- Explanation for step 1
- The incidence of radiocontrast-induced nephropathy is up to 24 %
- The risk factors for radiocontrast-induced nephropathy are:
- Concomitant diabetes and hypertension
- Age more than 75 years
- Low blood pressure
- The high volume of contrast
- Use of other nephrotoxic drugs
- Decreased renal hypoxia
- Direct toxic effect on renal tubular structures
- Explanation for step 2
- Contrast agents cause an increase in the level of asymmetrical dimethylarginine.
- This inhibits nitric oxide.
- Nitric oxide is a vasodilator, antioxidant, and anti-inflammatory in nature.
- At the same time, the contrast causes an increase in the adenosine and endothelin levels. These are vasoconstrictors.
- The contrast by itself stimulates the smooth muscle in the media of the blood vessels and causes vasoconstriction.
- The net effect is vasoconstriction. This leads to renal hypoxia.
- This is particularly evident in the renal medulla.
- The contrast increases the viscosity of blood and reduces the capacity of the RBCs to change shape. This adds to ischemia.
- This leads to a reduced blood supply to the metabolically active cells of the renal tubules.
- This leads to the release of oxygen-free radicals.
- The contrast damage the cells of the proximal renal tubule.
- This leads to a 25% increment in serum creatinine within 48 hours.
- Acute deterioration in renal function (up to 7 days) is called acute kidney injury. History of Diabetes and Coronary Heart Disease Essay Example
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- Explanation for step 3
- Creatinine moves freely out of the glomerular vessels into the tubules.
- In the proximal convoluted tubule, 10 - 30% is secreted into the tubules.
- Contrast causes damage to the renal tubules.
- Therefore, the removal of creatinine in the urine is reduced.
- This leads to an increase in the blood levels of creatinine in contrast-induced nephropathy.
- Explanation for step 4
- Diabetes is characterized by hyperglycemia.
- Hyperglycemia causes oxidative stress in the nephrons.
- It causes afferent arteriolar vasodilation and efferent arteriolar vasoconstriction.
- This lead to an increase in the pressure inside the glomerulus.
- There is also mesangial expansion and apoptosis of the podocytes.
- There is a thickening of the extracellular matrix
- This leads to proteinuria.
- Explanation for step 5
- Pulmonary congestion occurs either due to cardiac causes or non-cardiac causes.
- The cardiac cause is usually due to left heart failure. This leads to pulmonary venous congestion due to back pressure changes.
- Non-cardiac causes for pulmonary congestion result from direct injury to the pulmonary capillaries.
- Contrast causes pulmonary congestion via both the above-mentioned ways:
- The contrast increases the intravascular volume.
- A patient with coronary heart disease will not be able to tolerate the excess volume.
- This can lead to pulmonary congestion.
- At the same time, the contrast can cause damage to the vascular endothelium of the pulmonary capillaries.
- This will lead to an increase in capillary permeability. Thus leading to pulmonary congestion.
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