Kidneys

Degenerations and infiltrations nephrosis.

Nephrosis: Non inflammatory renal lesions occur in kidney.

1. Cloudy swelling and hydropic degeneration of the renal tubular epithelium is seen with hypoxic or toxic effect (Fig 1).

2. Fatty change is seen in the epithelium of renal tubules (Fig 2).

3. Moreover amyloid infiltration are seen in the glomeruli and around the renal tubules (Fig 3 & 4).

4.Visceral gout is seen in birds and dogs (Figs 5& 6).

5. Moreover, glycogen infiltration and pigments as hemosiderosis, bile pigment, melanin, sulfonamides beside hemoglobin and myoglobin are seen (Fig 7).

Congenital and hereditary anomalies

Aplasia or agenesis

Aplasia or agenesis of one or both kidneys are reported. Absence of both kidneys is fatal and encountered only in fetus, newborn of still born animal.

Aplasia of one kidney results in compensatory hypertrophy of the remaining kidney. It is common in swine, dogs and cattle, but less common in cats, horse and others.

Renal hypoplasia Ectopic kidneys are misplaced from their normal sublumbar location by abnormal migration during fetal development.

Horseshoe kidney results from fusion of the anterior or posterior poles of the kidneys during nephrogenesis (Fig. 8).  

Cysts in kidney: Kidneys may contain single or multiple cysts (Fig 9)   . Polycystic kidneys occur sporadically in many species but can be inherited as an autosomal dominant lesion in pigs (Fig 10)   . Acquired renal cysts occur as a results of fibrosis

Figure 1: Kidney showing cloudy swelling of the renal epithelium. The lumen of some alveoli may be completely obliterated. H&E

Figure 2: Kidney showing fatty change. The fat stain black with Sudan black.

Figure 3: Kidney amyloidosis leading to enlarged pale kidney.

Figure 4: Renal amyloidosis showing pale Eosinophilic materials deposit under the endothelial lining of glomerular tuft. H&E

Figure 5: Microscopic picture of visceral gout characterized by precipitation of uric acid and urate in th renal tubules. Moreover, the renal epithelium showing necrosis and the gouty material surrounded with granuolomatous inflammation. H&E

Figure 6: Microscopic picture of visceral gout characterized by precipitation of uric acid and urate in th renal tubules. Moreover, the renal epithelium showing necrosis and the gouty material surrounded with granuolomatous inflammation. H&E

Figure 7: Hemoglobinuric nephrosis represented by dark black color kidneys.

Figure 8: Horseshoe results from fusion of the anterior or posterior poles.

Figure 9: Kidney showing congenital medullary cyst.

Figure 10: Kidney of pig showing polycystic kidney.

Circulatory Disturbances

Hyperemia or congestion may be active, passive or hypostatic (Fig11).

Hemorrhage. Renal cortical and medullary hemorrhages are associated with many septicemic diseases and result from vasculitis and vascular necrosis. Petechial hemorrhages are commonly seen on the surface and through the cortex of kidneys from infected with hog cholera, African swine fever or salmonellosis (Fig. 12).

Figure 12: Kidney showing extravagation of erythrocytes among renal tubules (hemorrhage). H&E.

Infarction.

Renal infarctions are areas of coagulative necrosis that results from the ischemia of vascular occlusion (Figs 13 &14).

Figure 13: Kidney showing red infarction. The renal epithelium showing coagulative necrosis. \moreover extravasations of erythrocytes are seen among renal tubules. H&E.

Figure 14: Kidney showing pale infarction represented by coagulative necrosis surrounded an infiltrated by inflammatory cells. H&E.

Nephritis

It is the inflammation of the kidneys. Nephritis can be classified according to:

1. Route of infection into:

a. Hematogenic descending..                 b. Urinogenic ascending..

2. Anatomically into:

a. Glomerulonephritis.                            b. Interstitial nephritis.

3. The type of exudate into:

a.  Suppurative nephritis which can be subdivided into embolic descending. nephritis, interstitial. nephritis and pyelonephritis ascending. nephritis.                                   

b. Non suppurative, which can be subdivided into glomerulonephritis Proliferative, membranous and membranoprolifrative. or Lymphatic interstitial. nephritis.

Glomerulonephritis

Etiology:

It may be toxic or antigenic reaction secondary to persistent tonsilitis, bronchitis, endocarditis, myocarditis, splenic abscess and pneumonia.

Microscopic picture Proliferative.:

The glomeruli are swollen, nearly a vascular and fill Bowman’s capsule. Numerous large endothelial and mesangial cells beside neutrophils increase the cellularity of the glomeruli acute. (Fig 15) . Deposits of immune complex are seen in the epithelial side of the basement membrane, within the lamina densa or in the sub endothelial portion of the basement membrane.

Later on subacute., the proliferated epithelium of the Bowman’s capsule adds to the glomerular hypercellularity, and adhesions between visceral and parietal layers with the formation of epithelial crescents. Such crescents persists during the chronic stage together with collapsed and hyalinized glomeruli.

Membranous glomerulonephritis:

Immunoglobulins G and A. are deposited on the glomerular basement membrane which is thickened (Fig. 16) . The podocytes lose their foot processes. Later on the glomeruli become hypercellular and bloodless. The glomerular space is rarely obliterated even in chronic stage without epithelial crescents or Membranoprolifrative glomerulonephritis

It is a combination of the lesions of both types with a marked increase in the mesangial cells and thickened basement membranes by deposition of immunoglobulins.

Macroscopic picture:

The kidneys, in acute form, are slightly swollen with petechial hemorrhage throughout the cortex acute.. Moreover, the kidneys in chronic glomerulonephritis appear gray, slightly smaller and firmer than normal with tiny cysts in the cortex small white granular contracted kidney.. Microscopically, some glomeruli are hyalinized (Fig. 17).

Figure 15: Kidney showing proliferative glomerulonephritis represented by swelling and   a vascular glomeruli which fill Bowman’s capsule. Numerous large endothelial and mesangial cells beside neutrophils increase the cellularity of the glomeruli. H&E

Figure 16: Kidney showing membranous glomerulonephritis characterize by thickened  basement

 and the podocytes lose their foot processes. Later on the glomeruli become hypercellular and bloodless. H&E

Figure 17: Kiney showing membrano-proliferative glomerulonephritis. Some glomeruli are hyalinizd. H&E

Acute non.suppurative interstitial nephritis lymphocytic.

Causes

 Many generalized infections particularly leptospirosis.

Macroscopically:

Increase in size, pale in color and soft. The capsule strips easily. Grayish streaks or foci at the corticomedullary junction.

Microscopically:

1. Numerous tiny foci of lymphocytes in the inner cortex between renal tubules beside few neutrophils may be present (Fig 18)

2. Cloudy swelling, fatty change and even necrosis may be seen in the renal tubules.

3. Casts frequently occlude the renal tubules.

Subacute non.suppurative interstitial nephritis white spotted kidney.

Causes:

1. It is usually follows the acute as in Leptospirosis.

2. It is usually associated with renal infection, pneumonia and enteritis in calves.

Macroscopically, the kidneys are slightly atrophic and firm in consistency. Moreover, large white or grayish nodular masses in the outer medulla (Fig 19).

Microscopically, the nodules composed from lymphocytes with macrophages and few fibrous tissues (Fig 20) . Some renal tubules showed cystic dilatation (Fig 21).

Figure 18: Acute lymphocytic nephritis represented by round cell infiltration between the renal tubules beside congestion of renal blood vessels. H&E.

Figure 19: Sub acute lymphocytic nephritis. the kidneys are slightly atrophic and firm in consistency. Moreover, large white or grayish nodular masses in the outer medulla

Figure 20: Sub acute lymphocytic interstitial nephritis showing aggregation of lymphocytes between renal tubules besides cystic dilatation of some renal tubules and few fibroblasts. H&E.

Figure 21: Sub acute lymphocytic interstitial nephritis showing aggregation of lymphocytes between renal tubules besides cystic dilatation of some renal tubules and few fibroblasts. H&E.

Chronic non suppurative interstitial nephritis

Causes:

After subacute form.

Macroscopically:

Small in size, firm in consistency, pale in color with irregular and nodular surface. The capsule is thickened and adherent to the under lying tissue (Fig 22).

Microscopically:

1. Irregular fibroblastic bands through cortex and medulla besides chronic inflammatory cells and cystic dilatation of some renal tubules (Fig 23).

2. Fibrosis replaces the renal parenchyma.

Figure 22: Chronic non suppurative interstitial nephritis showing small kidney, firm in consistency, pale in color with irregular and nodular surface. The capsule is thickened.

Figure 23: Chronic interstitial nephritis showing replacement of the renal tissue by fibrous connective tissue besides cystic dilatation of some renal tubules. H&E.

Suppurative nephritis

a. Pyemic or embolic suppurative nephritis

Causes:

Specific pyogenic infections as Shigilla equiruilis, Streptococcus, Escherichia coli and Corynebacterium pyogenes. Which reach the kidneys via the blood stream and rarely ascend through ureters ascending pyelonephritis..

Macroscopically:

1. Both kidneys are usually involved.

2. Kidneys are congested.

3. Irregular yellow or gray areas are seen under the surface of the capsule (Fig 24).

Microscopically:

1. Widespread infiltration of neutrophils in the intertubular spaces.

2. Liquifactive necrosis followed by fibrosis (Fig 25).

Figure 24: Kidneys showing embolic nephritis showing congestion and abscesses.

Figure 25: Kidney, showing microscopic picture of acute suppurative interstitial nephritis characterized by focal infiltration of renal parenchyma with neutrophils. H&E.

a. Pyelonephritis

Causes:

• Corynebacterium renalis.

• Infection usually enters through the lower urinary tract specially after parturition.

Macroscopically:

• One or both kidneys may be affected.

• Grayish white foci are seen on the renal surface.

• Cut surface shows sloughing and necrosis of the renal papillae.

Microscopically:

1. Neutrophils infiltrate the renal corpuscles and periglomerular tissue.

2. Neutrophils infiltrate papillae (Fig 26).

Figure 26: Kidney, pyelonephritis showing suppurative pylitis with necrosis of renal papillae. The suppurative inflammation extend into medulla. H&E

Neoplasms of kidneys

Primary tumors are rare e.g. embryonic nephromablastoma (Figs 27 & 28) and hypernephroma.

Figure 27: Kidney showing nephroblastoma. H&E.

Figure 28: Kidney showing nephroblastoma. H&E.

Secondary tumors of all kinds are seen in the kidneys specially malignant lymphoma.

 Hydronephrosis

It is a pathological stagnation of urine in renal pelvis which expanded gradually at the expense of renal parenchyma.

Causes:

Incomplete or intermittent obstruction of urine outflow.

Macroscopically:

• The early stage reveals a distention in the renal pelvis from the pressure of the retained urine then renal cortex, due to collapsed and disappearance of tubules, make kidney similar to a hallow sac (Fig 29).

• Cysts may be found in the medullary substance and communicate with pelvis.

Microscopically:

Atrophied renal tubular epithelium with collapsed glomeruli. Later on, renal corpuscles become hyalinized beside interstitial fibrosis and lymphocytic infiltration (Fig 30).

Figure 29: Kidney, gross picture of hydronephrosis.

Figure 30: Kidney, microscopic picture of hydronephrosis characterize by severe dilatation of renal tubules with interstitial fibrosis. H&E

Results:

1. The bilateral cases are usually fatal from uremia.

2. The unilateral cases the renal function is performed by the other kidney.

Urolithiasis

It is the formation of stony precipitate anywhere in the urinary passages. The stone is called urolith or urinary calculus. The calculi are most common in the bladder and called cystic calculi.

Types

The types of calculi are oxalate stone, uric acid calculi, phosphate calculi, xanthine stones, cystine stones and siliceous calculi.

Uremia

It is a pathological condition in which blood urea and harmful waste product, which are normally eliminated in the urine as uric acid and ammonia. remain in circulating blood, as a result of compete or partial failure of urinary excretion.

Signs

1. The animals not drink or eat.                       2. Vomiting.

3. Mucous membrane congested.                    4. Oligouria.

5. Skin dry rough and less elastic basal mucous membrane resulted in uremic stomatitis.

Lesions of uremia

1. Hyperemia of the mucous membrane.

2. Inflammation of the mucous membrane of the alimentary tract sometime with ulcer formation. Hemorrhagic gastritis and enteritis.

3. Dehydration and debility associated with lesion of alimentary tract.

4. Urinous bad odor in skin, the buccal cavity because the excretory function of the kidney diminish the other excretory organ take a part in excreting the urea as intestine, skin, sweat gland then uremia result.

5. Skin lesions as crust, eczyma and the animal is itching acute uremia can develop and this type exist 2.3 weeks after which the animal die or recovery.

6. Uremic arteriosclerosis lead to hypertension in uremic animal feels hard pulse the heart later hypertrophic due to over function specially in the left side, then decompensatory hypertrophy, cardiac insufficiency manifested by:

1. C.V.C.                                                     2. Edema.

3. Ascites.                                                    4. Hydropericardium.

5. Hydrothorax.                                            6. Edematous limb.

7. Ostermalacia:

Microscopic areas of calcification are frequent in the intema of the aorta and the other blood vessels, beneath the endocardium.

In dog, there is ulcer in tongue and gum called uremic ulcer.

Urea has irritating effect cause hyperemia in all internal organs. N prolonged uremia, toxic injury of the bone marrow may occur Toxic aplastic anemia.

Ureter

Inflammation: ureteritis may be a part of inflammation of the whole urinary tract.

Dilatation: in case of pyelonephritis.

Narrowing: may be congenital or inflammatory.

Urinary bladder

Inflammation Cystitis.

Caused by stagnation of urine or trauma by urolith. Bacteria are the usual direct cause.

Acute catarrhal, fibrinous, purulent of hemorrhagic cystitis may be seen (Fig 31 & 32).

Chronicity leads to irregular thickening of subepithelial connective tissue.

Torsion: partial or compete is uncommon.

Inversion: It is permitted through the short wide female urethra of large animals especially cow and mare. It is seen during straining or after parturition.

Rupture of bladder: It may be caused by occlusion of urethra, trauma or cystitis.

Neoplasms of bladder

Secondary tumors are rare.

Primary tumors are frequent.

Epithelial tumors are common either benign or malignant leiomyoma is recorded.

Urethra

.Atretic urethral opening is reported.

Urethritis is common in animals due to urolith and corynebacterium renale infection.

Obstruction of urethra by urinary calculi is frequent in sigmoid flexure of steers and sheep.

Figure 31: urinary bladder showing hemorrhagic cystitis.

Figure 32: Urinary bladder showing chronic catarrhal cystitis.