Acute Kidney Injury
By the end of this section, you will be able to:
- Identify debris within the nephron tubule and explain how it is an indication of kidney injury
- Recognize changes in cellular populations in the glomeruli and correlate with pathology
- Identify the loss of cellular components (e.g. nuclei, cell volume, brush border) and correlate with the pathology
As mentioned in a previous section, AKI is a clinical diagnosis defined by an increase in serum creatinine or an abnormal decrease in urine output. Therefore, when discussing histopathology, the term AKI doesn’t really apply and instead we describe the pathological changes we see within the kidney itself.
The categories of causes of AKI (prerenal, intrarenal, and postrenal) don’t apply to the histopathology either. Generally, we will see only intrarenal damage when observing the kidneys microscopically, but this could be a result of any of AKI from any of the 3 categories.
Review the following sections and videos to learn more about the histopathology of AKI.
As we discussed earlier, medical shock occurs when there is a serious decrease in either effective or absolute circulating blood volume and may cause a prerenal AKI. A persistent prerenal AKI can cause intrarenal kidney damage, when the high metabolic demands of the cells in the renal tubules are not met and they begin to degenerate.
The following video reviews the histological findings in the kidney of someone with hemorrhagic shock.
Histopathology of kidney experiencing shock. DHPLC specimen PATH 425-058 presented by Lyz Boyd
Video Summary – Clinical context: The patient was a 29 year old male who was involved in a traffic accident and fractured his pelvis. Pelvic fractures are often associated with massive internal bleeding, which in this case caused shock and therefore a prerenal cause of AKI. He developed AKI and died 7 days later.
Pathology: The blood loss caused hemorrhagic shock which resulted in a type of prerenal kidney injury. Prolonged lack of blood to the kidneys resulted in pathology that can be seen microscopically, termed acute tubular injury.
Histopathological findings: The following changes to the renal tubules can be observed:
– Renal tubules are filled with debris and/or blood as a result of damage to the tubules and degradation of the epithelial cells lining the tubules.
– Nuclei of the cells lining the tubules disappear or appear faint.
– The brush border of the proximal convoluted tubules is lost or reduced.
– The cells lining the tubules flatten, making the lining of the tubules appear thinner.
– Mitotic figures are present, indicating that the surviving cells are attempting to divide and regenerate the tubules.
As mentioned in a previous section, glomerulonephritis is an inflammatory response that targets the glomeruli and interferes with their function. In this case, glomerulonephritis was triggered by strep throat.
The following video outlines the histopathological findings of glomerulonephritis.
Histopathology of glomeruloneprhitis. DHPLC specimen PATH 425-049 presented by Lyz Boyd
Clinical context: The patient was a 10 year old child who had a strep throat infection, which is an infection with a bacteria called streptococcus. A couple of weeks later they developed fever, edema, headaches, and “smoky” urine. Their urine contained protein, red blood cells, and white blood cells and their blood contained excess urea, a metabolic waste product.
Pathology: In some cases, a streptococcus infection results in a misguided immune response that attacks the glomeruli of the kidneys, termed streptococcal glomerulonephritis.
– The tubules of the kidney have observable debris and damage, similar to the shock kidney.
– The glomeruli are hypercellular because they are filled with inflammatory cells that are impairing the function of the glomeruli.
– Some glomeruli demonstrate crescents, which are areas of scarring in response to the inflammatory damage; others have been entirely obliterated.
Histologically, the damage caused in AKI is quite dramatic. In shock kidney, blood is not perfusing the nephrons causing starvation and death of cells. As a result, the nephron tubules are filled with debris and/or blood with signs of nuclear activity (i.e. life in the cell) waning as cellular structures appear faint (e.g. nuclei) or diminished (e.g. loss of brush border in PCT, flattened cells). Similarly in glomerulonephritis, the damage to glomeruli by antibody complexes are evident in observable debris and damage in the nephrons. Glomeruli are hypercellular because they are filled with inflammatory cells in addition to the glomerular capillaries and blood. Taken together with the changes in gross anatomy, the damage to nephrons are serious.