Læknablaðið - 01.09.1979, Blaðsíða 48

192
LÆKNABLAÐIÐ
Tom Berganl
Antibiotic treatment of patients with
reduced renal functions
Drugs which are eliminated mainly through
the kidneys are subject to a prolonged elimi-
nation in patients with reduced renai function.
In order to avoid toxic reactions, it is import-
ant to adjust the dose. This must be done in
such a way, however, that therapeutic efficacy
against the infection is maintained. This is
achieved by maintaining the same ratio bet-
ween dosage interval and serum half-life in
all patients, regardless renal function. Prefer-
able drugs in renal impairment are penicillins,
cehalosporins, macrolides, metronidazole, and,
after careful adjustments, aminoglycosides. -—
The half-life may be determined in the indivi-
dual patient or stipulated temporarily from
renal function determined by renal clearance.
Serum creatinine determinations are not suffi-
cient for assessment of the normalcy of renal
function, because the clearance is markedly
reduced in ages above 70 years, although the
serum creatinine levels are maintained within
normal limits. Increased elimination time only
starts with renally eliminated drugs when the
kidney function is below a glomerular filtra-
tion of 30 ml/min.
l Departments of Microbiology, Aker sykehus and
Institute of Pharmacy, University of Oslo.
Ragnarsson, J., M.D., Pohl, M.A., MD., Valenzuela,
R., M.D.
Gold nephropathy — Resolution of
membraneous nephropathy induced
by gold therapy
A 28-year-old black female with sero positive
rheumatoid arthritis developed nephrotic syn-
drome following a second course of gold thera-
py. SLE and other secondary causes of nephro-
tic syndrome were excluded by appropriate
laboratory tests. Renal biopsy in March of 1976
demonstrated typical membraneous nephro-
pathy with electron dense deposits on electron
microscopy. X-ray dispersion analysis docu-
mented gold particles in the renal tubular
cells and the interstitial macrophages. Follow-
ing cessation of goid therapy the nephrotic
syndrome resolved and the second renal biopsy
fourteen months later showed resolution of
the membranecous lesion. The electron micro-
scopy showed dramatic resolution of the elee-
tron dense deposits in the glomerular base-
ment membrane and immunomicroscopy showed
much weaker staming of the ímmunogioounns
in the basement membrane. Gold was not de-
monstrated by X-ray dispersion analysis. In
patients with gold nephropathy the prognosis
is generally favourable, however, serial renal
biopsies are lacking and therefore, histologi-
cal resolution of gold induced membraneous
lesions have not been previousiy demonstrated.
The possible pathogenic mechanisms are revi-
ewed, and we speculate that gold leads to
release of renal tubuiar cell antigens. These
antigens could then lead to the formation of
soluable immune complexes that are trapped
in the glomerular basement membrane or these
renal tubular epitheiial cell antigens could
lodge in the glomerular basement membrane
and attract circulating antibodies to form an
immune complex in the glomerular base-
ment membrane. Similar mechamsm has been
invoked as the cause of membraneous glome-
rulopathy, both in humans and in animal mo-
dels. When the gold therapy is stopped and
the stimulus for the release of these antigens
should disappear and the membraneous de-
posits might be expected to resolve. In con-
clusion we have described a patient who de-
veloped nephrotic syndrome with changes of
an immune complex membraneous nephro-
pathy following goid therapy. When gold tera-
py was discontinued, the clincal nephrotic
syndrome disappeared and the renal lesion re-
gressed histologically. These observations are
consistent with the notion that gold nephropat-
hy is an autoiogous immune complex giome-
rulopathy induced by the release of renal
tubuiar epithelial cell antigen.
Sigurður B. Þorsteinsson and Pall Asmundsson
Methicillin hypersensitivity-Iike
syndrome — Report of five cases
Methicillin hypersensitivity-like syndrome is
a potentially live threatening complication
associated with Methicillin therapy. The
syndrome includes any combination of fever,
skin, rash, eosinophilia, neutropenia, haema-
turia, pyuria, and interstitial nephritis with
renal failure of varying severity. The possible
pathogenic mechanisms accounting for the
renal affection will be briefly discussed.
We describe five patients aged 10-67 years
with methicillin hypersensitivity, the duration
of methicillin treatment varied from 15 to
21 days. The signs of methicillin toxicity ap-
peared after 11-14 days of treatment. All had
fever and eosinophilia and abnormal urina-
lysis. Two patients had skin rash and two
developed renal failure, one moderate and