Cardiovascular
In general, the fluid volume overload experienced in ARF may lead to hypertension, pulmonary edema, peripheral
edema, and arrhythmias. The kidneys fail to excrete excess potassium which may lead to the following: muscle
weakness, neuromuscular irritability, bradycardia, heart block, asystole, or other arrhythmias (Campbell,
2003).
Respiratory
Dyspnea may result from the decrease in oxygenation either from associated anemia or from fluid volume overload and
pulmonary edema associated with ARF. The dyspnea may be at rest or worsen with exertion. Auscultation of lung field
may reveal crackles.
Hematologic
ARF patients are anemic secondary to the impaired RBC production, hemolysis, bleeding, hemodilution, and decrease
RBC survival. Damaged kidneys produce less erythropoietin to stimulate RBC production and the damaged red blood
cells are not replaced. The decrease in hemoglobin leads to insufficient oxygenation manifested by dyspnea.
Gastrointestinal
Uremia may cause nausea, vomiting, anorexia, gastric ulcers and colitis which places the patient at risk for GI
bleeding. The increase in urea may also cause the patient’s breath to smell like foul urine.
Exceptions for John’s case study
John exhibited the majority of the above symptoms; however, he did not experience hypertension, pulmonary edema,
peripheral edema, and arrhythmias common to ARF due to the vasodilation effect of the sepsis. Conversely, he was
hypotensive and required volume replacement and intraveneous vasopressors. His blood gases revealed metabolic
acidosis,
resulting from the lactic acid produced from the sepsis.
Diagnostic Tools
Conventional Biomarkers
The conventional methods of diagnosing ARF are urine output, creatinine, and urea. However, the presence or absence
of urine does not necessarily denote renal malfunction. The output is more indicative of renal hemodynamics than
actual renal function. The excretion of sodium and urea has not been proven to be sensitive in early ARF because
the tubular functions may remain intact unless clinical conditions such as sepsis alter tubular function. Urine
protein is present in other diseases such as diabetes, shock, and chronic kidney disease (Kosinski, 2009).
New Biomarkers
Acute renal failure can be diagnosed earlier utilizing the following biomarkers in addition to the conventional
markers listed above: Cystatin C, Interlukin 18 (IL 18), Neutrophil Gelatinas-Associated Lipocalin (NGAL), and
Kidney injury Molecule (KIM-1). Cystatin C is a marker of the glomelular filtration rate and is independent of age,
sex, and muscle mass. Cystatin C has a small molecular mass and can be filtered more freely at the glomerulus.
Interlukin 18 is an inflammatory cytokine which enters urine in the proximal tubule. NGAL propagates with injured
endothelium of the lungs, stomach, colon, and kidneys and rises with acute infections. Kidney injury molecule
(KIM-1) is a transmembrane protein that is excreted in the proximal tubule and detected in ischemic kidney disease.
Cystatin C and NGAL are measured in the serum. IL-18, KIM-1, and NGAL are measured in the urine.
Diagnostic Imaging
Diagnostic imaging may also be needed in determining the underlying disease and differentiating between acute and
chronic disease. The following may be utilized as diagnostic procedures: X rays, computed tomography scan (CT),
magnetic resonance imaging (MRI), ultrasound, arteriogram, and renal biopsy. Ultrasounds of x rays of the ureters
and bladder may also be included.
Rifle Criteria
The RIFLE criteria (Thurman, 2009) is evidence-based practice tool used for the diagnosis of ARF. The diagnosis of
ARF can be the result of changes in the serum creatinine level, a change in the urinary output, or both. The RIFLE
tool assesses the following: risk of renal dysfunction, injury to the kidney, failure of kidney function, loss of
kidney function and end-stage kidney disease.
|
