<<snip>>
decrease in rate of progression of renal failure over the 21-day study
period
<<snip>>

Titre du document / Document title
Toxicity of tubule fluid iron in the nephrotic syndrome
Auteur(s) / Author(s)
ALFREY A. C. ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
Univ. Colorado medical cent., Denver veterans affairs hosp., Denver CO
80220, ETATS-UNIS

Résumé / Abstract
This study was carried out in rats with nephrotoxic serum nephritis
after autologous phase proteinuria was well established to determine
the effect of tubule fluid iron chelation on the course of this
disease. Deferoxamine administration caused a reduction in urinary
iron potentially capable of catalyzing hydroxyl radical (.OH)
formation and kidney iron uptake (224±60 vs. 398±152 mg/kg). This was
associated with a decrease in rate of progression of renal failure
over the 21-day study period (creatinine clearance -0.199±0.152 vs.
-0.509±0.336 ml/min, P<0.05) and improved survival (8/8 vs. 4/8,
P<0.05)
Revue / Journal Title
American journal of physiology. Renal, fluid and electrolyte
physiology  (Am. j. physiol., Renal fluid electrolyte physiol.)  ISSN
0363-6127   CODEN AJPFDM
Source / Source
1992, vol. 32, no4, pp. F637-F641 (31 ref.)
Langue / Language
Anglais

Editeur / Publisher
American Physiological Society, Bethesda, MD, ETATS-UNIS (1977- 1996)
(Revue)

Mots-clés anglais / English Keywords
Rat ; Animal ; Nephrotic syndrome ; Membranous glomerulonephritis ;
Pathophysiology ; Pathogenesis ; Urinary system disease ; Experimental
disease ; Iron ; Free radical ; Catalysis ; Transferrin ; Rodentia ;
Mammalia ; Vertebrata ;
Mots-clés français / French Keywords
Rat ; Animal ; Néphrotique syndrome ; Néphropathie glomérulaire
extramembraneuse ; Physiopathologie ; Pathogénie ; Appareil urinaire
pathologie ; Pathologie expérimentale ; Fer ; Radical libre ;
Catalyse ; Transferrine ; Rodentia ; Mammalia ; Vertebrata ;

002b14a01 ;
Mots-clés espagnols / Spanish Keywords
Rata ; Animal ; Nefrótico síndrome ; Glomerulonefritis membranosa ;
Fisiopatología ; Patogenia ; Aparato urinario patología ; Patología
experimental ; Hierro ; Radical libre ; Catálisis ; Transferrina ;
Rodentia ; Mammalia ; Vertebrata ;
Localisation / Location
INIST-CNRS, Cote INIST : 670 F, 35400003206993.0090

Copyright 2006 INIST-CNRS. All rights reserved

Toute reproduction ou diffusion même partielle, par quelque procédé ou
sur tout support que ce soit, ne pourra être faite sans l'accord
préalable écrit de l'INIST-CNRS.
No part of these records may be reproduced of distributed, in any form
or by any means, without the prior written permission of INIST-CNRS.

Nº notice refdoc (ud4) : 4362365

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kidney failure ..<<

The last article speaks to the problem of kidney failure in the Maori
and Pacific Islanders and their .. **specific** problem OF .. lupus ..
and how 'coincidentally' they also are closely followed by type 2
diabetes kidney failure .. ANOTHER .. **erythrocytotic** .. related ..
high iron .. related .. disease.

And it seems the latest study has found the highest iron levels of
ANYONE in the world to BE .. somewhere around the Pacific ..
islanders .. http://tinyurl.com/yp486o

This article shows the results of increased red blood cell
production / polycythemia / erythrocytosis ..

"Glomerulomegaly is a histologic finding in polycythemic states"

Journal of the American Society of Nephrology, Vol 8, 1966-1970,
Copyright © 1997 by American Society of Nephrology
--------------------------------------------------------------------------------

REGULAR ARTICLES

Glomerulomegaly and proteinuria in a patient with idiopathic pulmonary
hypertension
F Faustinella, C Uzoh, D Sheikh-Hamad, LD Truong and JJ Olivero
Department of Medicine, Baylor College of Medicine, Houston, Texas
77030, USA.

Glomerulomegaly is a histologic finding present in idiopathic
pulmonary hypertension, congenital cyanotic heart disease, morbid
obesity associated with sleep apnea syndrome, sickle cell disease, and
polycythemic states. This study examines the case of a 34-yr-old woman
with idiopathic pulmonary artery hypertension who presented with
nephrotic-range proteinuria. Kidney biopsy revealed enlarged glomeruli
with mesangial-proliferative glomerulonephritis. A review of the
pertinent literature and a discussion of the proposed pathophysiologic
mechanisms leading to glomerulomegaly are presented.

Oxford Journals Medicine Nephrology Dialysis Transplantation Volume
19, Number 3 Pp. 678-685
Nephrol Dial Transplant (2004) 19: 678-685
Nephrol Dial Transplant Vol. 19 No. 3 (c) ERA-EDTA 2004; all rights
reserved

--------------------------------------------------------------------------------

http://ndt.oxfordjournals.org/cgi/content/full/19/3/678

"the excess in Maori and Pacific Island people was confined to type II
diabetic nephropathy, hypertensive renal disease and
glomerulonephritis (especially lupus nephritis and type I
mesangiocapillary glomerulonephritis]"

Original Article

The incidence of treated end-stage renal disease in New Zealand Maori
and Pacific Island people and in Indigenous Australians
John H. Stewart1, Margaret R. E. McCredie2 and Stephen P. McDonald3
1Department of Renal Medicine, Westmead Hospital, Westmead, NSW,
Australia, 2Department of Preventive and Social Medicine, University
of Otago, Dunedin, New Zealand and 3Australia and New Zealand Dialysis
and Transplant Registry, Queen Elizabeth Hospital, Woodville, SA,
Australia

Correspondence and offprint requests to: Dr Margaret McCredie,
Department of Preventive and Social Medicine, University of Otago, PO
Box 913, Dunedin, New Zealand. Email:
margaret.mccredie@stonebow.otago.ac.nz

   Abstract

Background. Although Indigenous Australians, New Zealand Maori and
Pacific Island people comprise an unduly high proportion of patients
treated for end-stage renal disease (ESRD) in the two countries, no
population-based age- and disease-specific rates have been published.

Methods. From data provided to the Australia and New Zealand Dialysis
and Transplant Registry (ANZDATA), truncated age- and sex-standardized
incidence rates were calculated for treated ESRD due to all causes and
by primary renal disease, in four broad age groups of Maori, Pacific
Island people and all 'other' New Zealanders and Indigenous and non-
indigenous Australians, for the period 1992-2001.

Results. The incidence of ESRD did not differ in persons aged 0-14
years. In adults, Maori and Pacific Island people had similar rates of
ESRD, a little more than half those of Indigenous Australians except
in persons aged 65 years and over in whom the rates were nearly equal,
but two to ten times the rates in 'other' New Zealanders and non-
indigenous Australians. The excess of ESRD in Indigenous Australians
was due principally to type II diabetic nephropathy and
glomerulonephritis (all common types except lupus nephritis), but was
seen also in respect of type I diabetic nephropathy, hypertensive
renal disease and analgesic nephropathy, while the excess in Maori and
Pacific Island people was confined to type II diabetic nephropathy,
hypertensive renal disease and glomerulonephritis (especially lupus
nephritis and type I mesangiocapillary glomerulonephritis, but not
mesangial IgA disease).

Conclusions. The incidence and pattern of treated ESRD differs
quantitatively and qualitatively between Maori, Pacific Island people
and other New Zealanders, and Indigenous and non-indigenous
Australians.

Keywords: end-stage renal disease; glomerulonephritis; incidence;
Indigenous Australians; New Zealand Maori; Pacific Island people

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complexes, which happen to be HUGE molecules, getting stuck in the
glomeruli<<

This article shows the **iron overload** IN this disease CAUSED all
the **symptoms** / lab work OF  .. "immune complexes" .. which happen
to BE .. "huge molecules which get stuck in the glomeruli" ..

GVHD - graft-versus-host disease which again 'coincidentally' causes
lupus like symptoms .. or by some to be considered to BE .. one ..
and .. the .. same ..

Biol Blood Marrow Transplant. 2006 May;12(5):506-10.  Links
Iron overload manifesting as apparent exacerbation of hepatic graft-
versus-host disease after allogeneic hematopoietic stem cell
transplantation.Kamble RT, Selby GB, Mims M, Kharfan-Dabaja MA, Ozer
H, George JN.
Oklahoma University Health Sciences Center, Oklahoma City, Oklahama
73190, USA. kamble@sbcglobal.net

Iron overload presenting as exacerbation of hepatic graft-versus-host
disease (GVHD) after allogeneic hematopoietic stem cell
transplantation has not been previously described. We report 6
patients with established hepatic GVHD in whom iron overload (median
serum ferritin, 7231 mug/dL; median transferrin saturation, 77%)
resulting from a lifetime median of 20 units of packed red blood cell
transfusions was manifested by worsening of liver function. Liver
biopsies performed in 4 patients confirmed severe iron overload and
also hepatic GVHD. Analysis for the C282Y and H63D hemochromatosis
gene mutation was negative for the homozygous state in all 6 patients.
Erythropoietin-assisted phlebotomy resulted in normalization of liver
function at a median of 7 months and of serum ferritin at a median of
11 months. Immunosuppressive therapy was successfully tapered in all 4
patients who completed the phlebotomy program, and this supported the
impression that iron overload, rather than GVHD, was the principal
cause of liver dysfunction. At a median follow-up of 50 months (range,
18-76 months) from the transplantation and 25 months (range, 5-36
months) from ferritin normalization, all 4 patients require
maintenance phlebotomy. We conclude that iron overload can mimic GVHD
exacerbation, thus resulting in unnecessary continuation or
intensification of immunosuppressive therapy for GVHD, and that
maintenance phlebotomy is necessary after successful iron-reduction
therapy.

PMID: 16635785 [PubMed - indexed for MEDLINE]

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