صور باثولوجى : Pathology Slides : Kidney Patholoy

Pathology Slides :  Kidney Patholoy

 

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Depending on the affected segment, non-tumor nephropathies can be divided into : glomerular and tubulo-interstitial nephropaties.

Primary glomerulonephritis :
acute diffuse proliferative glomerulonephritis (nephritic syndrome)

rapidly progressive (crescentic) glomerulonephritis

lipoid nephrosis (minimal change disease) (nephrotic syndrome)

membranous glomerulonephritis (membranous nephropathy) (nephrotic syndrome)

membranoproliferative glomerulonephritis (nephrotic syndrome)

focal segmental glomerulosclerosis (nephrotic syndrome)

IgA nephropathy (Berger's disease)

chronic glomerulonephritis

Secondary glomerulonephritis may appear during some systemic diseases, such as: systemic lupus erythematosus, diabetes mellitus, amyloidosis, Goodpasture's syndrome, polyarteritis nodosa, Wegener's granulomatosis, Henoch-Schonlein purpura, bacterial endocarditis.

Tubulo-intestitial nephropaties are represented by : acute tubular necrosis (nephrotoxic or ischemic), inflammatory lesions of the tubules and interstitium (acute and chronic pyelonephritis, interstitial nephritis, including drug-induced interstitial nephritis).

Renal tumors are : benign (cortical adenoma, fibroma, angiomyolipoma, oncocytoma, urothelial papilloma) and malignant (renal cell carcinoma - Grawitz tumor, nephroblastoma - Wilms' tumor, urothelial carcinoma, sarcomas).

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Poststreptococcal acute diffuse proliferative glomerulonephritis

Acute postinfectious (poststreptococcal) diffuse proliferative glomerulonephritis is a primary glomerulonephritis, which produces nephritic syndrome (hematuria, oliguria, uremia, hypertension and mild proteinuria).

• "Acute" - because it occurs 2 weeks after a streptococcal (group A beta-hemolytic) pharyngitis. It becomes chronic only in 10 - 15 % of cases, especially in adults.
• "Diffuse" - because almost all the glomeruli are affected (about 80 %).
• "Proliferative" - due to proliferation of endothelial cells and mesangial cells.

The mechanism of poststreptococcal acute diffuse proliferative glomerulonephritis is immune : granular deposits of IgG and C3 ("humps") on the external (subepithelial) side of the basement glomerular membrane. These humps can be seen in electron microscopy and immunofluorescence microscopy.

Acute postinfectious diffuse proliferative glomerulonephritis. Almost all glomeruli are enlarged (hypercellular) due to proliferation of endothelial cells and mesangial cells, swelling of endothelial cells and inflammatory infiltrate (neutrophils and monocytes). This will result in compression of capillaries and Bowman space, which is reduced in size. Initially, tubules are not affected, but with evolution, they may present hydropic change. (H&E, ob. x10)

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Rapidly progressive ("crescentic") glomerulonephritis

Rapidly progressive ("crescentic") glomerulonephritis is a primary glomerulonephritis, which produces nephritic syndrome (hematuria, oliguria, uremia, hypertension and mild proteinuria). The prognosis is severe, with rapid and irreversible evolution to renal failure.

Etiology of rapidly progressive crescentic glomerulonephritis : streptococcal infection, systemic lupus, vasculitis, Goodpasture's syndrome, idiopathic.

Rapidly progressive ("crescentic") glomerulonephritis - the majority of glomeruli present "crescents". Formation of crescents is initiated by passage of fibrin into the Bowman space as a result of increased permeability of glomerular basement membrane. Fibrin stimulates the proliferation of parietal cells of Bowman capsule, and an influx of monocytes. Rapid growing and fibrosis of crescents compresses the capillary loops and decreases the Bowman space which leads to renal failure within weeks or months. (H&E, ob. x20)

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Chronic glomerulonephritis

Chronic glomerulonephritis represents the end-stage of all glomerulonephritis with unfavorable evolution. This general (glomerular, vascular and interstitial) affection constitutes the so-called "end stage kidney". In most cases, it is associated with systemic hypertension.

Chronic glomerulonephritis. The majority of the glomeruli are affected. Depending on the stage of the disease, they may present different degrees of hyalinization (hyalinosclerosis - total replacement of glomeruli and Bowmann's space with hyaline). The hyaline is an amorphous material, pink, homogenous, resulted from combination of plasma proteins, increased mesangial matrix and collagen. Totally hyalinised glomeruli are atrophic (smaller), lacking capillaries, hence these glomeruli are non-functional. Few glomeruli may still present changes which permit to discern the etiology of chronic glomerulonephritis. Obstruction of blood flow will produce secondary tubular atrophy, interstitial fibrosis and thickening of the arterial wall by hyaline deposits. In the interstitium is present an abundant inflammatory infiltrate (mostly with lymphocytes). (Hematoxylin-eosine, ob. x20)

Chronic glomerulonephritis. Functional nephrons have dilated tubules, often with hyaline casts in the lumens. (Hematoxylin-eosine, ob. x20)

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Diabetic glomerulosclerosis

In diabetes, basement membranes of majority of capillaries in the body are thickened by deposits of nonenzymatic glycosilated proteins (diabetic microangiopathy): retinopathy, coronary arteries, and peripheral vessels.
In kidney, diabetic nephropathy includes : diabetic glomerulosclerosis, arteriolosclerosis and papillary necrosis, with an increased risk for pyelonephritis.

Diabetic glomerulosclerosis is characterized by thickening of glomerular basement membrane with increased permeability. With time, the mesangial space becomes larger by deposits of proteins (collagen IV), initially diffuse, then nodular.

Diffuse diabetic glomerulosclerosis. The deposits appear diffusely on the basement membranes of capillary loops of the glomeruli, as well as on basement membranes of tubules and arterioles. (PAS, ob. x40)

In nodular diabetic glomerulosclerosis, PAS-positive nodular deposits (containing mucopolysaccharides, fibrils and collagen) may appear in the mesangial space, at the periphery of the glomerulus, pushing the capillaries. The lesion is focal (glomeruli are not entirely affected), and some of them are spared. This pattern is also called Kimmelstiel-Wilson lesion. (PAS, ob. x20)

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Amyloidosis (kidney)

Amyloid (an abnormal protein) accumulates as extra-cellular deposits, nodular or diffuse, as pink, amorphous material. Initially, the deposits appear in the glomeruli: within the mesangial matrix and along the basement membranes of the capillary loops. Continuous accumulation of the amyloid will compress and obliterate the capillary tuft. With progression, amyloid deposits appear also peritubular and within the arteriolar wall, narrowing them. Congo red is a special staining, elective for amyloid. (Congo Red, ob. x20)

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Toxic tubular necrosis

Acute tubular necrosis is a pathological entity characterized by destruction of tubular epithelial cells, followed by acute renal failure (oliguria, proteinuria, blood retention of urea and creatinine).

Depending on etiology, there are two types of acute tubular necrosis :

• toxic acute tubular necrosis, after ingestion or inhalation of toxic substance ethylene glycol, mercury, lead, carbon tetrachloride, methyl alcohol, nephrotoxic drugs
• ischemic acute tubular necrosis - in shock

Toxic acute tubular necrosis is characterized by proximal tubular epithelium necrosis (no nuclei, intense eosinophilic homogenous cytoplasm, but preserved shape) due to interference of ingested toxic agents (poisons, organic solvents, drugs, heavy metals) with epithelial cell metabolism. Necrotic cells fall into the tubule lumen, obliterating it, and determining acute renal failure (oligo-anuria). Basement membrane is intact, so the tubular epithelium regeneration is possible, if the patient survives. The interstitium and glomeruli are not affected. (H&E, ob. x20)

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Acute pyelonephritis

Acute pyelonephritis is an exudative purulent localized inflammation of kidney and renal pelvis. The renal parenchyma presents in the interstitium abscesses (suppurative necrosis), consisting in purulent exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils). Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, glomeruli and vessels are normal. (Hematoxylin-eosine, ob. x10)

Acute pyelonephritis (Hematoxylin-eosine, ob. x10)

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Nephroblastoma (Wilms' Tumor)

Wilms' tumor (nephroblastoma) is a malignant mixed tumor containing metanephric blastema, stromal and epithelial derivatives. It is the most frequent renal tumor in children before age of 5 years (peak of incidence: 2 year-old).

Etiology of Wilms' tumor (nephroblastoma) : mutations of WT1 gene on chromosome 11 and nephroblastematosis (persistence of renal blastema in kidney tissue).

Wilms' tumor (nephroblastoma). The tumor consists in tumor epithelial component (abortive tubules and glomeruli) surrounded by metanephric blastema and tumor immature spindled cell stroma. The stroma may include differentiated (muscle, cartilage, bone, fat tissue, fibrous tissue) or anaplastic elements. The tumor (photo, left) compresses the normal kidney parenchyma ( photo, right) (H&E, ob. x10)

Nephroblastoma (Wilms' Tumor) (detail)

Wilms' tumor (nephroblastoma) : metanephric blastema, stromal and epithelial components. (H&E, ob. x20)

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Renal cell carcinoma (Grawitz tumor)

Renal clear cell carcinoma (Grawitz tumor) is a malignant epithelial tumor resulted from proliferation of tubule cells. Tumor cells form cords, papillae, tubules or nests, and are atypical, polygonal and large. Because these cells accumulate glycogen and lipids, their cytoplasm appears "clear", lipid-laden, the nuclei remain in the middle of the cells, and the cellular membrane is evident. Some cells may be smaller, with eosinophilic cytoplasm, resembling normal tubular cells. The stroma is reduced, but well vascularized. The tumor grows in large front, compressing the surrounding parenchyma, producing a pseudocapsule. (H&E, ob. x20)

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