PMID- 9445347
OWN - NLM
STAT- MEDLINE
DCOM- 19980211
LR  - 20190727
IS  - 0039-2499 (Print)
IS  - 0039-2499 (Linking)
VI  - 29
IP  - 1
DP  - 1998 Jan
TI  - Proteinuria precedes cerebral edema in stroke-prone rats: a magnetic resonance 
      imaging study.
PG  - 167-74
AB  - BACKGROUND AND PURPOSE: Stroke-prone spontaneously hypertensive rats (SHRSP) 
      subjected to high sodium intake develop severe hypertension, cerebral edema, and 
      proteinuria, culminating in organ damage and early death. MRI, which can be 
      applied serially, provides the unique opportunity to study temporal and 
      quantitative relations between these changes and whether diminution of sodium 
      intake can attenuate established cerebral edema. METHODS: SHRSP were subjected to 
      1% NaCl in drinking water. Cerebral MRI, proteinuria and systolic blood pressure 
      (SBP) were measured serially. After detection of cerebral edema (T2-weighted 
      MRI), 6 rats were killed for histology, to confirm the diagnosis of cerebral 
      edema. The others were followed up for 7 more days while salt loading was 
      continued (n = 10, group 1) or after sodium intake was normalized (n = 7, group 
      2). RESULTS: SHRSP invariably developed cerebral edema in 30 days (range, 8 to 54 
      days). At this point neurological signs were absent in 16 of 23 rats. SBP rose 
      until 1 week before detection of cerebral edema, and then stabilized at 
      approximately 265 mm Hg. Proteinuria invariably preceded cerebral edema, with a 
      concentration exceeding 40 mg/d predicting development of cerebral edema in 9 
      days (range, 3 to 15 days). There was linear correlation (R=.62, P<.0001) between 
      proteinuria and cerebral edema (pixels with an intensity above a defined 
      threshold). Rats in group 1 showed an increase in cerebral edema (from 5.8+/-1.1% 
      to 12.5+/-2.8%; P<.05), and proteinuria remained high (from 305+/-44 to 338+/-29 
      mg/d); and 2 died spontaneously. Rats in group 2 showed no significant change in 
      edema (from 4.9+/-0.5% to 6.9+/-1.3%) but a marked fall in proteinuria (from 
      294+/-24 to 119+/-10 mg/d; P<.05), both significantly different from group 1 
      (P<.05); all survived. SBP remained unaltered in both groups. CONCLUSIONS: Our 
      data establish MRI as a sensitive method for detection of cerebral edema, often 
      prior to neurological signs, in SHRSP. Proteinuria predicts cerebral edema, and 
      these two variables, both obtained noninvasively, are quantitatively related. 
      Moreover, in SHRSP normalizing sodium intake after salt loading attenuates 
      development of cerebral edema and reduces proteinuria.
FAU - Blezer, E L
AU  - Blezer EL
AD  - Department of Nephrology, University Hospital Utrecht, The Netherlands.
FAU - Schurink, M
AU  - Schurink M
FAU - Nicolay, K
AU  - Nicolay K
FAU - Bar, P R
AU  - Bar PR
FAU - Jansen, G H
AU  - Jansen GH
FAU - Koomans, H A
AU  - Koomans HA
FAU - Joles, J A
AU  - Joles JA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
RN  - 0 (Sodium, Dietary)
RN  - 9NEZ333N27 (Sodium)
RN  - AYI8EX34EU (Creatinine)
SB  - IM
MH  - Animals
MH  - Blood Pressure
MH  - Brain Edema/diagnosis/*etiology/pathology/physiopathology
MH  - Cause of Death
MH  - Cerebrovascular Disorders/*complications/diagnosis/pathology/physiopathology
MH  - Creatinine/blood/urine
MH  - Diet, Sodium-Restricted
MH  - Follow-Up Studies
MH  - Hypertension/etiology/physiopathology
MH  - *Magnetic Resonance Imaging
MH  - Male
MH  - Proteinuria/*etiology/physiopathology/urine
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Sodium/urine
MH  - Sodium, Dietary/administration & dosage/adverse effects
MH  - Survival Rate
MH  - Systole
MH  - Time Factors
MH  - Water Supply
EDAT- 1998/01/28 00:00
MHDA- 1998/01/28 00:01
CRDT- 1998/01/28 00:00
PHST- 1998/01/28 00:00 [pubmed]
PHST- 1998/01/28 00:01 [medline]
PHST- 1998/01/28 00:00 [entrez]
AID - 10.1161/01.str.29.1.167 [doi]
PST - ppublish
SO  - Stroke. 1998 Jan;29(1):167-74. doi: 10.1161/01.str.29.1.167.