  - Serum Albumin/*deficiency
EDAT- 1992/03/01 00:00
MHDA- 1992/03/01 00:01
CRDT- 1992/03/01 00:00
PHST- 1992/03/01 00:00 [pubmed]
PHST- 1992/03/01 00:01 [medline]
PHST- 1992/03/01 00:00 [entrez]
AID - 10.1152/ajprenal.1992.262.3.F333 [doi]
PST - ppublish
SO  - Am J Physiol. 1992 Mar;262(3 Pt 2):F333-7. doi: 10.1152/ajprenal.1992.262.3.F333.