Contrast nephropathy is a preventable disease. Diagnosis of contrast nephropathy depends primarily on the clinical finding and excluding other causes.
Contrast-induced
nephropathy
Clinical features and diagnosis
Contrast
nephropathy is usually a reversible type of AKI (acute kidney injury) that
presents immediately after the addition of radiocontrast media in radiological examination.
The underlying mechanism of this injury still uncertain. However, animal
studies the occurrence of ATN (acute tubular necrosis), an acute form of kidney
failure that could be related to vasoconstriction (blood vessel wall
contraction) and toxic impacts of the contrast itself with other systemic
effects like dehydration and obstructive events inside the kidney.
Risk factors
The
prevalence of contrast nephropathy depends greatly on the associated risk
factors, particularly the underlying chronic kidney disease. If the baseline
kidney function was normal, this means smaller risk to develop this disease,
however, with the presence of associated kidney function abnormality, the risk
will increase proportionally with severity of kidney dysfunction particularly
among diabetics. Moreover, the risk is also higher with associated heart
failure or hemodynamically unstable (low blood pressure and poor circulation).
In
addition, higher doses of the contrast media may be associated with increased
risks of contrast nephropathy, on the other hand, there is lower limit to be
considered a safe limit to prevent disease occurrence. Types of the contrast e.g.
hyperosmolar ionic also affect disease incidence.
Clinically,
disease manifestations can be observed within 24-48 hours from contrast administration.
Contrast nephropathy is mostly non-oliguric (no diminution of urine output),
but rather a modest rise in serum creatinine that might return to its normal
level within 3-7 days. Proteinuria (protein in urine) is usually mild or absent
and urine sediment (after centrifugation) is that of the classic ATN (form of
acute kidney failure) findings.
Diagnosis
of contrast nephropathy depends primarily on the clinical finding and excluding
other causes. There are no specific criteria for diagnosis of contrast
nephropathy. Lack of other criteria on urine analysis such as WBCs, WBCs casts
or dysmorphic RBCs or RBCs or RBCs cast would exclude other diagnoses such as interstitial
nephritis and glomerular diseases. On the other hand, the presence of WBCs,
WBCs cast, RBCs dysmorphia or RBCs casts is in favor of other causes of AKI. No
role for ultrasound for early diagnosis of contrast nephropathy in patients with
a positive history of contrast exposure, however, this technique may have a
role later on to exclude other causes of AKI e.g., obstructive uropathy.
In
addition, kidney biopsy has no role in the diagnosis of contrast nephropathy
considering the focal nature of this disease as well as its short course and lack
of specifity. However, kidney biopsy may be the last resort for diagnosis of
cases presented clinically with atypical course.
Differential diagnosis (DD)
DD
may include ischemic ATN, acute interstitial nephritis, and kidney atherosclerotic
emboli. Both ischemic ATN and acute interstitial nephritis may need additional
insults e.g. sepsis or hypotension, or drug exposure that can be excluded by
history taking. Atherosclerotic emboli in kidney tissues can be recognized via
the finding of other embolic manifestations (one toe for example) or livedo
reticularis, and temporary eosinophilia with low complement. Furthermore, AKI
onset resulting from atheroembolism usually presented lately after weeks from
contrast exposure with no resumption of kidney function.
https://www.wjgnet.com/2220-3230/full/v6/i4/682.htm
N.B. This Blogger is created to declare how much dangerous to the kidney to expose your kidney to certain contrast.
COMMENTS