Acute Kidney Injury
By the end of this chapter, you will be able to:
- Identify changes in colour and size of kidney and relate it to the pathology
- Identify absence and presence of gross anatomy structures and relate it to the pathology
- Correlate pre-renal, intra-renal, and post-renal causes and the pathological changes in gross anatomy specimens
In this section, we’ll learn about examples of different causes of AKI using gross pathology specimens from the DHPLC.
Prerenal: Shock Kidney
Recall that prerenal acute kidney injury occurs when there is inadequate blood flow to the kidneys for them to be able to continue their function of excreting waste and balancing fluid and electrolytes. In this example, the cause of the AKI was hemorrhagic shock.
Aneurysms are bulges in arteries that can occur as a result of weak connective tissue or prolonged hypertension. This 58 year old patient with a history of hypertension and diabetes had an aneurysm of their abdominal aorta. Due to the weakened vessel walls, this aneurysm ruptured. The abdominal aorta carries all the blood supply for the lower body, so with rupture of the aneurysm, there was massive bleeding into the abdominal cavity, resulting in hemorrhagic shock. In addition to the blood loss and other negative consequences of the ruptured aneurysm, this shock state also caused an AKI in this patient.
The rupture of the aneurysm caused severe abdominal pain and the blood loss caused shock, which presented as an extremely low blood pressure of 60/0 mmHg (normal: approximately 120/80 mmHg). Surgeons attempted to repair the rupture with a graft, but after the operation the patient had persistent hypotension and anuria (lack of urination), which reflected the AKI that accompanied this pathology.
Gross Pathology Features
Compared to the normal kidney, the cortex is pale and the medulla is darkened. These findings are typical of prolonged shock.
Shock kidney – DHPLC specimen D0310 presented by Jennifer Kong
Intrarenal causes of AKI are a group of conditions that cause kidney damage via a process that occurs within the tissue of the kidney. In this example, the cause was glomerulonephritis which is an inflammatory response that targets the glomeruli.
The term glomerulonephritis encompasses a group of causes of kidney disease that all involve damage done to components of the glomerulus by the immune system. For example systemic lupus erythematosus (colloquially known as “lupus”) is an autoimmune condition that involves deposition of immune complexes and inflammatory responses in a wide array of body systems. One of these is the kidneys and this ongoing immune insult to the kidneys may affect renal function. Another example of a cause of glomerulonephritis is post-streptococcal glomerulonephritis. After an infection with streptococcal bacteria, some people develop a damaging immune response in the kidneys that affects the glomeruli. There are many other causes of glomerulonephritis, but in most cases the recruitment of immune cells and proteins (like antibodies) impair the ability of the glomerulus to perform filtration. Not all of these causes usually result in AKI; some of them have a tendency to cause more gradual changes to kidney function which is termed Chronic Kidney Disease (CKD).
The impaired filtration and damage to the glomeruli results in protein and red blood cells that would normally be too large for the filtration barrier of the glomerulus leaking into the urine. This can result in inadequate protein in the blood, decreasing the osmotic force drawing fluid back into the blood and resulting in edema. The nephron has an internal mechanism of sensing filtration and adjusting blood pressure accordingly, so when filtration is impaired, factors are released in an attempt to increase kidney perfusion. Unlike prerenal causes where activation of mechanisms to raise blood pressure may be helpful, in glomerulonephritis the systemic blood pressure is usually normal to begin with, so this effect may cause dangerously elevated blood pressure.
In the case of the specimen we will see shortly, clinicians were unable to determine a precise cause, but acute glomerulonephritis was confirmed to be present.
In this patient, the initial symptoms were facial and peripheral edema (swelling in the face and extremities), which were likely related to protein loss in the urine. They then developed headaches, blurred vision, and dark urine. When they presented for medical care, their blood pressure was extremely elevated at 220/120 and their urine contained protein and red blood cells. The headaches were most likely caused by the increased blood pressure, as was the blurred vision. The small blood vessels that supply the retina are delicate and can burst when blood pressure is extremely elevated. Dark urine was caused by the leakage of red blood cells through the damaged glomeruli and into the filtrate. The patient died from a bleed in their brain (cerebral hemorrhage) before treatment could be completed, which was also caused by the highly elevated blood pressure because the blood vessels could not continue to withstand the pressure.
Gross Pathology Features
Glomerulonehpritis – DHPLC specimen D0201 presented by Jennifer Kong
In the cortex of the kidney that we can see on the cross section view of the specimen there are many small red dots. These are called petechiae and they represent hemorrhages resulting from the damage the disease caused to the glomeruli. These dots are only present in the cortex because that is where the glomeruli are located.
Two examples of AKI are shock kidney and glomerulonephritis. Shock kidney is a prerenal cause as shock is preventing blood flowing to the kidney. As such, the kidneys are pale and the pyramids are showing signs of necrosis. Glomerulonephritis is an intrarenal cause where antibodies have damaged the glomeruli. As such, damage is evident in the cortex is pale with signs of bleeds (petechia) whereas the medulla (loop of Henle & collecting ducts) are spared.