By Guenevere Rae, Ph.D., William Newman, M.D., Supriya Donthamsetty, M.D., Robin McGoey, M.D.

Transcription

1 The Cadaver s Kidney P.G. Pathology Guide By Guenevere Rae, Ph.D., William Newman, M.D., Supriya Donthamsetty, M.D., Robin McGoey, M.D. There are many aspects of kidney pathology that are evident via gross inspec6on. Use the following protocol as a guide for gross examina6on of the cadaver s kidneys. The size and weight The normal weight of the kidney is g for men and g for females. Kidneys above or below those values have a higher likelihood that a disease process is present in the affected organ. The nature of the disease process may be determined by the organ s other gross and microscopic characterisdcs. 1A 1B Figure 1- A- normal bean shaped kidney. 1b- The altered shape of a kidney with metasta6c cancer and scarred cortex. The Shape of the Organ The kidney is generally a bean shaped organ. However, several condidons such as neoplasms, pyelonephrids and hypertension can cause an irregularity in the overall shape of the kidney. The amount of funcdonal parenchyma is more indicadve of whether the person had any loss of renal funcdon than is the overall shape of the organ. 1

2 The surface features The smoothness of the surface The normal kidney has a smooth, shiny outer cortex (Fig. 2A). If the surface is not smooth, then it usually has either a fine granularity or more irregular deep piong. The presence of a fine granular surface, called nephrosclerosis (Figure 2B), is associated with arteriolosclerosis and glomerulosclerosis. These condidons occur with clinical essendal hypertension. More irregular, deep pit on the surface is suggesdve of cordcal scarring commonly seen in cases of chronic pyelonephrids (Fig. 2C). 2A 2B 2C Figure 2- A- normal smooth surface, B- fine granular surface seen in nephrosclerosis, C- deep pieng of the cor6cal surface. Fine granular surface (nephrosclerosis) The gross finding of diffuse, bilateral nephrosclerosis (figure 2B) is associated with the histologic features of both arteriolosclerosis and glomerulosclerosis. Most commonly, taken together these findings suggest essendal hypertension. 1 Arteriolosclerosis (figure 3B) is a disease process that can affect any organ of the body, but frequently is seen in the kidney. Due to the anatomic importance of the afferent and efferent arterioles that service the glomeruli, there are many changes in the kidney that ensue due to this disease process. Any cause of endothelial damage can cause changes in the structure of the arteriolar wall. HyalinizaDon is one way in which arterioles can change over Dme, even with the normal aging process. During the process of hyalinosis, deposits of proteins (specifically ic3b) get deposited in the walls of the arterioles of the kidney (Figure 3B). Some disease processes, such as hypertension and diabetes, increase the rate of protein accumuladon to accelerate the arteriolosclerosis. The numerous hyaline deposits can affect the flow of blood through the lumen of the vessel. 2

3 Glomerulosclerosis is a glomerular alteradon that involves scarring of structures contained in the glomerulus. The scars are mostly made of collagen fibers but can also include proteins or hyaline. Many forms of renal injury to the tubules, glomeruli and blood vessels can cause scarring of the glomeruli, and the glomeruli can be affected segmentally or globally (Figure 3C). Sclerosis of the glomerulus can constrict the capillaries within this fragile structure, leading to decreased glomerular filtraDon rate (GFR). The other glomeruli that are not affected in the kidney can enlarge to compensate for the loss of funcdonal nephrons and, therefore, have increased GFR. There are different types of glomerulosclerosis according to the pa[ern of scarring and the content of the accumulated material. For example, diabedc individuals are more likely to exhibit with patchy or nodular appearing accumuladons of hyaline within the mesangial matrix of the glomerulus (Figure 3D). 3A 3B 3C 3D Figure 3- A= Histologic appearance of normal glomeruli. B- arteriosclerosis in a afferent/efferent arteriole, characteried by concentric onion skinning and thickening of the vascular layers (arrow). C- global glomerulosclerosis, D- nodular glomerulosclerosis as seen in diabe6c nephropathy (arrows). 3

4 Deep pits or corecal scars Deep pifng of the corecal surface (or corecal scars) is associated with chronic pyelonephries. Chronic PyelonephriEs is a disorder that typically involves tubulointersddal inflammadon as a result of chronic infecdon. The invading microbes usually originate from the distal urinary tract with retrograde reflux into the kidney tubules and intersddum. Chronic pyelonephrids is one of the few tubulointersddal diseases that cause damage to the calyces. Grossly, chronic pyelonephrids can produce dilated, blunted or deformed calyces and renal papillae that appear blunted or fla[ened. Also, the kidney can have a dilated pelvis (4B). Histologically, chronic pyelonephrids is associated with glomerulosclerosis, infiltradon of the renal intersddum by lymphocytes and plasma cells and thyroidizadon of tubules (4C). Regardless of the cause, chronic pyelonephrids can lead to end stage kidney disease. 4A 4B 4C Figure 4A- C- A- The gross presenta6on of chronic pyelonephri6s with deep broad cor6cal scars, B- a dilated pelvis in a kidney with chronic pyelonephri6s, C- The histologic presenta6on of chronic pyelonephri6s showing focal regions of: lymphocytes (blue arrow), glomerulosclerosis (red arrow) and thyroidiza6on of tubules(yellow arrow). 4

5 The inner features CorEcal (outer) pallor with medullary inner redness The inner features of a kidney can be assessed a\er the organ is halved. The usual approach is via a linear cut in the verdcal axis aiming from the lateral surface towards the renal hilum. Halving the kidney this way permits inspecdon of the outer rim of cortex, the underlying medulla and the innermost calyceal system. A bright red medullary parenchyma with a diffusely pale cortex may be an indicadon of acute kidney injury (AKI). Acute kidney injury (AKI) is an acute condidon that involves damage to the tubules of the kidney. Usually, the kidneys swell and reach weights above normal in a process called nephromegaly. The damage usually occurs due to reduced blood flow such as that which occurs in cases of shock or hemorrhage. There has been a marked increase in drug related AKI in recent years, pardcularly in individuals >65 years of age. Non- steroidal and- inflammatory drugs, andbiodcs and proton pump inhibitors are frequent insuldng agents leading to AKI. The tubules are pardcularly suscepdble to injury due to ischemia and toxins and, therefore, demonstrate acute tubular necrosis (ATN) histopathologically. ATN is characterized by epithelial sloughing into the tubule lumen and a peripheral surrounding cle\ where the epithelium separates from the tubular basement membrane. The gross features and corresponding histology are seen below in figures 5A- 5C. 5A 5B 5C Figure 5- A- B- These sec6oned kidneys have areas of bright red parenchyma (primarily medullary). These lesions may be an indica6on of AKI or chronic inters66al nephri6s, C- Epithelial necrosis of the proximal convoluted tubule including the peripheral cler between the epithelium and the basement membrane (arrows). 5

6 Hard lesions Like in other organs, hard lesions are o\en neoplasms (or tumors). In the kidney, neoplasms can be primary or metastadc and benign or malignant. AddiDonally, the outer surface of the kidney may be grossly distorted and the surface may appear pale due to the obstrucdon of blood to the cordcal surface caused by invading tumor cells (Figure 6). 6A 6B Figure 6- The gross (A) and histologic (B) appearance of a metasta6c tumor in a sec6oned kidney (pancrea6c adenocarcinoma). The yellow outline highlights the palpable mass within the organ. Kidney Stones Nephrolithiasis is the presence of renal calcificadons (kidney stones) which is a common occurrence (Figure 7A). The generadon of a stone begins with the linking of salts to form a crystalline nucleus. Most of the lithiases of the kidney are formed by calcium oxalate. The main concern regarding nephrolithiasis is obstrucdon of the urinary flow and progression into a chronic kidney condidon. Stones are more prevalent in individuals suffering from other diseases such as: hypertension, diabetes and cardiac disease. 7A 7B Figure 7- A- the gross appearance of kidney stones. B- The histologic appearance of coarse calcium deposits in the kidney tubules as a result of chronic injury (arrow). 6

7 ArEfacts of the Embalming Process Small dark vessels on the outside The appearance of small dark vessels on the outside of the kidney may be an ardfact of the embalming process and not necessarily related to any pardcular pathologic process (Figure 8). These spiderweb- like vessels may be more pronounced in kidneys with a fine granular cordcal surface (see smoothness of the surface). 8A 8B Figure 8- A&B- The gross appearance of the spiderweb- like vessels on the outside of the kidney. These dark lines are ardfacts of the embalming process. 9A Red discoloraeons within the parenchyma or a speckled- looking cortex The parenchyma may have dark red splotches or a speckled appearance intermingled with areas of normal looking cortex. These discoloradons are most likely ardfacts of the embalming process but may be more pronounced in kidneys with arteriolosclerosis. The sclerodc vessels may have prohibited the embalming fluid from penetradng the endre organ and, therefore, these areas may represent focal regions of autolysis. 9B 9C Figure 9- A&C Red discoloradons within the parenchyma of a secdoned kidney (arrows). Note that the consistency is similar to the consistency of the surrounding Dssue.

8 Other non- pathologic gross characterisecs Cysts Simple cysts can be visible on the outside of the kidney or within the parenchyma of the organ itself (Figure 10). These cysts may be filled with fluid, gel- like colloid or even blood. They are not correlated with any pardcular pathologic process and most likely they did not impair renal funcdon in the individual. In contrast, polycysdc kidney disease is a common condidon that affects 1 out of every births. In this condidon most of the parenchyma consists of innumerable cysts and barely and residual architecture. This type of cysdc kidney disease is always bilateral and does significantly impair renal funcdon. The difference in the gross appearance of simple cysts versus polycysdc kidney disease is very nodceable. 10A 10B 10C Figure 10- A- B- examples of simple cysts (arrows); C- fetal polycys6c kidney. Fetal lobulaeons Fetal lobuladons of the kidney are a normal variant in the adult kidney and are a result of incomplete fusion of the renal lobules (figures 11A- C). This common characterisdc is not a sign of any pathologic process. 11A 11B 11C Figure 11A- C- Fetal lobuladons on the cordcal surface of the kidney. 8

9 References and Suggested Readings Cooke, R., Stewart, B. (2004). Colour atlas of anatomical pathology. Philadelphia, PA.: Saunders Elsevier. Kumar, V., Abbas, A., Fausto, N., Aster, J. (2010). Robbins and Cotran pathologic basis of disease, eighth edidon. Philadelphia, PA.: Saunders Elsevier. Riede, U.- N., Werner, M. (2004). Color atlas of anatomic pathology. New York: Thieme. 9